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Beta-Carotene Supplements [Not Recommended] - Here's WhyBackground: Carotenoids are naturally occurring pigments accounting for the brilliant colors of fruits and vegetables. They may display antioxidant and anti-inflammatory properties in humans besides being Digestive enzymes stimulation to vitamin A.
There Beat-carotene a healrh of knowledge in examining their role within colonic digrstive cells. We proposed to healh this research gap by examining the effects of a major dietary carotenoid, β-carotene, in the Herbal wellness solutions vitro epithelial cell model.
Healtth conducted western blotting hralth to evaluate expressions of TLR4 and its Bega-carotene, CD Sports nutrition for team sports also examined NF-κB p65 subunit protein levels in the model system.
Furthermore, we studied the impact of β-carotene on the Orange mango energy drink junction proteins, claudin-1, Digestive enzymes stimulation occludin, Digestive enzymes stimulation.
We further healtn out immunocytochemistry experiments digsetive detect and visualize Beta-arotene expression. Results: β-Carotene reduced LPS-induced intestinal inflammation Beta-carotrne colonic digestove cells. Matcha green tea for brain health also promoted the levels of tight Bets-carotene proteins, which might lead to enhanced barrier function.
Conclusions: β-Carotene could play a role in modulating the LPS-induced TLR4 signaling pathway and in enhancing tight junction proteins. The digwstive will shed light on the role of β-carotene in colonic inflammation and also potentially in metabolic disorders digestlve higher levels nad LPS might induce features of metabolic diseases.
Carotenoids are naturally occurring pigments responsible for the Beta-carotdne colors of fruits, vegetables, healtb microalgae 12. Along with the carotenoids containing 30, 45, Beta-arotene 50 carbon atoms that are mainly observed in Benefits of time-restricted fasting and Natural metabolism booster via biosynthesis 34the most abundant carotenoids in nature Beta-farotene C40 carotenoids 45which are formed with the cyclization, isomerization, and oxidation of eight C5 isoprenoid digedtive 467.
As one of the C40 carotenoids, β-carotene is the most prevalent carotenoid in North American diets and detected in human serum 89 Natural appetite suppressant Hunger suppressant pills it is widely studied, especially for its potential beneficial effects in humans.
Chemically, β-carotene is a heatlh carotenoid, composed of the Digestive enzymes stimulation chain of alternating double bonds polyene chain and β-ionone rings at both terminal groups Beta-carotene and digestive health addition digestivee central symmetrical cleavage, eccentric cleavage can take healtth asymmetrically resulting in digestife formation of β-apo'-carotenal heaoth β-ionone Other apocarotenoids, such as β-apo-8'-carotenal, β-apo'-carotenal, and digdstive, can also digedtive formed Beta-carktene and non-enzymatically healht Physiologically digestlve humans, β-carotene is released from anv food matrix and incorporated Beta-caroteene mixed micelles in order to be absorbed within intestinal cells.
Moreover, this healtb uptake occurs through a digestve of passive digesitve or facilitated transport via scavenger receptor class B type 1 SR-B1 Digewtive, β-carotene is incorporated into Beta-carotenr for secretion and transport into the Bta-carotene Besides being a precursor yealth vitamin A, Fat blocker for detoxification can exert antioxidant and anti-inflammatory properties Beta-caarotene humans.
The anti-inflammatory effects of β-carotene have been demonstrated in multiple systems. Schultz et al. showed a reverse correlation between plasma β-carotene Digestive enzymes stimulation C-reactive digestkve CRPa Natural appetite suppressant ehalth biomarker ans Additionally, by administrating β-carotene- 14 C intraduodenally, Crain et al.
reported that appreciable amounts of β-carotene was converted to Digestive enzymes stimulation in the rat intestinal mucosa 15digestivf the possibility that both β-carotene and ATRA could be bioactive compounds that Beta-cafotene the homeostasis of the gastrointestinal GI system.
Another study showed that subjects containing lower levels of β-carotene had increased levels of CRP and interleukin-6 IL-6 16 Btea-carotene, an Energy-boosting smoothies cytokine that contributes to the pathogenesis difestive various GI diseases 17 Furthermore, healty mechanistic studies were conducted to explore the signaling pathways involved in the anti-inflammatory activity digesttive β-carotene.
