留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

姜黄素改善非酒精性脂肪性肝病的研究进展

孙秋爽 郭雅婷 庄玉 黄芳 邱志霞

孙秋爽, 郭雅婷, 庄玉, 黄芳, 邱志霞. 姜黄素改善非酒精性脂肪性肝病的研究进展[J]. 南京中医药大学学报, 2021, 37(4): 625-631. doi: 10.14148/j.issn.1672-0482.2021.0625
引用本文: 孙秋爽, 郭雅婷, 庄玉, 黄芳, 邱志霞. 姜黄素改善非酒精性脂肪性肝病的研究进展[J]. 南京中医药大学学报, 2021, 37(4): 625-631. doi: 10.14148/j.issn.1672-0482.2021.0625
SUN Qiu-shuang, GUO Ya-ting, ZHUANG Yu, HUANG Fang, QIU Zhi-xia. Research Progress of Curcumin for the Prevention and Treatment of Non-Alcoholic Fatty Liver Disease[J]. Journal of Nanjing University of traditional Chinese Medicine, 2021, 37(4): 625-631. doi: 10.14148/j.issn.1672-0482.2021.0625
Citation: SUN Qiu-shuang, GUO Ya-ting, ZHUANG Yu, HUANG Fang, QIU Zhi-xia. Research Progress of Curcumin for the Prevention and Treatment of Non-Alcoholic Fatty Liver Disease[J]. Journal of Nanjing University of traditional Chinese Medicine, 2021, 37(4): 625-631. doi: 10.14148/j.issn.1672-0482.2021.0625

姜黄素改善非酒精性脂肪性肝病的研究进展

doi: 10.14148/j.issn.1672-0482.2021.0625
基金项目: 

“重大新药创制”科技重大专项 2017ZX09301026

详细信息
    作者简介:

    孙秋爽,女,硕士研究生,E-mail: sunqiushuangsqs@163.com

    通讯作者:

    邱志霞,女,副教授,主要从事内源性物质代谢调控与代谢性疾病关联研究,E-mail: qiuzhixia_cpu@163.com

  • 中图分类号: R285.5

Research Progress of Curcumin for the Prevention and Treatment of Non-Alcoholic Fatty Liver Disease

  • 摘要: 非酒精性脂肪性肝病(Non-alcoholic fatty liver disease,NAFLD)是目前全球最常见的慢性肝病之一,发病率呈现不断上升的趋势。姜黄素是从姜科植物姜黄中提取的具有多种生物活性的多酚类化合物。大量研究证实姜黄素具有良好的降脂、抗炎、抗氧化、抗纤维化等药理活性,并且对NAFLD、肥胖、胰岛素抵抗等多种代谢性疾病疗效显著,因而有着重要的临床价值和广阔的应用前景。就姜黄素治疗NAFLD的药理学作用及相关机制研究进行综述,旨在为姜黄素治疗代谢性疾病的研究提供参考,并推广其预防和改善NAFLD以及其它脂质代谢紊乱相关疾病可能的临床应用。

     

