Research progress of curcumin in the treatmentof non-alcoholic fatty liver disease
-
摘要: 非酒精性脂肪性肝病(NAFLD)是慢性肝损伤的原因之一,发病机制复杂。胰岛素抵抗、氧化应激、肠-肝轴和线粒体功能障碍等共同导致NAFLD的发生、发展。姜黄素是一种天然多酚类物质,是治疗NAFLD的潜在药物,并已广泛开展了实验研究。本研究对NAFLD的发病机制及姜黄素对NAFLD的治疗作用进行综述。Abstract: Non-alcoholic fatty liver disease (NAFLD) is one of causes of chronic liver injury, and the pathogenesis is complex. Insulin resistance, oxidative stress, intestinal-hepatic axis and mitochondrial dysfunction lead to the occurrence and development of NAFLD. Curcumin, a natural polyphenol, is a potential drug for the treatment of NAFLD, and has been widely studied in experimental researches. This study reviewed pathogenesis of NAFLD and the therapeutic effect of curcumin on NAFLD.
-
-
[1] COBBINA E, AKHLAGHI F. Non-alcoholic fatty liver disease (NAFLD)-pathogenesis, classification, and effect on drug metabolizing enzymes and transporters[J]. Drug Metab Rev, 2017, 49(2): 197-211. doi: 10.1080/03602532.2017.1293683
[2] NEUSCHWANDER-TETRI B A. Non-alcoholic fatty liver disease[J]. BMC med, 2017, 15(1): 45-53. doi: 10.1186/s12916-017-0806-8
[3] EASL-EASD-EASO. Clinical practice guidelines for the management of non-alcoholic fatty liver disease[J]. Obes Facts, 2016, 9(2): 65-90. doi: 10.1159/000443344
[4] GOH G B, MCCULLOUGH A J. Natural history of nonalcoholic fatty liver disease[J]. Dig Dis Sci, 2016, 61(5): 1226-1233. doi: 10.1007/s10620-016-4095-4
[5] YOUNOSSI Z M, KOENIG A B, ABDELATIF D, et al. Global epidemiology of nonalcoholic fatty liver disease-Meta-analytic assessment of prevalence, incidence, and outcomes[J]. Hepatology, 2016, 64(1): 73-84. doi: 10.1002/hep.28431
[6] LI Z Z, XUE J, CHEN P, et al. Prevalence of nonalcoholic fatty liver disease in mainland of China: a meta-analysis of published studies[J]. J Gastroenterol Hepatol, 2014, 29(1): 42-51. doi: 10.1111/jgh.12428
[7] ESLAMPARAST T, TANDON P, RAMAN M. Dietary composition independent of weight loss in the management of non-alcoholic fatty liver disease[J]. Nutrients, 2017, 9(8): 800-811. doi: 10.3390/nu9080800
[8] BORRELLI A, BONELLI P, TUCCILLO F M, et al. Role of gut microbiota and oxidative stress in the progression of non-alcoholic fatty liver disease to hepatocarcinoma: Current and innovative therapeutic approaches[J]. Redox Biol, 2018, (15): 467-479. http://europepmc.org/abstract/MED/29413959
[9] MARCHESINI G, PETTA S, GRAVE R D. Diet, weight loss, and liver health in nonalcoholic fatty liver disease: Pathophysiology, evidence, and practice[J]. Hepatology, 2016, 63(6): 2032-2043. doi: 10.1002/hep.28392
[10] DE CASTRO GS, CALDER PC. Non-alcoholic fatty liver disease and its treatment with n-3 polyunsaturated fatty acids[J]. Clin Nutr, 2018, 37(1): 37-55. doi: 10.1016/j.clnu.2017.01.006
[11] FRIEDMAN S L, NEUSCHWANDER-TETRI B A, RINELLA M, et al. Mechanisms of NAFLD development and therapeutic strategies[J]. Nat Med, 2018, 24(7): 908-922. doi: 10.1038/s41591-018-0104-9
[12] PERDOMO C M, FRÜHBECK G, ESCALADA F J. Impact of nutritional changes on nonalcoholic fatty liver disease[J]. Nutrients, 2019, 11(3): 677-683. doi: 10.3390/nu11030677
[13] TILG H, MOSCHEN A R. Evolution of inflammation in nonalcoholic fatty liver disease: the multiple parallel hits hypothesis[J]. Hepatology, 2010, 52(5): 1836-1846. doi: 10.1002/hep.24001
