Actions of  Berk.Sacc and its Effective Components on Reversing Liver Fibrosis Induced by Dimethylnitrosamine in Rats

LI Feng-hua; Liu Ping; WANG Chun-shu

doi:CNKI:11-3495/R.20110314.0942.010

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Actions of Berk.Sacc and its Effective Components on Reversing Liver Fibrosis Induced by Dimethylnitrosamine in Rats

更新时间：2024-01-04

- Actions of Berk.Sacc and its Effective Components on Reversing Liver Fibrosis Induced by Dimethylnitrosamine in Rats
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 17, Issue 9, Pages: 164-168(2011)
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- DOI：CNKI:11-3495/R.20110314.0942.010
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- Published：2011
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LI Feng-hua, Liu Ping, WANG Chun-shu. Actions of Berk.Sacc and its Effective Components on Reversing Liver Fibrosis Induced by Dimethylnitrosamine in Rats[J]. Chinese journal of experimental traditional medical formulae, 2011, 17(9): 164-168.
DOI：

LI Feng-hua, Liu Ping, WANG Chun-shu. Actions of Berk.Sacc and its Effective Components on Reversing Liver Fibrosis Induced by Dimethylnitrosamine in Rats[J]. Chinese journal of experimental traditional medical formulae, 2011, 17(9): 164-168. DOI： CNKI:11-3495/R.20110314.0942.010.

摘要

目的: 研究虫草菌丝治疗二甲基亚硝胺(DMN)模型大鼠肝纤维化的有效组分及其作用机制。方法: 大鼠ip DMN 5 mg ·kg-1

每周连续3d

共4周。造模结束后

模型大鼠随机分组

治疗组分别以虫草菌丝(CsB)及其组分(C12)以生药800

5 mg ·kg-1ig

每日1次

共2周;正常组及模型组以等量生理盐水ig。分别检测血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)活性

检测肝组织羟脯氨酸(Hyp)、丙二醛(MDA)含量

超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)和谷胱甘肽-S转移酶(GST)活性

观察肝组织胶原沉积变化

免疫组织化学和蛋白印迹法(Western)检测α-平滑肌肌动蛋白(α-SMA)

转化生长因子-β1(TGF-β1)和图像分析肿瘤坏死因子-α(TNF-α)阳性面积百分比

观察肝组织病理及胶原沉积变化。结果: 与模型组比较

CsB及C12治疗组大鼠血清ALT

AST活性显著降低( P <0.05)。与6周模型组比较

CsB及C12治疗组大鼠肝组织Hyp含量显著降低( P <0.05)。模型组大鼠肝组织可见炎性细胞浸润

胶原增生明显

大多数形成较厚的完全间隔

假小叶形成。CsB及C12治疗组的坏死出血、炎性细胞浸润、胶原增生、纤维间隔形成有所改善。与6周模型组相比

CsB及C12治疗组的 SOD

GSH-Px活性显著升高

MDA含量

GST活性显著降低( P <0.01)。与6周模型组比较

CsB及C12治疗组大鼠肝组织α-SMA

TGF-β1及TNF-α的蛋白表达显著减少( P <0.01)。结论: CsB及C12能够显著改善肝功能

有显著抗肝纤维化作用。CsB及C12能够显著减轻过氧化损伤

保护肝细胞

减少胶原生成

阻断和逆转二甲基亚硝胺大鼠肝纤维化。CsB和C12 抑制库普弗细胞(KCs)活化和细胞因子TNF-α

TGF-β1的释放

抑制肝星状细胞(HSCs)活化

合成和分泌细胞外基质。

Abstract

Objective: To study the effect and mechanism of Cordyceps sinensis Berk Sacc(CsB) and its effective components on liver fibrosis induced by dimethylnitrosamine (DMN) in rats. Method: From the 1st to 4th week

rats were treated with intraperitoneal injection of DMN (5 mg ·kg-1) for three continuous days each week. After modeling

normal group and model group were given saline (10 mL ·kg-1) intragastrically

and rats in drug treatment group were treated separately with CsB and its componentsC12 (800 mg ·kg-1 ·d-1 and 5 mg ·kg-1 ·d-1) for 2 weeks.All the rats were sacrificed to harvest blood and liver tissue sample. Serum alanine aminotransferase(ALT) and aspartate transferase (AST) were detected

maleic dialdehyde (MDA)

superoxide dismutase (SOD)

glutathione peroxidase (GSH-Px) and glutathiones s transferase (GST) in liver tissue were assayed biochemically. Content of hydroxyproline (Hyp) in liver tissue was assayed biochemically;Histological changes with collagen deposition with sirus red staining in rat liver tissue were observed. Expression of α-smooth muscle action (α-SMA)

transforming growth factor-β1 (TGF-β1)

hepatocyte growth factor (HGF-α) and tumor necrosis factor-α (TNF-α) were detected immunohistologically. Result: Compared to 6 wk model group

serum ALT and AST in CsB and C12 group were lowered( P <0.05).Compared to 6 wk model group

Hyp content in liver tissue in CsB and C12 group was decreased significantly ( P <0.05). Large area of hemorrhage and necrosis

swelling of large amount of hepatocytes

widened portal area

inflammatory cells infiltration

increased collagen deposition

and pseudolobule were seen in liver tissue in the model group. Some histological improvement was seen in CsB group and C12 group. Compared to 6 wk model group

CsB and C12 could increase SOD and GSH-Px activity

meanwhile decrease MDA and GST activity ( P <0.01). Compared to 6w model group

expression of α-SMA

TGF-β1 and TNF-α in CsB and C12 was decreased obviously ( P <0.01). Conclusion: CsB and C12 blocks development and formation of liver fibrosis induced by dimethylnitrosamine

through protecting hepatocytes to resist liver injury

decreasing synthesis of collagen

inhibiting oxidative stress. CsB and C12 inhibit KCs activation and release of cytokines

which further inhibits HSCs’ activation

synthesis and secretion of ECM.

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Related Institution

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