  • 图  1  姜黄素通过调控脂质代谢、抗炎、抗纤维化等改善NAFLD

    表  1  姜黄素防治NAFLD的药理作用及机制

    药理作用 作用机制 靶点名称 参考文献
    降脂作用 抑制脂质从头合成 ACLY、SLC13A5、ACC、FAS [28, 34, 45, 50]
    降低脂质摄取 CD36、FATP2、FATP5
    降低脂质异位转移 PKA/HSL
    促进脂肪酸的处置利用 CPT-1、CPT-2
    抗炎作用 减少炎症相关因子的合成和分泌 NF-κB、HIF-1α、IL-6、IL-1β、TNF-α [12, 61, 66-67]
    抗纤维化作用 抑制肝星状细胞的异常激活及TGF-β1的活化 TGF-β1、Col1α、Col3α、Col6α [51, 75]
    其他 调节相关核转录因子、激酶和沉默调节蛋白 SREBPs、ChREBP、PXR、LXR、FXR、AMPK、SIRT [29, 46-47, 51, 68, 77]
    下载: 导出CSV
  • [1] COTTER TG, RINELLA M. Nonalcoholic fatty liver disease 2020: The state of the disease[J]. Gastroenterology, 2020, 158(7): 1851-1864. doi: 10.1053/j.gastro.2020.01.052
    [2] YOUNOSSI Z, ANSTEE QM, MARIETTI M, et al. Global burden of NAFLD and NASH: Trends, predictions, risk factors and prevention[J]. Nat Rev Gastroenterol Hepatol, 2018, 15(1): 11-20. doi: 10.1038/nrgastro.2017.109
    [3] SANYAL AJ. Past, present and future perspectives in nonalcoholic fatty liver disease[J]. Nat Rev Gastroenterol Hepatol, 2019, 16(6): 377-386. doi: 10.1038/s41575-019-0144-8
    [4] WU YK, ZHENG Q, ZOU BY, et al. The epidemiology of NAFLD in mainland China with analysis by adjusted gross regional domestic product: A meta-analysis[J]. Hepatol Int, 2020, 14(2): 259-269. doi: 10.1007/s12072-020-10023-3
    [5] WANG XJ, MALHI H. Nonalcoholic fatty liver disease[J]. Ann Intern Med, 2018, 169(9): ITC65-ITC80. doi: 10.7326/AITC201811060
    [6] RINELLA ME. Nonalcoholic fatty liver disease: A systematic review[J]. JAMA, 2015, 313(22): 2263-2273. doi: 10.1001/jama.2015.5370
    [7] NEUSCHWANDER-TETRI BA. Therapeutic landscape for NAFLD in 2020[J]. Gastroenterology, 2020, 158(7): 1984-1998. doi: 10.1053/j.gastro.2020.01.051
    [8] SUMIDA Y, YONEDA M. Current and future pharmacological therapies for NAFLD/NASH[J]. J Gastroenterol, 2018, 53(3): 362-376. doi: 10.1007/s00535-017-1415-1
    [9] YAN TT, YAN NN, WANG P, et al. Herbal drug discovery for the treatment of nonalcoholic fatty liver disease[J]. Acta Pharm Sin B, 2020, 10(1): 3-18. doi: 10.1016/j.apsb.2019.11.017
    [10] ESATBEYOGLU T, HUEBBE P, ERNST IM, et al. Curcumin: From molecule to biological function[J]. Angew Chem Int Ed Engl, 2012, 51(22): 5308-5332. doi: 10.1002/anie.201107724
    [11] 崔晶, 翟光喜, 娄红祥. 姜黄素的研究进展[J]. 中南药学, 2005, 3(2): 108-111. doi: 10.3969/j.issn.1672-2981.2005.02.019
    [12] MENON VP, SUDHEER AR. Antioxidant and anti-inflammatory properties of curcumin[J]. Adv Exp Med Biol, 2007, 595: 105-125. http://pdfs.semanticscholar.org/01b2/367ae40b4a9fd32a1523d71306314dd04c34.pdf
    [13] AGGARWAL BB. Targeting inflammation-induced obesity and metabolic diseases by curcumin and other nutraceuticals[J]. Annu Rev Nutr, 2010, 30: 173-199. doi: 10.1146/annurev.nutr.012809.104755
    [14] KUNNUMAKKARA AB, 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
    [15] SALEHI B, STOJANOVIC-RADIC Z, MATEJIC J, et al. The therapeutic potential of curcumin: A review of clinical trials[J]. Eur J Med Chem, 2019, 163: 527-545. doi: 10.1016/j.ejmech.2018.12.016
    [16] GUPTA SC, PATCHVA S, AGGARWAL BB. Therapeutic roles of curcumin: Lessons learned from clinical trials[J]. Aaps J, 2013, 15(1): 195-218. doi: 10.1208/s12248-012-9432-8
    [17] RAHMANI S, ASGARY S, ASKARI G, et al. Treatment of non-alcoholic fatty liver disease with curcumin: A randomized placebo-controlled trial[J]. Phytother Res, 2016, 30(9): 1540-1548. doi: 10.1002/ptr.5659
