• صفحه اصلی
  • اهمیت اسیدهای چرب زنجیر کوتاه سنتز شده توسط میکروارگانیسم‌‌های روده، به عنوان یک عامل اپی ژنتیک، در کاهش ابتلا به سرطان کولون

اشتراک گذاری

آدرس مقاله


کد مقاله : SJOAPB-2210-1396 (R1) بازدید : 375 صفحه: 59 - 86

نوع مقاله: پژوهشی

اهمیت اسیدهای چرب زنجیر کوتاه سنتز شده توسط میکروارگانیسم‌‌های روده، به عنوان یک عامل اپی ژنتیک، در کاهش ابتلا به سرطان کولون

محورهای موضوعی : ژنتیک

شیوا دارابی 1 , فاطمه کشاورزی 2 , پرویز اشتری 3 , فرحناز معتمدی سده 4 , بهروز علیرضاپور 5

1 - دانشجوی دکتری بیوشیمی، گروه زیست‌شناسی، واحد سنندج، دانشگاه آزاد اسلامی، سنندج، ایران.
2 - دانشیار، گروه زیست‌شناسی، واحد سنندج، دانشگاه آزاد اسلامی، سنندج، ایران
3 - دانشیار، دانشکده تحقیقات کاربردی پرتو، پژوهشکده علوم و فناوری هسته‌ای، کرج، ایران
4 - دانشیار، گروه دامپزشکی و علوم دامی، مرکز تحقیقات کشاورزی هسته‌ای، پژوهشکده علوم و فناوری هسته‌ای، کرج، ایران.
5 - دانشیار، مرکز تحقیقات کاربردی پرتو، پژوهشکده علوم و فناوری هسته‌ای، تهران، ایران.

تاریخ دریافت : 1401/01/21 تاریخ پذیرش : 1401/03/16 تاریخ انتشار : 1401/04/01

کلید واژه: فاکتورهای اپی ژنتیک, رژیم غذایی, اسیدهای چرب زنجیره کوتاه (SCFAs), سرطان کولون,  میکروبیوتای روده,

چکیده مقاله :

هدف: مکانیسم‌های درگیر در پاتوژنز سرطان کولورکتال هنوز به درستی شناخته نشده‌اند، اما رژیم غذایی فاکتور اصلی است که اثرات چند جانبه‌ای از جمله تغییر در متابولوم و ترانسکریپتوم میزبان دارد. متابولیت‌‌هایی که از رژیم غذایی حاصل می‌‌شوند، می‌‌توانند به طور مستقیم بر متابولیسم کل بدن تاثیر بگذارند. هدف پژوهش حاضر، مرور تاثیر میکروبیوتای روده به واسطه سنتز اسیدهای چرب زنجیره کوتاه (استات، بوتیرات و پروپیونات)، و در نتیجه القای بیان ژن سیتوکروم P4501A1 در پیشگیری و درمان سرطان کولون است.مواد و روش‌ها: با استفاده از کلمات کلیدی، جستجو و جمع‌آوری مقالات از پایگاه‌های اطلاعاتی و استنادی پابمد (PubMed)، آی.‌ اس. آی. ‌(ISI web of Knowledge)، اسکوپوس (SCOPUS)، گوگل‌ اسکالر (Google Scholar)، پروکوئست‌(ProQuest) ، اکسفورد (Oxford) و اویدو(Ovid) و نیز معروف‌ترین‌ پایگاه‌های اطلاعاتی داخلی شامل پایگاه جهاد دانشگاهی (SID)، ایرانمدکس ‌(Iranmedex)، مگیران (Magiran)، ایرانداک (Irandoc) و مدلیب‌(MedLib) انجام شد.یافته‌ها: مواد ترکیبات غذایی هضم نشده که وارد روده بزرگ می‌‌شوند، توسط میکروبیوتای روده تخمیر شده و متابولیت‌‌های تخمیری تولید می‌‌شود که طیف گسترده‌ای از عملکرد‌‌های موثر را انجام می‌‌دهند. برخی از این متابولیت‌‌ها با سیستم ایمنی روده تعامل دارند، از جمله اسید‌‌های چرب زنجیره کوتاه، لیگاند‌‌های گیرنده آریل هیدروکربن و متابولیت‌‌های اسید‌‌‌‌های صفراوی که در القای هموستاز ایمنی روده نقش دارند. به نظر می‌‌رسد که اثرات حفاظتی اسید‌‌های چرب زنجیره کوتاه سنتز شده توسط میکروارگانیسم‌ها، در سرطان کولون به واسطه مهار فعالیت هیستون د‌‌استیلازی و تقویت گیرنده آریل هیدروکربن و در نتیجه حفاظت از DNA در برابر آسیب‌های ناشی از کارسینوژن‌ها، با فعال‌سازی آنزیم‌‌‌های متابولیزه‌کننده زنوبیوتیک، مانند سیتوکروم P4501A1، اعمال شود.نتیجه‌گیری: پژوهش حاضر دیدگاه جدیدی را در رابطه با اهمیت میکروبیوتا روده به واسطه تولید اسیدهای چرب زنجیره کوتاه به ویژه استات، بوتیرات و پروپیونات به عنوان اهداف دارویی در جهت پیشگیری و حتی درمان سرطان کلورکتال ارائه داد.