[14] AKINOBU T, DAISUKE K, KAZUHIDE Y. Multiple hits, including oxidative stress, as pathogenesis and treatment target in non-alcoholic steatohepatitis(NASH)[J]. Int J Mol Sci, 2013, 14(10): 20704-20728. doi: 10.3390/ijms141020704
[15] PEVERILL W, POWELL L W, SKOIEN R. Evolving concepts in the pathogenesis of NASH: beyond steatosis and inflammation[J]. Int J Mol Sci, 2014, 15(5): 8591-8638. doi: 10.3390/ijms15058591
[16] JIANG C T, XIE C, LI F, et al. Intestinal farnesoid X receptor signaling promotes nonalcoholic fatty liver disease[J]. Clin Invest, 2015, 125(1): 386-402. doi: 10.1172/JCI76738
[17] HENAO-MEJIA J, ELINAV E, JIN C C, et al. Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity[J]. Nature, 2012, 482(7384): 179-185. doi: 10.1038/nature10809
[18] DE MINICIS S, RYCHLICKI C, AGOSTINELLI L, et al. Dysbiosis contributes to fibrogenesis in the course of chronic liver injury in mice[J]. Hepatology, 2014, 59(5): 1738-1749. doi: 10.1002/hep.26695
[19] CANI P D, DELZENNE N M. The role of the gut microbiota in energy metabolism and metabolic disease[J]. Curr Pharm Des, 2009, 15(13): 1546-1558. doi: 10.2174/138161209788168164
[20] BUZZETTI E, PINZANI M, TSOCHATZIS E A, et al. The multiple-hit pathogenesis of non-alcoholic fatty liver disease(NAFLD)[J]. Metabolism, 2016, 65(8): 1038-1048. doi: 10.1016/j.metabol.2015.12.012
[21] CHEN Y, SUN H H, BAI Y Z, et al. Gut dysbiosis-derived exosomes trigger hepatic steatosis by transiting HMGB1 from intestinal to liver in mice[J]. Biochem Biophys Res Commun, 2019, 509(3): 767-772. doi: 10.1016/j.bbrc.2018.12.180
[22] JANSSEN A W F, HOUBEN T, KATIRAEI S, et al. Modulation of the gut microbiota impacts nonalcoholic fatty liver disease: a potential role for bile acids[J]. J Lipid Res, 2017, 58(7): 1399-1416. doi: 10.1194/jlr.M075713
[23] WOUDENBERG-VRENKEN T E, CONDE DE LA ROSA L, BUIST-HOMAN M, et al. Metformin protects rat hepatocytes against bile acid-induced apoptosis[J]. PloS One, 2013, 8(8): e71773. doi: 10.1371/journal.pone.0071773
[24] SODEMAN T, BRONK S F, ROBERTS P J, et al. Bile salts mediate hepatocyte apoptosis by increasing cell surface trafficking of Fas[J]. Am J Physiol Gastrointest Liver Physiol, 2000, 278(6): G992-G999. doi: 10.1152/ajpgi.2000.278.6.G992
[25] HIGUCHI H, BRONK S F, TAKIKAWA Y, et al. The bile acid glycochenodeoxycholate induces TRAIL-receptor 2/DR5 expression and apoptosis[J]. J Biol Chem, 2001, 276(42): 38610-38618. doi: 10.1074/jbc.M105300200
[26] FRCKERT P, FUCHSBICHLER A, MARSCHALL H U, et al. Lithocholic acid feeding induces segmental bile duct obstruction and destructive cholangitis in mice[J]. Am J Pathol, 2006, 168(2): 410-422. doi: 10.2353/ajpath.2006.050404
[27] ARANHA M M, CORTEZ-PINTO H, COSTA A, et al. Bile acid levels are increased in the liver of patients with steatohepatitis[J]. Eur J Gastroenterol Hepatol, 2008, 20(6): 519-525. doi: 10.1097/MEG.0b013e3282f4710a
[28] DAY C P, JAMES O F. Steatohepatitis: A tale of two "hits"[J]. Gastroenterology, 1998, 114(4): 842-845. doi: 10.1016/S0016-5085(98)70599-2