    [18] AGGARWAL BB, SUNG B. Pharmacological basis for the role of curcumin in chronic diseases: An age-old spice with modern targets[J]. Trends Pharmacol Sci, 2009, 30(2): 85-94. doi: 10.1016/j.tips.2008.11.002
    [19] GENG Y, FABER KN, DE MEIJER VE, et al. How does hepatic lipid accumulation lead to lipotoxicity in non-alcoholic fatty liver disease?[J]. Hepatol Int, 2021, 15(1): 21-35. doi: 10.1007/s12072-020-10121-2
    [20] GINSBERG HN. Selective trafficking of fatty acids in the liver: Add Them2 to the list of influencers[J]. Hepatology, 2019, 70(2): 462-464. doi: 10.1002/hep.30800
    [21] DONNELLY KL, SMITH CI, SCHWARZENBERG SJ, et al. Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease[J]. J Clin Invest, 2005, 115(5): 1343-1351. doi: 10.1172/JCI23621
    [22] ARAB JP, ARRESE M, TRAUNER M. Recent insights into the pathogenesis of nonalcoholic fatty liver disease[J]. Annu Rev Pathol, 2018, 13: 321-350. doi: 10.1146/annurev-pathol-020117-043617
    [23] LAMBERT JE, RAMOS-ROMAN MA, BROWNING JD, et al. Increased de novo lipogenesis is a distinct characteristic of individuals with nonalcoholic fatty liver disease[J]. Gastroenterology, 2014, 146(3): 726-735. doi: 10.1053/j.gastro.2013.11.049
    [24] WEI ZC, LIU N, TANTAI XX, et al. The effects of curcumin on the metabolic parameters of non-alcoholic fatty liver disease: A meta-analysis of randomized controlled trials[J]. Hepatol Int, 2019, 13(3): 302-313. doi: 10.1007/s12072-018-9910-x
    [25] JANG EM, CHOI MS, JUNG UJ, et al. Beneficial effects of curcumin on hyperlipidemia and insulin resistance in high-fat-fed hamsters[J]. Metabolism, 2008, 57(11): 1576-1583. doi: 10.1016/j.metabol.2008.06.014
    [26] AMEER F, SCANDIUZZI L, HASNAIN S, et al. De novo lipogenesis in health and disease[J]. Metabolism, 2014, 63(7): 895-902. doi: 10.1016/j.metabol.2014.04.003
    [27] MAITHILIKARPAGASELVI N, SRIDHAR MG, SWAMINATHAN RP, et al. Curcumin inhibits hyperlipidemia and hepatic fat accumulation in high-fructose-fed male Wistar rats[J]. Pharm Biol, 2016, 54(12): 2857-2863. doi: 10.1080/13880209.2016.1187179
    [28] CUNNINGHAM RP, MOORE MP, MOORE AN, 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
    [29] KABIRIFAR R, GHORESHI ZAS, REZAIFAR A, et al. Curcumin, quercetin and atorvastatin protected against the hepatic fibrosis by activating AMP-activated protein kinase[J]. J Funct Foods, 2018, 40: 341-348. doi: 10.1016/j.jff.2017.11.020
    [30] NTAMBI JM. Hepatic de novo lipogenesis and regulation of metabolism[M]. Cham: Springer International Publishing, 2016.
    [31] IACOBAZZI V, INFANTINO V. Citrate: New functions for an old metabolite[J]. Biol Chem, 2014, 395(4): 387-399. doi: 10.1515/hsz-2013-0271
    [32] WILLIAMS NC, O'NEILL LAJ. A role for the Krebs cycle intermediate citrate in metabolic reprogramming in innate immunity and inflammation[J]. Front Immunol, 2018, 9: 141. doi: 10.3389/fimmu.2018.00141
    [33] BIRKENFELD AL, LEE HY, GUEBRE-EGZIABHER F, et al. Deletion of the mammalian INDY homolog mimics aspects of dietary restriction and protects against adiposity and insulin resistance in mice[J]. Cell Metab, 2011, 14(2): 184-195. doi: 10.1016/j.cmet.2011.06.009
    [34] 牛群, 孙秋爽, 邱志霞, 等. SLC13A5作为代谢性疾病潜在药物作用靶点的研究进展[J]. 中国药科大学学报, 2020, 51(5): 607-613. https://www.cnki.com.cn/Article/CJFDTOTAL-ZGYD202005014.htm