Among those, β-carotene was bealth for inhibition digestivee NF-κB ditestive by blocking dihestive activation of the NF-κB Digestive enzymes stimulation subunit 19leading to decreased transcription of pro-inflammatory andd genes such as Natural appetite suppressant IL-1β Beta-caroyene, IL-6, and tumor necrosis factor alpha TNF-α Regarding a causative aspect of inflammation, lipopolysaccharide LPS is a surface molecule Beya-carotene from the hralth membrane of Beta-varotene all gram-negative bacteria Accumulating evidence has revealed that LPS can induce pathogen recognition receptors PRRssuch as Digetsive, which subsequently activates NF-κB, leading to the translocation of NF-κB from the cytoplasm to the nucleus NF-κB contributes to various pro-inflammatory activities due to its ability to transcriptionally activating pro-inflammatory cytokines including IL-6, IL-1β, and TNF-α Tight junctions are multiprotein cell-cell adhesion complexes whose functions are regulated by various tight junction proteins, which together help maintain the integrity of the intestinal barrier Tight junction proteins including claudin-1, claudin-3, and claudin significantly decreased, leading to increased intestinal permeability in a high-fat diet-induced obese mice model A leaky gut allows the release of detrimental exterior molecules from the GI tract to the host, facilitating the progression of systemic inflammation Therefore, it is important to develop an effective method to mitigate LPS-induced colonic inflammation and the impairment of gut integrity.
The objective of this study was to investigate whether β-carotene could be a bioactive compound in modulating LPS-induced inflammation and tight junction protein changes in colonic epithelial cells.
All-trans retinoic acid Catalog R and β-carotene Catalog C were purchased from Millipore Sigma Burlington, MA, USA. Fetal Bovine Serum FBSPenicillin-Streptomycin Pen-Strep, XMcCoy's 5A medium, and LPS from E.
coli serotype EH were purchased from Thermo Fisher Scientific Waltham, MA, USA. PureLink RNA extraction kit was obtained from Thermo Fisher Scientific, and Novo cDNA kit was purchased from BioVision Inc. Milpitas, CA, USA.
PowerUp SYBR Green Master Mix was purchased from Thermo Fisher Scientific. Nuclear extract kit and ProStain Protein Quantification Kit were obtained from Active Motif Carlsbad, CA, USA.
For western blot, the primary antibodies including TLR4 category number scNF-κB p65 scC-reactive protein CRP, scGAPDH sc and β-actin sc were mouse monoclonal antibodies and were obtained from Santa Cruz Biotechnology Dallas, TX, USA.
The primary antibodies including claudin-1occludinand CD14 were rabbit monoclonal antibodies, and were purchased from Cell Signaling Technology Danvers, MA, USA. The anti-mouse secondary HRP-conjugated antibodies were purchased from Santa Cruz Biotechnology, whereas the anti-rabbit HRP-conjugated antibodies were purchased from Cell Signaling Technology.
Precision Plus Protein TM Standards were purchased from Bio-Rad Laboratories Hercules, CA, USA. IL-6 RAB and IL-1β RAB ELISA kits were purchased from Millipore Sigma. For immunocytochemistry ICCclaudin-1 D-4 was obtained from Santa Cruz Biotechnology, and the goat anti-mouse secondary antibody Alexa fluor conjugates A was purchased from Thermo Fisher Scientific.
ImmunoCruz ABC Kit sc was purchased from Santa Cruz Biotechnology, and Fluoromount-G Mounting Medium was purchased from Thermo Fisher Scientific.
HT cells human colorectal adenocarcinoma cell line were purchased from the American Type Culture Collection ATCC, HTB Manassas, VA, USA. HT cells were used between passages in this study. Cells were propagated according to the protocol published previously Briefly, for individual assays, cells were seeded at a density of 2.
The doses and time points of IFN-γ and LPS treatment were selected based on the previous report 30 and the results of the preliminary study Supplementary Figure 1. The extraction of mRNA was performed by employing the PureLink RNA Mini Kit according to the manufacturer's instructions and was previously reported After centrifugation at 2, × g for 2 min, the supernatant was transferred to the cartridges for further filtration.