[29] ZENG X, YANG J, HU O, et al. Dihydromyricetin ameliorates nonalcoholic fatty liver disease by improving mitochondrial respiratory capacity and redox homeostasis through modulation of SIRT3 signaling[J]. Antioxid Redox Signal, 2019, 30(2): 163-183. doi: 10.1089/ars.2017.7172
[30] ALLISON C, NURIA M. The crosstalk between the gut microbiota and mitochondria during exercise[J]. Front Physiol, 2017, 8: 319-327. doi: 10.3389/fphys.2017.00319
[31] CUNNINGHAM K E, VINCENT G, SODHI C P, et al. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) protects against experimental murine colitis[J]. J Biol Chem, 2016, 291(19): 10184-10200. doi: 10.1074/jbc.M115.688812
[32] CHEN M T, HUI S C, LANG H D, et al. SIRT3 deficiency promotes high-fat diet-induced nonalcoholic fatty liver disease in correlation with impaired intestinal permeability through gut microbial dysbiosis[J]. Mol Nutr Food Res, 2018, 63(4): e1800612. http://www.ncbi.nlm.nih.gov/pubmed/30525304
[33] ROLE A P, TEODORO J S, PALMEIRA C M, et al. Role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis[J]. Free Radic Biol Med, 2012, 52(1): 59-69. doi: 10.1016/j.freeradbiomed.2011.10.003
[34] TAKAKI A, KAWAI D, YAMAMOTO K. Multiple hits, including oxidative stress, as pathogenesis and treatment target in non-alcoholic steatohepatitis(NASH)[J]. Int J Mol Sci, 2013, 14(10): 20704-20728. doi: 10.3390/ijms141020704
[35] WANG L, YIN L, YAO H X, et al. Curcumin prevents the non-alcoholic fatty hepatitis via mitochondria protection and apoptosis reduction[J]. Int J Clin Exp Pathol, 2015, 9(8): 11503-11509.
[36] KUNNUMAKKARA A B, BORDOLOI D, PADMAVATHI G, et al. Curcumin, the golden nutraceutical: multitargeting for multiple chronic diseases[J]. Br J Pharmacol, 2017, 174(11): 1325-1348. doi: 10.1111/bph.13621
[37] ALVES R C, FERNANDES R P, FONSECA-SANTOS B, et al. A critical review of the properties and analytical methods for the determination of curcumin in biological and pharmaceutical matrices[J]. Crit Rev Anal Chem, 2019, 49(2): 138-149. doi: 10.1080/10408347.2018.1489216
[38] GOPI S, JACOB J, VARMA K, et al. Comparative oral absorption of curcumin in a natural turmeric matrix with two other curcumin formulations: an open-label parallel-arm study[J]. Phytother Res, 2017, 31(12): 1883-1891. doi: 10.1002/ptr.5931
[39] KOTHA R, LUTHRIA D. Curcumin: biological, pharmaceutical, nutraceutical, and analytical aspects[J]. Molecules, 2019, 24(16): 2930-2937. doi: 10.3390/molecules24162930
[40] GHOSH S, BANERJEE S, SIL P C. The beneficial role of curcumin on inflammation, diabetes and neurodegenerative disease: A recent update[J]. Food Chem Toxicol, 2015, 83: 111-124. doi: 10.1016/j.fct.2015.05.022
[41] GIORDANO A, TOMMONARO G. Curcumin and Cancer[J]. Nutrients, 2019, 11(10): 2376. doi: 10.3390/nu11102376
[42] MOMTAZI-BOROJENI A A, HAFTCHESHMEH S M, ESMAEILI S A, et al. Curcumin: A natural modulator of immune cells in systemic lupus erythematosus[J]. Autoimmun Rev, 2018, 17(2): 125-135. doi: 10.1016/j.autrev.2017.11.016
[43] SAHEBKAR A. Are curcuminoids effective C-reactive protein-lowering agents in clinical practice Evidence from a meta-analysis[J]. Phytother Res, 2014, 28(5): 633-642. doi: 10.1002/ptr.5045
[44] MOLTENI M, GEMMA S, ROSSETTI C, et al. The role of toll-like receptor 4 in infectious and noninfectious inflammation[J]. Mediat Inflamm, 2016, 2016: 6978936.