    [35] SUITER C, SINGHA SK, KHALILI R, et al. Free fatty acids: Circulating contributors of metabolic syndrome[J]. Cardiovasc Hematol Agents Med Chem, 2018, 16(1): 20-34. doi: 10.2174/1871525716666180528100002
    [36] KAZANTZIS M, STAHL A. Fatty acid transport proteins, implications in physiology and disease[J]. Biochim Biophys Acta, 2012, 1821(5): 852-857. doi: 10.1016/j.bbalip.2011.09.010
    [37] GOUNDEN V, VASHISHT R, JIALAL I. Hypoalbuminemia[EB/OL]. (2021-04-01)[2021-06-29]. https://www.statpearls.com/articlelibrary/viewarticle/23253/.
    [38] BLINDAUER CA, KHAZAIPOUL S, YU R, et al. Fatty acid-mediated inhibition of metal binding to the multi-metal site on serum albumin: Implications for cardiovascular disease[J]. Curr Top Med Chem, 2016, 16(27): 3021-3032. doi: 10.2174/1568026616666160216155927
    [39] WILSON CG, TRAN JL, ERION DM, et al. Hepatocyte-specific disruption of CD36 attenuates fatty liver and improves insulin sensitivity in HFD-fed mice[J]. Endocrinology, 2016, 157(2): 570-585. doi: 10.1210/en.2015-1866
    [40] ENOOKU K, TSUTSUMI T, KONDO M, et al. Hepatic FATP5 expression is associated with histological progression and loss of hepatic fat in NAFLD patients[J]. J Gastroenterol, 2020, 55(2): 227-243. doi: 10.1007/s00535-019-01633-2
    [41] DOEGE H, BAILLIE RA, ORTEGON AM, et al. Targeted deletion of FATP5 reveals multiple functions in liver metabolism: Alterations in hepatic lipid homeostasis[J]. Gastroenterology, 2006, 130(4): 1245-1258. doi: 10.1053/j.gastro.2006.02.006
    [42] PEREZ VM, GABELL J, BEHRENS M, et al. Deletion of fatty acid transport protein 2 (FATP2) in the mouse liver changes the metabolic landscape by increasing the expression of PPARα-regulated genes[J]. J Biol Chem, 2020, 295(17): 5737-5750. doi: 10.1074/jbc.RA120.012730
    [43] CHEN AP, TANG YC, DAVIS V, et al. Liver fatty acid binding protein (L-Fabp) modulates murine stellate cell activation and diet-induced nonalcoholic fatty liver disease[J]. Hepatology, 2013, 57(6): 2202-2212. doi: 10.1002/hep.26318
    [44] FURUHASHI M, HOTAMISLIGIL GS. Fatty acid-binding proteins: Role in metabolic diseases and potential as drug targets[J]. Nat Rev Drug Discov, 2008, 7(6): 489-503. doi: 10.1038/nrd2589
    [45] MUN J, KIM S, YOON HG, et al. Water extract of Curcuma longa L. ameliorates non-alcoholic fatty liver disease[J]. Nutrients, 2019, 11(10): E2536. doi: 10.3390/nu11102536
    [46] LIU Y, CHENG F, LUO YX, et al. PEGylated curcumin derivative attenuates hepatic steatosis via CREB/PPAR-γ /CD36 pathway[J]. Biomed Res Int, 2017, 2017: 8234507. http://gooa.las.ac.cn/external/download/1424705/5944300/8234507.pdf
    [47] DING LL, LI JM, SONG BL, et al. Curcumin rescues high fat diet-induced obesity and insulin sensitivity in mice through regulating SREBP pathway[J]. Toxicol Appl Pharmacol, 2016, 304: 99-109. doi: 10.1016/j.taap.2016.05.011
    [48] ROSEN ED, SPIEGELMAN BM. Adipocytes as regulators of energy balance and glucose homeostasis[J]. Nature, 2006, 444(7121): 847-853. doi: 10.1038/nature05483
    [49] LANGIN D. Adipose tissue lipolysis as a metabolic pathway to define pharmacological strategies against obesity and the metabolic syndrome[J]. Pharmacol Res, 2006, 53(6): 482-491. doi: 10.1016/j.phrs.2006.03.009