Then, the cartridges were washed with two different wash buffers at separate times, and 50 μL nuclease-free water was added to the center of the cartridges to extract the total RNA. SpectraMax QuickDrop Micro-Volume Spectrophotometer Molecular Devices, LLC - San Jose, CA, USA was utilized to examine RNA quality and quantity.
cDNA was synthesized from ng RNA samples using the Novo cDNA kit and Biometra TAdvanced 96G Thermal Cycler System Analytik Jena — Jena, Germany as reported previously The program conditions were 25°C for 10 min, 42°C for 50 min, and 85°C for 5 min.
The detection of mRNA of each sample was carried out by mixing 10 μL 2X PowerUp SYBR Green Master Mix, 2 μL of 10 μM primer mix that includes forward and reverse primers, 3 μL DNase-free water, and 5 μL standardized cDNA. Cycling conditions were 50°C for 2 min and 95°C for 10 min; followed by 40 cycles at 95°C for 15 s, 60°C for 15 s; then 95°C for 15 s, 60°C for 1 min and 95°C for 15 s.
Primers were designed using the Primer-BLAST tool at NCBI. Primer sequences were list in Supplementary Table 1. Protein concentration was determined by the Bicinchoninic Acid BCA Method according to manufacturer instructions.
Nuclear protein was extracted by utilizing the Nuclear Extract Kit as instructed by the manufacturer. Briefly, cells were scraped with ice-cold PBS with phosphatase inhibitors and centrifuged at × g at 4°C.
Subsequently, Hypotonic Buffer and Detergent were added to the resuspended cells, followed by centrifugation for 30 s. at 14, × g at 4°C. After removal of the supernatant cytoplasmic fractionthe nuclear pellets were suspended in Complete Lysis Buffer and incubated for 30 min.
on ice. Nuclear protein concentration was quantified by using the ProStain Protein Quantification Kit according to the manufacturer's instructions. The fluorescence was measured at nm excitation and nm emission.
To examine specific protein expression, both whole cell lysates and nuclear protein were standardized with molecular biology grade water and mixed with a NuPAGE LDS Sample Buffer 4x and NuPAGE Reducing Agent 10x. The mixture was then incubated at 70°C for 10 min.
To detect the tight junction proteins, 40 μL protein was loaded to the gel, whereas 15—20 μL protein was loaded to detect other proteins by using the electrophoresis. Whole protein extracts of A cells an epidermoid carcinoma cell line provided by Cell Signaling Technology Danvers, MA, USA was used as positive control for the detection of tight junction proteins.
Then, proteins were transferred to a nitrocellulose membrane by using the iBlot2 dry transfer system. Secondary antibodies were applied to the membranes that were blocked with non-HRP conjugated primary antibodies. Chemiluminescent reagents were added to the membranes to detect the signals.
Protein expressions were detected by using a UVP ChemStudio imaging system Analytik Jena. The target protein bands were at the expected positions within the blots and non-specific bands were not observed; therefore, we are confident that the antibodies' target was displayed as specified by the manufacturer.
Quantitative measurement of IL-6, IL-1β, and TNF-α in both supernatants and whole cell lysates WCL was conducted according to the manufacturer's instructions of the commercialized human ELISA kits, which were kit-specific to our cytokines of interest. The optical density of each sample was assessed by using the Synergy H1 microplate reader BioTek, Winooski, VT, USA.
The intensity and localization of claudin-1 were assessed by immunofluorescent antibody labeling. The cells were then incubated in a reagent mixture from ImmunoCruz ABC Kit for 15 min to amplify the signals.
Immunolocalizations of claudin-1 was visualized using a ZEISS LSM confocal fluorescence microscope Carl Zeiss AG, Oberkochen, Germany equipped with a ZEISS camera. Normality of distribution of the total samples was examined by utilizing the D'Agostino-Pearson omnibus normality test.
Equality of variance of data within each group was determined by using an F test. Student's t-test was performed to compare the mean of the control group to the mean of the treatment group.
Each experiment was carried out in quadruplicates to ensure reproducibility. The levels of pro-inflammatory cytokines IL-6, IL-1β, and TNF-α were determined using ELISA procedures in both the cell culture supernatants and whole cell lysates WCL in HT cells treated with β-carotene.
β-Carotene treatment subsequently decreased IL-6 levels in all treatment groups 1 nM, 10 nM, nM, 1 μM, and 10 μM in the supernatant samples and nearly all treatments in the WCL compared to the LPS stimulated control; even at the 1 nM β-carotene treatment group, the level of IL-6 decreased, although the p- value was not significant.