[45] ROSADINI C V, KAGAN J C. Early innate immune responses to bacterial LPS[J]. Curr Opin Immunol, 2017, 44(14): 19-26. http://europepmc.org/abstract/med/27842237
[46] MIURA K, OHNISHI H. Role of gut microbiota and toll-like receptors in nonalcoholic fatty liver disease[J]. World J Gastroenterol, 2014, 20(23): 7381-7391. doi: 10.3748/wjg.v20.i23.7381
[47] BEUTLER B, HOEBE K, DU X, et al. How we detect microbes and respond to them: the Toll-like receptors and their transducers[J]. J Leukor Biol, 2003, 74(4): 479-485. doi: 10.1189/jlb.0203082
[48] MILIC S, LULIC D, STIMAC D. Non-alcoholic fatty liver disease and obesity: biochemical, metabolic and clinical presentations[J]. World J Gastroenterol, 2014, 20(28): 9330-9337.
[49] YAN C, ZHANG Y R, ZHANG X X, et al. Curcumin regulates endogenous and exogenous metabolism via Nrf2-FXRLXR pathway in NAFLD mice[J]. Biomed Pharmacother, 2018, 105: 274-281. doi: 10.1016/j.biopha.2018.05.135
[50] PANAHI Y, KIANPOUR P, MOHTASHAMI R, et al. Efficacy of phospholipidated curcumin in nonalcoholic fatty liver disease: a clinical study[J]. J Asian Nat Prod Res, 2019, 21(8): 798-805. doi: 10.1080/10286020.2018.1505873
[51] CUNNINGHAM R P, MOORE M P, MOORE A N, et al. Curcumin supplementation mitigates NASH development and progression in female Wistar rats[J]. Physiol Rep, 2018, 6(14): e13789. doi: 10.14814/phy2.13789
[52] GHEIBI S, GOUVARCHIN GHALEH H E, MOTLAGH B M, et al. Therapeutic effects of curcumin and ursodexycholic acid on non-alcoholic fatty liver disease[J]. Biomed Pharmacother, 2019, 115: 108938. doi: 10.1016/j.biopha.2019.108938
[53] BING C, MRACEK T, GAO D, et al. Zinc-α2-glycoprotein: an adipokine modulator of body fat mass[J]. Int J Obes, 2010, 34(11): 1559-1565. doi: 10.1038/ijo.2010.105
[54] LIU W, BAKER R D, ZHU L, et al. Antioxidant mechanisms in nonalcoholic fatty liver disease[J]. Curr Drug Targ, 2015, 16(12): 1301-1314. doi: 10.2174/1389450116666150427155342
[55] LI C P, LI J H, CHEN Y, et al. Effect of curcumin on visfatin and zinc-α2-glycoprotein in a rat model of fatty liver disease[J]. Acta Cir Bras, 2016, 31(11): 706-713. doi: 10.1590/s0102-865020160110000001
[56] FENG D, ZOU J, SU D, et al. Curcumin prevents high-fat diet-induced hepatic steatosis in ApoE(-/-) mice by improving intestinal barrier function and reducing endotoxin and liver TLR4/NF-κB inflammation[J]. Nutr Metab, 2019, 16: 79-87. doi: 10.1186/s12986-019-0410-3
[57] HOU H T, QIU Y M, ZHAO H W, et al. Effect of curcumin on intestinal mucosal mechanical barrier in rats with non-alcoholic fatty liver disease[J]. Zhonghua Gan Zang Bing Za Zhi, 2017, 25(2): 134-138. http://www.ncbi.nlm.nih.gov/pubmed/28297801
[58] FENG W H, WANG H D, ZHANG P Z, et al. Modulation of gut microbiota contributes to curcumin-mediated attenuation of hepatic steatosis in rats[J]. BBA-Gen Subjects, 2017, 1681(7): 1801-1812.