    [50] WANG LL, ZHANG BL, HUANG F, et al. Curcumin inhibits lipolysis via suppression of ER stress in adipose tissue and prevents hepatic insulin resistance[J]. J Lipid Res, 2016, 57(7): 1243-1255. doi: 10.1194/jlr.M067397
    [51] QIU ZX, ZHANG SH, LI AY, et al. The role of curcumin in disruption of HIF-1α accumulation to alleviate adipose fibrosis via AMPK-mediated mTOR pathway in high-fat diet fed mice[J]. J Funct Foods, 2017, 33: 155-165. doi: 10.1016/j.jff.2017.03.035
    [52] REDDY JK, RAO MS. Lipid metabolism and liver inflammation. Ⅱ. Fatty liver disease and fatty acid oxidation[J]. Am J Physiol Gastrointest Liver Physiol, 2006, 290(5): G852-G858. doi: 10.1152/ajpgi.00521.2005
    [53] HOUTEN SM, WANDERS RJ. A general introduction to the biochemistry of mitochondrial fatty acid β-oxidation[J]. J Inherit Metab Dis, 2010, 33(5): 469-477. doi: 10.1007/s10545-010-9061-2
    [54] PAWLAK M, LEFEBVRE P, STAELS B. Molecular mechanism of PPARα 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
    [55] BONNEFONT JP, DJOUADI F, PRIP-BUUS C, et al. Carnitine palmitoyltransferases 1 and 2: Biochemical, molecular and medical aspects[J]. Mol Aspects Med, 2004, 25(5/6): 495-520. http://www.onacademic.com/detail/journal_1000035417370710_44fa.html
    [56] EJAZ A, WU DY, KWAN P, et al. Curcumin inhibits adipogenesis in 3T3-L1 adipocytes and angiogenesis and obesity in C57/BL mice[J]. J Nutr, 2009, 139(5): 919-925. doi: 10.3945/jn.108.100966
    [57] UM MY, HWANG KH, AHN J, et al. Curcumin attenuates diet-induced hepatic steatosis by activating AMP-activated protein kinase[J]. Basic Clin Pharmacol Toxicol, 2013, 113(3): 152-157. doi: 10.1111/bcpt.12076
    [58] FRIEDMAN SL, NEUSCHWANDER-TETRI BA, 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
    [59] SCHUSTER S, CABRERA D, ARRESE M, et al. Triggering and resolution of inflammation in NASH[J]. Nat Rev Gastroenterol Hepatol, 2018, 15(6): 349-364. doi: 10.1038/s41575-018-0009-6
    [60] BRAUNERSREUTHER V, VIVIANI GL, MACH F, et al. Role of cytokines and chemokines in non-alcoholic fatty liver disease[J]. World J Gastroenterol, 2012, 18(8): 727-735. doi: 10.3748/wjg.v18.i8.727
    [61] JURENKA JS. Anti-inflammatory properties of curcumin, a major constituent of Curcuma longa: A review of preclinical and clinical research[J]. Altern Med Rev, 2009, 14(2): 141-153. http://www.ncbi.nlm.nih.gov/pubmed/19594223/
    [62] ZHOU HY, BEEVERS CS, HUANG SL. The targets of curcumin[J]. Curr Drug Targets, 2011, 12(3): 332-347. doi: 10.2174/138945011794815356
    [63] WEI W, PENG J, LI J. Curcumin attenuates hypoxia/reoxygenation-induced myocardial injury[J]. Mol Med Rep, 2019, 20(6): 4821-4830. http://www.ncbi.nlm.nih.gov/pubmed/31638219
    [64] WIECKOWSKA A, PAPOUCHADO BG, LI ZZ, et al. Increased hepatic and circulating interleukin-6 levels in human nonalcoholic steatohepatitis[J]. Am J Gastroenterol, 2008, 103(6): 1372-1379.
    [65] CRESPO J, CAYON A, FERNANDEZ-GIL P, et al. Gene expression of tumor necrosis factor alpha and TNF-receptors, p55 and p75, in nonalcoholic steatohepatitis patients[J]. Hepatology, 2001, 34(6): 1158-1163. doi: 10.1053/jhep.2001.29628
    [66] AFRIN R, ARUMUGAM S, RAHMAN A, et al. Curcumin ameliorates liver damage and progression of NASH in NASH-HCC mouse model possibly by modulating HMGB1-NF-κB translocation[J]. Int Immunopharmacol, 2017, 44: 174-182. http://www.ncbi.nlm.nih.gov/pubmed/28110063