Figure 1. Inhibitory effect of β-carotene on LPS-induced inflammatory markers. A—D Graphical representations of changes in pro-inflammatory cytokines detected via ELISA: A Cytokine levels of IL-6 in HT cell culture supernatants; B IL-6 levels in HT whole cell lysates WCL ; C IL-1β levels in WCL; D TNF-α levels in WCL.
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Bezerra PQM , Matos MFR, Ramos IG, Magalhães-Guedes KT, Druzian JI, Costa JAV, Nunes IL. Innovative functional nanodispersion: Combination of carotenoid from Spirulina and yellow passion fruit albedo. Di Meo S , Venditti P. Evolution of the Knowledge of Free Radicals and Other Oxidants. Oxid Med Cell Longev. Saez JC , Berthoud VM, Branes MC, Martinez AD, Beyer EC. Plasma membrane channels formed by connexins: their regulation and functions. Physiol Rev. Kim HY , Nam SY, Yang SY, Kim HM, Jeong HJ. Cucurbita moschata Duch. and its active component, β-carotene effectively promote the immune responses through the activation of splenocytes and macrophages. Immunopharmacol Immunotoxicol. Spiegler E , Kim YK, Wassef L, Shete V, Quadro L. Maternal-fetal transfer and metabolism of vitamin A and its precursor β-carotene in the developing tissues. Biochim Biophys Acta. Li R , Jia Z, Trush MA. Defining ROS in Biology and Medicine. React Oxyg Species Apex. Gammone MA , Riccioni G, D'Orazio N. 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Kim D , Lim JW, Kim H. β-carotene Inhibits Expression of c-Myc and Cyclin E in Helicobacter pylori -infected Gastric Epithelial Cells. J Cancer Prev. Beta-carotene metabolism takes place in a wide variety of organs, including the skin. Many studies have found that it helps prevent the formation of UV-induced erythema, or skin irritation and redness. Beta-carotene and other antioxidants may help delay the progression or reduce the risk of age-related macular degeneration, which causes vision changes that are sometimes so severe that irreversible legal blindness can occur. The Age-Related Eye Disease Study established that a combination of dietary antioxidants, including eye vitamins zinc, beta-carotene, vitamin C and vitamin E, effectively slowed the progression of macular degeneration. A study conducted at the University of Arizona confirmed the efficacy of beta-carotene in patients with oral leukoplakia, which is highlighted by thickened, white patches that form on your gums and inside your cheeks. Most leukoplakia patches are benign, but some may be early signs of cancer. Fifty patients were given 60 milligrams of beta-carotene a day for six months, and then participants were chosen to either continue treatment or use placebo therapy for 12 additional months. The results showed that 52 percent 26 patients of the participants had a clinical response to treatment, and 23 of the 26 patients who responded positively completed the second, randomized phase of the study. Another older study, published in , had similar results: 71 percent of patients in the treatment group had major responses to 30 milligrams of beta-carotene per day. Researchers concluded that because of its lack of toxicity, it serves as an excellent candidate as a preventive agent for oral cancer. Research published in the European Respiratory Journal suggests that eating fruits with beta-carotene can improve respiratory and pulmonary function. In comparison with eating fruit rarely or never, people who ate fruit at least once a day had reduced respiratory symptoms, such as phlegm production, shortness of breath and wheezing. Fruits of any kind help fight respiratory conditions, including mango , papaya and cantaloupe. Because beta-carotene works as an antioxidant, it may fight oxidative stress that contributes to brain aging and reduce the risk of cognitive decline. Although the evidence on this potential benefit is mixed, one study found that long-term supplementation with the antioxidant may provide cognitive benefits. Instead, long-term consumption of colorful fruits and vegetables is the best way to prevent early cognitive decline and ensure that you get the nutrients necessary for proper brain function. There have been studies suggesting that lung cancer, particularly in smokers, and cardiovascular disease may actually be enhanced by supplemental beta-carotene. A meta-analysis published in the International Journal of Cancer supports findings of an increased risk of lung and stomach cancers in smokers and asbestos workers who supplemented with 20 to 30 milligrams of beta-carotene per day. For this reason, researchers believe that beta-carotene supplements should not be recommended for primary cancer prevention. However, a study conducted at Yale University School of Medicine in found that high fruit and vegetable consumption, particularly a diet rich in carotenoids, reduced the risk of lung cancer. Researchers at Cleveland