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姜辣素通过抑制促炎和促纤维化介质来预防大鼠实验性肝纤维化。

Gingerol protects against experimental liver fibrosis in rats via suppression of pro-inflammatory and profibrogenic mediators.

作者信息

Algandaby Mardi M, El-Halawany Ali M, Abdallah Hossam M, Alahdal Abdulrahman M, Nagy Ayman A, Ashour Osama M, Abdel-Naim Ashraf B

机构信息

Medicinal Plants Research Group, Deanship of Scientific Research, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.

Department of Biological Sciences, Faculty of Science, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 2016 Apr;389(4):419-28. doi: 10.1007/s00210-016-1210-1. Epub 2016 Jan 26.

DOI:10.1007/s00210-016-1210-1
PMID:26809353
Abstract

6-Gingerol (Gin) is known to possess hepatoprotective effects. Liver fibrosis is a major health concern that results in significant morbidity and mortality. There is no FDA-approved medication for liver fibrosis. The present work aimed at exploring the beneficial effects of Gin against liver fibrosis in rats. Experimental fibrosis was induced by challenging animals with CCl4 for 6 weeks. Gin significantly ameliorated the increase in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, albumin, total cholesterol (TC) and triglyceride (TG) concentrations, and liver index. These effects were confirmed by light and electron microscopic examinations. The antifibrotic effects were confirmed by examining Masson trichrome-stained liver sections which indicated reduced collagen deposition in Gin-treated animals. Further, Gin administration hampered alpha-smooth muscle actin (α-SMA) expression and significantly reduced hepatic content of transforming growth factor-beta (TGF-β). Also, Gin elicited profound antioxidant actions as indicated by preventing reduced glutathione (GSH) depletion and lipid peroxide accumulation. The observed antifibrotic activities involved decreased production of nuclear factor κB (NF-κB), tumor necrosis factor alpha (TNF-α), expression of toll-like receptor 4 (TLR4), intercellular adhesion molecule (ICAM), and vascular cell adhesion molecule (VCAM). Involvement of Gin anti-inflammatory activity was verified by the decreased expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in livers of animals treated with Gin. Thus, it can be concluded that Gin protects against CCl4-induced liver fibrosis in rats. This can be ascribed, at least partly, to its antioxidant, anti-inflammatory effects as well as the inhibition of NF-κB/TLR-4 expression.

摘要

已知6-姜酚(Gin)具有肝脏保护作用。肝纤维化是一个主要的健康问题,会导致显著的发病率和死亡率。目前尚无美国食品药品监督管理局(FDA)批准的用于治疗肝纤维化的药物。本研究旨在探讨Gin对大鼠肝纤维化的有益作用。通过用四氯化碳(CCl4)刺激动物6周诱导实验性纤维化。Gin显著改善了血清丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)活性、白蛋白、总胆固醇(TC)和甘油三酯(TG)浓度以及肝脏指数的升高。这些作用通过光镜和电镜检查得到证实。通过检查Masson三色染色的肝脏切片证实了抗纤维化作用,该切片显示Gin处理的动物中胶原沉积减少。此外,给予Gin阻碍了α-平滑肌肌动蛋白(α-SMA)的表达,并显著降低了转化生长因子-β(TGF-β)的肝脏含量。而且,Gin引发了显著的抗氧化作用,表现为防止还原型谷胱甘肽(GSH)耗竭和脂质过氧化物积累。观察到的抗纤维化活性涉及核因子κB(NF-κB)、肿瘤坏死因子-α(TNF-α)的产生减少,Toll样受体4(TLR4)、细胞间黏附分子(ICAM)和血管细胞黏附分子(VCAM)的表达降低。Gin抗炎活性的参与通过给予Gin的动物肝脏中诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)表达的降低得到证实。因此,可以得出结论,Gin可保护大鼠免受CCl4诱导的肝纤维化。这至少部分可归因于其抗氧化、抗炎作用以及对NF-κB/TLR-4表达的抑制。

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本文引用的文献

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Kang-Xian Pills Inhibit Inflammatory Response and Decrease Gut Permeability to Treat Carbon Tetrachloride-Induced Chronic Hepatic Injury through Modulating Gut Microbiota.康仙丸通过调节肠道菌群抑制炎症反应并降低肠道通透性以治疗四氯化碳诱导的慢性肝损伤。
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