    [67] LECLERCQ IA, FARRELL GC, SEMPOUX C, et al. Curcumin inhibits NF-kappaB activation and reduces the severity of experimental steatohepatitis in mice[J]. J Hepatol, 2004, 41(6): 926-934. http://www.onacademic.com/detail/journal_1000035406130310_82c0.html
    [68] LEE DE, LEE SJ, KIM SJ, et al. Curcumin ameliorates nonalcoholic fatty liver disease through inhibition of O-GlcNAcylation[J]. Nutrients, 2019, 11(11): E2702. http://www.ncbi.nlm.nih.gov/pubmed/31717261
    [69] ELTZSCHIG HK, CARMELIET P. Hypoxia and inflammation[J]. N Engl J Med, 2011, 364: 656-665. http://pubmedcentralcanada.ca/pmcc/articles/PMC3930928/
    [70] SEMENZA GL. Hypoxia-inducible factor 1 (HIF-1) pathway[J]. Sci STKE, 2007, 2007(407): cm8.
    [71] HUANG Y, DENG X, LIANG J. Modulation of hepatic stellate cells and reversibility of hepatic fibrosis[J]. Exp Cell Res, 2017, 352(2): 420-426. http://www.sciencedirect.com/science?_ob=ShoppingCartURL&_method=add&_eid=1-s2.0-S0014482717300927&originContentFamily=serial&_origin=article&_ts=1488297029&md5=5b234bb35a369f7eebcd8137c9e9eeb2
    [72] CHEN Z, JAIN A, LIU H, et al. Targeted drug delivery to hepatic stellate cells for the treatment of liver fibrosis[J]. J Pharmacol Exp Ther, 2019, 370(3): 695-702. http://jpet.aspetjournals.org/content/early/2019/03/18/jpet.118.256156.full.pdf
    [73] COLL M, PEREA L, BOON R, et al. Generation of hepatic stellate cells from human pluripotent stem cells enables in vitro modeling of liver fibrosis[J]. Cell Stem Cell, 2018, 23(1): 101-113. http://www.sciencedirect.com/science?_ob=ShoppingCartURL&_method=add&_eid=1-s2.0-S1934590918302820&originContentFamily=serial&_origin=article&_ts=1530281809&md5=14651e031a8d452f6dc320d414bfccda
    [74] XIONG WP, FRASCH SC, THOMAS SM, et al. Induction of TGF-β1 synthesis by macrophages in response to apoptotic cells requires activation of the scavenger receptor CD36[J]. PLoS ONE, 2013, 8(8): e72772. http://www.researchgate.net/profile/Courtney_Frasch/publication/255737725_Induction_of_TGF-b1_Synthesis_by_Macrophages_in_Response_to_Apoptotic_Cells_Requires_Activation_of_the_Scavenger_Receptor_CD36/links/5463980e0cf2cb7e9da99656/Induction-of-TGF-b1-Synthesis-by-Macrophages-in-Response-to-Apoptotic-Cells-Requires-Activation-of-the-Scavenger-Receptor-CD36.pdf
    [75] LIN JG, ZHENG SZ, CHEN AP. Curcumin attenuates the effects of insulin on stimulating hepatic stellate cell activation by interrupting insulin signaling and attenuating oxidative stress[J]. Lab Invest, 2009, 89(12): 1397-1409. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2787823/pdf/nihms-137922.pdf
    [76] TANG YC, ZHENG SZ, CHEN AP. Curcumin eliminates leptin's effects on hepatic stellate cell activation via interrupting leptin signaling[J]. Endocrinology, 2009, 150(7): 3011-3020. http://endo.endojournals.org/content/150/7/3011.full.pdf
    [77] ZENG KJ, TIAN LL, SIREK A, et al. Pak1 mediates the stimulatory effect of insulin and curcumin on hepatic ChREBP expression[J]. J Mol Cell Biol, 2017, 9(5): 384-394. http://europepmc.org/abstract/MED/28992163
  • 加载中
图(1) / 表(1)
计量
  • 文章访问数:  348
  • HTML全文浏览量:  36
  • PDF下载量:  222
  • 被引次数: 0
出版历程
  • 收稿日期:  2021-03-05
  • 网络出版日期:  2021-12-21
  • 刊出日期:  2021-07-10
  • 发布日期:  2021-07-15

目录

    /

    返回文章
    返回