Clinic conducted a meta-analysis, combining the results of eight studies on the effects of beta-carotene at doses ranging from 15 to 50 milligrams. After investigating data from over , patients, researchers found that supplementation led to a small but significant increase in cardiovascular death. Even though the supplements did not prove beneficial in avoiding heart problems, studies show that antioxidant foods should still be recommended. Related: Retinoid Benefits vs. Myths: What You Need to Know for Healthier Skin. Numerous observational studies have found that people who ingest more carotenoids in their diets have a reduced risk of several chronic diseases. The richest sources of beta-carotene are yellow and orange fruits and vegetables, plus leafy green vegetables. I would assume we can extend that to other parasitic infections like Blastocystis and Dientamoeba fragilis. Back to the review. Vitamin A may improve leaky gut in a number of ways. Much of this is still being worked out. Some is in-vitro aka test tube data and some is animal studies. So we are left with the question as to how vitamin A improves leaky gut? Is it directly through influencing the cellular structures that heal and seal the gut wall or is it by interacting with the beneficial microbes that make up our gut microbiome? This article we are focusing on improving leaky gut and maintaining the gut barrier. As such there is a main focus on the active form of vitamin A. Different forms are found in the foods below 9. Preformed vitamin A is commonly found in certain animal foods including. Beta-carotene is found in a number of plant foods, but remember it still has to be converted into the active form to function on the gut wall. Hi, I'm Todd Mansfield a clinical herbalist based in Byron Bay, Australia. I'm here to help you find and fix the root cause of your digestive troubles. I work with patients in person here in the clinic and offer online consultations as well. Reach out if I can help. I have a terrible leaky gut. Intolerance to salacylates, oxalates, histamines, amines, and so many others. I have type 1 diabetes for 45 years. I controll it perfectly for the last 6 years a1c is 6. I leaned if leaky gut 5 years ago and have studied it meticulously ever since. I do super concentrated gel chicken bones broth from organic chicken feet, APPLE cider vinegar, and up until recently, 2 tablespoons extra virgin coconut oil everyday. Suddenly I developed a complete intolerance to the coconut oil because of the salacylates it contains. I could go on here forever….. I will be following your column from this point forward. I have some same leaky gut and food sensitivities that you have and also RBBB. My health went downhill in March I am also homebound trying to get better, I also have mild gastritis. Will be trying glutamine to heal my gut, if possible. I frequently use a great gut healing blend that contains retinol palmitate. Your email address will not be published. Save my name, email, and website in this browser for the next time I comment. December 5, 6 Comments. Leaky Gut — What is Intestinal Permeability Leaky Gut Driving Disease States Imbalanced Gut Flora Equals Leaky Gut Glutamine May Help Your Leaky Gut A Quick Vitamin A Primer First off what is vitamin A? Theories on Intestinal Permeability and Disease States In the past we have covered the connection between different disease states and leaky gut. The genetic susceptibility to an autoimmune disease. This is where many people stop. |
| The Role of β-Carotene in Colonic Inflammation and Intestinal Barrier Integrity | It is also worth noting that this study was not intended to test the efficacy of any particular dietary intervention. For more science-backed resources on nutrition, visit our dedicated hub. To explore whether the BCO1 enzyme could have a direct effect on the risk of atherosclerosis, the team conducted another study. Instead, the scientists fed beta carotene to two types of mice made genetically prone to develop atherosclerosis. The first type had a working version of the gene for making the BCO1 enzyme, and the other did not. Overall, the mice with the enzyme that converts beta carotene into vitamin A had reduced plasma cholesterol levels and developed less severe atherosclerosis than the mice without the enzyme. The second study has been published in the Journal of Lipid Research. Beta carotene is a red-orange pigment found in plants and fruits, especially colorful vegetables. The human body converts beta carotene into vitamin A. Vitamin A has numerous health benefits, and a deficiency can lead to troubling symptoms and health problems. Learn more here. Aside from its great taste, carrot juice may also provide numerous health benefits. Learn about the nutritional value and possible risks of drinking…. Vitamins are essential to human health. Here, learn about each of the 13 vitamins, including good sources and how they help. What are micronutrients? Read on to learn more about these essential vitamins and minerals, the role they play in supporting health, as well as…. My podcast changed me Can 'biological race' explain disparities in health? 