[59] LEE D E, LEE S J, KIM S J, et al. Curcumin ameliorates nonalcoholic fatty liver disease through inhibition of O-GlcNAcylation[J]. Nutrients, 2019, 11(11): 2702-2709. doi: 10.3390/nu11112702
[60] DE FREITAS CARVALHO M M, LAGE N N, DE SOUZA PAULINO A H, et al. Effects of acai on oxidative stress, ER stress, and inflammation-related parameters in mice with high fat diet-fed induced NAFLD[J]. Sci Rep, 2019, 9(1): 8107-8116. doi: 10.1038/s41598-019-44563-y
[61] MOSCHEN A R, KASER A, ENRICH B, et al. Visfatin, an adipocytokine with proinflammatory and immunomodulating properties[J]. J Immunol, 2007, 178(3): 1748-1758. doi: 10.4049/jimmunol.178.3.1748
[62] OITA R C, FERDINANDO D, WILSON S, et al. Visfatin induces oxidative stress in differentiated C2C12 myotubes in an Akt-and MAPK-independent, NFκB-dependent manner[J]. Pflugers Arch, 2010, 459(4): 619-630. doi: 10.1007/s00424-009-0752-1
[63] GALLEGO-DURAN R, ROMERO-GOMEZ M. Epigenetic mechanisms in non-alcoholic fatty liver disease: An emerging field[J]. World J Hepatol, 2015, 7(24): 2497-2502. doi: 10.4254/wjh.v7.i24.2497
[64] LI Y Y. Genetic and epigenetic variants influencing the development of nonalcoholic fatty liver disease[J]. World J Gastroenterol, 2012, 18(45): 6546-6551. doi: 10.3748/wjg.v18.i45.6546
[65] CONTRERAS A V, TORRES N, TOVAR A R, et al. Ppar-alpha as a key nutritional and environmental sensor for metabolic adaptation[J]. Adv Nutr, 2013, 4(4): 439-452. doi: 10.3945/an.113.003798
[66] SOUZA M R, DINIZ MDE F, MEDEIROS-FILHO J E, et al. Metabolic syndrome and risk factors for non-alcoholic fatty liver disease[J]. Arq Gastroenterol, 2012, 49: 89-96. doi: 10.1590/S0004-28032012000100015
[67] SUN X, ZHANG Y, XIE M, et al. The role of peroxisome proliferator-activated receptor in the treatment of non-alcoholic fatty liver disease[J]. Acta Pharm, 2017, 67(1): 1-13. doi: 10.1515/acph-2017-0007
[68] LISS K H H, FINCK B N. Ppars and nonalcoholic fatty liver disease[J]. Biochimie, 2017, 136: 65-74. doi: 10.1016/j.biochi.2016.11.009
[69] PAWLAK M, LEFEBVRE P, STAELS B, et al. Molecular mechanismof pparalpha action and its impact on lipid metabolism, inflammation and fibrosis in non-alcoholic fatty liver disease[J]. J Hepatol, 2015, 62(3): 720-733. doi: 10.1016/j.jhep.2014.10.039
[70] HUANG Y Y, GUSDON A M, QU S, et al. Nonalcoholic fatty liver disease: Molecular pathways and therapeutic strategies[J]. Lipids Health Dis, 2013, 12: 171-179. doi: 10.1186/1476-511X-12-171
[71] GIBY V G, AJITH T A. Role of adipokines and peroxisome proliferator-activated receptors in nonalcoholic fatty liver disease[J]. World J Hepatol, 2014, 8: 570-579. http://europepmc.org/abstract/MED/25232450
[72] LI Y Y, TANG D, DU Y L, et al. Fatty liver mediated by PPAR-α DNA methylation can be reversed by a methylation inhibitor and curcumin[J]. J Dig Dis, 2018, 19(7): 421-430. doi: 10.1111/1751-2980.12610
[73] KUO J J, CHANG H H, TSAI T H, et al. Positive effect of curcumin on inflammation and mitochondrial dysfunction in obese mice with liver steatosis[J]. Int J Mol Med, 2012, 30(3): 673-679. doi: 10.3892/ijmm.2012.1049
[74] MARTINEZ-MORUA A, SOTO-URQUIETA M G, FRANCO-ROBLES E, et al. Curcumin decrases oxidative stress in mitochondria isolated from liver and kidneys of high-fat diet-induced obese mice[J]. Asian Nat Prod Res, 2013, 15(8): 905-915. doi: 10.1080/10286020.2013.802687
-
期刊类型引用(3)
1. 王梓杭,姜红丽,史绪生. 全球重症病人早期康复研究热点的可视化分析. 循证护理. 2024(14): 2554-2561 . 百度学术
2. 吴洪,温贤秀,雷花,毛孝容,潘俊青,曹海霞,卢婷,蓝梅. 新型冠状病毒肺炎患者早期康复及干预措施研究进展. 实用医院临床杂志. 2022(02): 211-214 . 百度学术
3. 宋宇杰,徐悦蓉,董佳颖,张明明. 新型冠状病毒肺炎所致心血管系统损伤的研究进展. 实用临床医药杂志. 2021(15): 114-118 . 本站查看
其他类型引用(0)
计量
- 文章访问数: 475
- HTML全文浏览量: 238
- PDF下载量: 29
- 被引次数: 3