چکیده انگلیسی:

Objective: The mechanisms involved in the pathogenesis of colorectal cancer are still not well understood, but diet is the main factor that has multifaceted effects, including changes in the host's metabolome and transcriptome. Metabolites obtained from diet can directly affect the metabolism of the whole body. The purpose ofthis study is to review the effect of intestinal microbiota through the synthesis ofshort chain fatty acids (acetate, butyrate and propionate), and as a result, the induction of cytochrome P4501A1 gene expression in the prevention and treatment of colon cancer.Materials and methods: Using keywords, searching and collecting articles from PubMed and citation databases, I.S. I. (ISI web of Knowledge), SCOPUS, Google Scholar, ProQuest, Oxford and Ovid, as well as the most famous internal databases including the Academic Jihad Database (SID), Iranmedex, Magiran, Irandoc and MedLib were performed.Findings: Undigested food ingredients that enter the large intestine are fermented by intestinal microbiota and fermentative metabolites are produced that perform a wide range of effective functions. Some of these metabolites interact with the intestinal immune system, including short-chain fatty acids, aryl hydrocarbon receptor ligands, and bile acid metabolites that play a role in inducing intestinal immune homeostasis.It seems that the protective effects of short chain fatty acids synthesized by microorganisms, in colon cancer by inhibiting the activity of histone deacetylase and strengthening the aryl hydrocarbon receptor and thus protecting DNA against damage caused by carcinogens, by activating xenobiotic metabolizing enzymes, such as Cytochrome P4501A1, apply.Conclusion: The present study presented a new perspective regarding the importance of intestinal microbiota through the production of short chain fatty acids, especially acetate, butyrate and propionate, as medicinal targets for the prevention and even treatment of colorectal cancer.