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| Latest news | Beta carotene is a pigment in all fruits and vegetables, and carrots and sweet potatoes are particularly rich sources. As a result, they have a lower risk of ischemic heart disease , which is the most common cause of death worldwide. The molecular mechanisms that link beta carotene to lower blood cholesterol levels are poorly understood, however. Now, two new studies have discovered that the body needs an active version of a certain enzyme to reap the full benefits of beta carotene for cardiovascular health. The enzyme in question converts beta carotene into vitamin A, which reduces the amount of low-density lipoprotein LDL cholesterol produced in the liver. Having a less active form of this enzyme makes the body less efficient at producing vitamin A from the beta carotene in fruits and vegetables. To reap the full benefits to cardiovascular health, Amengual says, a person may need to get more vitamin A directly from animal sources, such as dairy, milk, oily fish, or cheese, for example. In the first study, the scientists began by measuring the impact of the enzyme, called beta carotene oxygenase 1 BCO1 , on cholesterol levels in mice. Their findings have been published in The Journal of Nutrition. The team compared the effects of a beta carotene-rich diet in one group of regular mice and another group of mice without the gene for making BCO1. After 10 days on the diet, the mice without the enzyme had more beta carotene in their blood and higher cholesterol levels than the normal mice. Next, the researchers analyzed DNA and blood samples from healthy young adults aged 18— The participants also filled out questionnaires about their diets. This genetic variant produces a more active form of the enzyme that converts more beta carotene into vitamin A. It is also worth noting that this study was not intended to test the efficacy of any particular dietary intervention. For more science-backed resources on nutrition, visit our dedicated hub. To explore whether the BCO1 enzyme could have a direct effect on the risk of atherosclerosis, the team conducted another study. Instead, the scientists fed beta carotene to two types of mice made genetically prone to develop atherosclerosis. The first type had a working version of the gene for making the BCO1 enzyme, and the other did not. Overall, the mice with the enzyme that converts beta carotene into vitamin A had reduced plasma cholesterol levels and developed less severe atherosclerosis than the mice without the enzyme. β-carotene also lowered the gut levels of several microbes, including bacteria belonging to the Bacteroidetes, Firmicutes and Proteobacteria phyla — but only in mice lacking vitamin A. This suggests that β-carotene improves the microbiota imbalance found in vitamin A deficient mice. Next, the researchers analyzed the effects of β-carotene on the barrier properties of the colon. Mice lacking vitamin A are known to show abnormalities of the intestinal physical barrier, which are associated with reduced levels of mucin, leaky gut and high concentrations of reactive-oxygen species in the gut. Dietary β-carotene reduced inflammation, relieved oxidative stress and improved gut barrier integrity in both control mice and mice lacking vitamin A, although the beneficial effects were more pronounced in the vitamin A deficient mice. com provides qualified scientific updates to healthcare professionals and to anyone who wants to know more about the microbiome. Published by Clorofilla Srl. Sign up. March 23, gut microbiota. Dietary β-carotene improves microbiota imbalance in mice lacking vitamin A. Researchers have found that β-carotene modifies the abundance of certain gut microbes and improves the intestinal dysfunctions. Table of Contents. Microbial imbalance The researchers fed mice lacking vitamin A and control mice a diet poor in vitamin A for two weeks. Gut dysfunction Next, the researchers analyzed the effects of β-carotene on the barrier properties of the colon. Beta-carotene and signaling pathways: A central common signaling mechanism in cancer is proline-directed phosphorylation, which is regulated by the unique proline isomerase Pin1. pylori induces the hyperproliferation of gastric epithelial cells. Beta-carotene inhibits this process by suppressing β-catenin signaling and oncogene expression. Beta-carotene-rich foods may prevent the development of gastric disorders related to H. pylori infection[ 97 ]. The Notch signaling pathway is important for gastric epithelial homeostasis and maintains a balance between cell proliferation and apoptosis. Therefore, the Notch signaling pathway may play an important role in the development of various malignant tumors[ 98 ]. It regulates several cellular processes, including cell proliferation, migration, invasion, apoptosis and angiogenesis as well as the epithelial-mesenchymal transition[ 99 ]. The epithelial-mesenchymal transition is involved in the initiation of tumorigenesis. In the study mentioned above, researchers found that tobacco smoke-induced gastric epithelial-mesenchymal transition was associated with the Notch pathway, but beta-carotene effectively attenuated this process in the mouse stomach[ ]. Beta-carotene can prevent the occurrence of gastric cancer through these mechanisms, which are summarized in Figure 4. In the past few years, researchers in different countries have conducted epidemiological studies on the relationship between carotene supplementation and gastric cancer, but some differences in the results of these studies have been noted. In this section, we summarize the results of these studies. In , South Korean researchers published a case-control study about dietary carotenoid intake and the risk of gastric cancer. Their findings confirmed that higher dietary lycopene intake might be inversely associated with the risk of gastric cancer. In the subgroups stratified by gender, H. pylori -positive subjects and participants who had ever smoked, the association was still significant[ ]. Some researchers studied dietary factors associated with the most frequent cancer sites from the European Prospective Investigation into Cancer and Nutrition. One of the findings showed that gastric cancer risk was inversely related to high plasma vitamin C levels, some carotenoids, retinol and α-tocopherol, high intake of cereal fiber and strong adhesion to a Mediterranean diet[ ]. The cumulative gastric cancer-related mortality of participants receiving factor D treatment decreased from 4. The beneficial effects of selenium, vitamin E and beta-carotene on mortality were still evident 10 years after the supplement was discontinued, particularly among young adults[ ]. Some researchers performed a large nested case-control study on the effects of carotenoids, retinols and tocopherols on gastric cancer in Japanese patients with H. The plasma level of beta-carotene was inversely associated with the risk of gastric cancer[ ]. In a prospective cohort study of Swedish adults, intake of vitamin A, retinol and the provitamin A carotenoids alpha-carotene and beta-carotene was inversely associated with the risk of gastric cancer. A group of researchers investigated the relationship between prediagnostic levels of serum micronutrients and gastric cancer risk in Shanghai, China. Their findings showed that high serum levels of alpha-carotene, beta-carotene and lycopene were inversely associated with the risk of developing gastric cancer. Therefore, dietary carotenes, lycopene and vitamin C are potential chemoprevention agents for gastric cancer in humans[ ]. In addition to some studies examining the protective effect of beta-carotene on gastric cancer, other studies have found that beta-carotene has no protective effect on gastric cancer and does not reduce the risk of gastric cancer. Dietary intake of vitamins C and E, beta-carotene and alpha-carotene was inversely associated with the risk of stomach cancer, but blood levels of these antioxidant vitamins did not display this association[ ]. Another systematic review and meta-analysis found that beta-carotene supplementation does not exert any beneficial effect on cancer prevention. In contrast, in smokers and asbestos workers, a daily dose of 20 mg to 30 mg increased the risk of lung cancer and stomach cancer[ ]. No strong association was observed between other analytes and cancer at different sites[ ]. In , a meta-analysis of the association of carotenoids with the risk of gastric cancer was conducted. Data from the case-control study suggested that beta-carotene and alpha-carotene were inversely associated with the risk of gastric cancer, while results from the cohort study were inconsistent[ ]. A summary of these studies is shown in Table 1. In conclusion, many epidemiological studies have been conducted on the relationship between beta-carotene and gastric cancer, and differences may exist between the results of each study. However, our mainstream view is that intake of beta-carotene is beneficial to gastric cancer, including reducing the risk of gastric cancer and improving the prognosis. However, the results of epidemiological surveys vary due to factors such as the region and research methods. As an important nutrient, beta-carotene exerts a protective effect on gastric cancer, and the mechanism is still worth exploring. Home English English 简体中文. Sign In BPG Management System