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_||_

  1. Zheng P, Li Zh & Zhou Zh. Gut microbiome in type 1 diabetes: A comprehensive review. Diabetes Metab Res Rev. 2018; 34: e3043. DOI:org/10.1002/dmrr.3043
    2.
  2. Poppe J, Baarle L, Matteoli G & Verbeke K. How microbial food fermentation supports a tolerant gut. Molecular Nutrition & Food Research. 2020. DOI: 1002/mnfr.202000036
    3.
  3. Mayer EA, Savidge T & Shulman RJ. Brain-gut microbiome interactions and functional bowel disorders. Gastroenterology. 2014; 146:1500-12.
    DOI: 1053/j.gastro.2014.02.037
    4.
  4. Macfarlane, GT & Macfarlane, S. Bacteria,colonic fermentation and gastro intestinal health. AOAC Int. 2012; 95: 50-60.
    5.
  5. Xu W, Zhou Y & Hang X, Shen D. Current evidence on the relationship between CYP1B1 polymorphisms and lung cancer risk: a metaanalysis. Mol Biol Rep. 2012; 39(3): 2821-9.
    6.
  6. Beyerle J, Frei E, Stiborov M, Habermann N & Ulrich CM. Biotransformation of xenobiotics in the human colon and rectum and its association with colorectal cancer. Drug Metab Rev; 2015; 47: 199-221.
    7.
  7. Gutierrez-Vazquez C & Quintana FJ. Regulation of the immune response by the aryl hydrocarbon receptor. Immunity. 2018; 48(1): 19-33.
    8.
  8. Donaldson GP, Lee SM & Mazmanian SK. Gut biogeography of the bacterial microbiota. Nature reviews. Microbiology. 2016; 14(1): 20-32.
    9.
  9. Li H & et al. The outer mucus layer hosts a distinct intestinal microbial niche. Nature Communications. 2015; 6(1): 8292.
    10.
  10. Franzosa EA & et al. Identifying personal microbiomes using metagenomic codes. Proceedings of the National Academy of Sciences of the United States of America. 2015; 112(22): 2930-8.
    11.
  11. Costea PI & et al. Enterotypes in the landscape of gut microbial community composition. Nature Microbiology. 2017; 3(1): 8-16.
    12.
  12. Ha CW, Lam YY & Holmes AJ. Mechanistic links between gut microbial community dynamics, microbial functions and metabolic health. World Journal of Gastroenterology. 2014; 20(44): 16498-16517.
    13.
  13. Marinelli L, Martin-Gallausiaux C, Bourhis J-M, B_eguet-Crespel F, Blotti_ere HM & Lapaque N. Identification of the novel role of butyrate as Ahr ligand in human intestinal epithelial cells. Sci Rep. 2019; 9(1): 643.
    14.
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    15.
  15. Louis P, Hold G & Flint HJ.The gut microbiota, bacterial metabolites and colorectal cancer. Rev.Microbiol. 2014; 12: 661-672. DOI: 10.1038/nrmicro3344
    16.
  16. Reichardt N & et al. Phylogenetic distribution of three pathways forpropionate production within the human gut microbiota. ISMEJ. 2014; 8: 1323-1335.
    DOI:1038/ismej.2014.14
    17.
  17. Flint HJ, Duncan SH, Scott KP, & Louis P. Links between diet, gut microbiota composition and gut Proc.Nutr.Soc. 2015; 74:13-22.
    DOI: 10.1017/s0029665114001463
    18.
  18. Machiels K, & et al. Adecrease of the butyrate-producing species Roseburiahominis and Faecali bacterium prausnitzii defines dysbiosis in patients with Gut. 2014; 63:1275-1283. DOI: 10.1136/gutjnl-2013-304833.
    19.
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    20.
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    21.
  21. Macfarlane GT & Macfarlane S. Bacteria,colonic fermentation and gastro intestinal health. AOACInt. 2012; 95: 50-60.
    22.
  22. Jung TH, Park JH, Jeon WM & Han KS. Butyrate modulates bacterial adherence on LS174T human colorectal cells by stimulating mucin secretionand MAPK signaling pathway. Res.Pract. 2015; 9: 343-349. DOI: 10.4162/nrp.2015.9.4.343
    23.
  23. Den Besten G & et al. Short-chain fatty acids protect against high-fatdiet-induced obesity via a PPAR gamma-Dependent Switch from lipogenesist of at oxidation. 2015; 64: 2398-2408. DOI: 10.2337/db14-1213
    24.
  24. Canfora EE., Jocken JW. & Blaak EE. Short-chain fatty acids in control of body weight and insulin sensitivity. Rev.Endocrinol. 2015, 11: 577-591.     
    DOI: 10.1038/nrendo.2015.128.
    25.
  25. Keku TO, Dulal S, Deveaux A, Jovov, B & Han X. The gastro intestinal microbiota and colorectal cancer. J. Physiol. Gastrointest. LiverPhysiol. 2015, 308: G351-G363.
    DOI: 10.1152/ajpgi.00360.2012
    26.
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    27.
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    29.
  29. Wang G & et al. Role of SCFAs in gut microbiome and glycolysis for colorectal cancer therapy. Journal of cellular physiology. 2019. DOI:1002/jcp.28436.
    30.
  30. Han A, Bennett N, Macdonald A, Johnstone M, Whelan J & Donohoe DR. Cellular metabolism and dose reveal carnitine‐dependent and ‐independent mechanisms of butyrate oxidation in colorectal cancer cells. Journal of Cellular Physiology. 2016; 231: 1804-1813.
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  33. Binoy Shivanna, Ch Ch & Bhagavatula M. The Aryl Hydrocarbon Receptor (AHR): A Novel Therapeutic Target for Pulmonary Diseases? J. Mol. Sci. 2022; 23: 1516.
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    38.
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