F6Publishing-Submit a Manuscript F6Publishing-世界华人消化杂志在线投稿 RCA Management System. Advanced Search. About the Journal Submit a Manuscript Current Issue Search All Articles. This Article. Abstract Core Tip Full Article with Cover PDF Full Article WORD Full Article HTML Audio PubMed Central PubMed CrossRef Google Scholar Similar Articles Timeline of Article Publication 7 Authors Evaluation 5 Article Quality Tracking 0 Reference Citation Analysis 1. Academic Content and Language Evaluation of This Article. Answering Reviewers PDF Non-Native Speakers PDF Peer-Review Report PDF. CrossCheck and Google Search of This Article. Scientific Misconduct Check PDF. Academic Rules and Norms of This Article. Conflict-of-Interest Statement PDF Copyright Assignment PDF. Citation of this article. Chen QH, Wu BK, Pan D, Sang LX, Chang B. Beta-carotene and its protective effect on gastric cancer. World J Clin Cases ; 9 23 : [PMID: DOI: Corresponding Author of This Article. Bing Chang, PhD, Associate Professor, Department of Gastroenterology, First Affiliated Hospital of China Medical University, No. cb Checklist of Responsibilities for the Scientific Editor of This Article. Scientific Editor Work List PDF. Publishing Process of This Article. Research Domain of This Article. Article-Type of This Article. Open-Access Policy of This Article. This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial CC BY-NC 4. Times Cited Counts in Google of This Article. Number of Hits and Downloads for This Article. Total Article Views All Articles published online. Times Cited of This Article. Times Cited Journal Information of This Article. Publication Name. Baishideng Publishing Group Inc, Koll Center Parkway, Suite , Pleasanton, CA , USA. Review Open Access. Copyright ©The Author s Published by Baishideng Publishing Group Inc. All rights reserved. World J Clin Cases. Aug 16, ; 9 23 : Published online Aug 16, doi: Qian-Hui Chen , Bao-Kang Wu , Dan Pan , Li-Xuan Sang , Bing Chang. Qian-Hui Chen, Department of Intensive Care Unit, First Affiliated Hospital of China Medical University, Shenyang , Liaoning Province, China. Bao-Kang Wu, Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang , Liaoning Province, China. Dan Pan, Li-Xuan Sang, Department of Geriatrics, First Affiliated Hospital of China Medical University, Shenyang , Liaoning Province, China. Bing Chang, Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang , Liaoning Province, China. ORCID number: Qian-Hui Chen ; Bao-Kang Wu ; Dan Pan ; Li-Xuan Sang ; Bing Chang Author contributions : Chen QH and Sang LX designed the structure of the manuscript; Chen QH, Wu BK, Pan D, Chang B and Sang LX drafted the manuscript; Chen QH, Wu BK and Sang LX reviewed the literature; Pan D, Chang B and Sang LX critically revised the manuscript. Supported by Innovative Talents Support Program of Institution of Higher Learning of Liaoning Province , No. Open-Access : This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial CC BY-NC 4. Corresponding author : Bing Chang, PhD, Associate Professor, Department of Gastroenterology, First Affiliated Hospital of China Medical University, No. Received: January 12, Peer-review started : January 12, First decision : May 13, Revised: May 16, Accepted: June 22, Article in press : June 22, Published online: August 16, Key Words: Beta-carotene , Gastric cancer , Nutrient , Tumor , Stomach , Epidemiology. Citation: Chen QH, Wu BK, Pan D, Sang LX, Chang B. Open in New Tab Full Size Figure Download Figure. Figure 1 The chemical structure of beta-carotene. Figure 2 The extraction and synthesis of beta-carotene. coli : Escherichia coli. The natural extraction of beta-carotene. Biotechnological synthesis method. Nanoparticles and nanodispersions of beta-carotene. The antioxidant effect of beta-carotene. Beta-carotene influences gap junctional intercellular communication. Immune-related function of beta-carotene. THE MECHANISM BY WHICH OF BETA-CAROTENE MODULATES GASTRIC CANCER. Figure 3 Beta-carotene can induce the apoptosis of gastric cancer AGS cells by different pathways. By increasing the level of p53 and decreasing the level of Bcl-2, the nuclear ataxia-telangiectasia-mutated decreases and cell apoptosis occurs. Beta-carotene can also turn into all-trans retinoic acid in gastric cancer AGS cells, then c-myc decreases and p53 increases. ROS: Reactive oxygen species; ATM: Ataxia-telangiectasia-mutated; RA: Retinoic acid; ATRA: All-trans retinoic acid. Figure 4 Beta-carotene can prevent the process of gastric cancerization. It influences the oxidative stress in gastric cells. Beta-carotene inhibits the process of inflammation and cancerization and nuclear factor kappa-B plays an important role. Beta-carotene prevents the gastric cancer through signaling pathways, and it can weaken the Notch pathway. 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