Protection Mechanism of Total Flavones from Hemerocallis Fulva on Alcohol-induced Liver Injury in Mice

XU Bo; WU Wei-nan; LI Chuan-jia; CHEN Xue; ZHAO Dong-hai; LI Chang-hua; SHEN Nan

doi:10.13422/j.cnki.syfjx.2016230139

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Protection Mechanism of Total Flavones from Hemerocallis Fulva on Alcohol-induced Liver Injury in Mice

更新时间：2024-01-04

- Protection Mechanism of Total Flavones from Hemerocallis Fulva on Alcohol-induced Liver Injury in Mice
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 22, Issue 23, Pages: 139-143(2016)
- 作者机构：
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- DOI：10.13422/j.cnki.syfjx.2016230139
  CLC： R285.5
- Published：2016
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XU Bo, WU Wei-nan, LI Chuan-jia, et al. Protection Mechanism of Total Flavones from Hemerocallis Fulva on Alcohol-induced Liver Injury in Mice[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(23): 139-143.
DOI：

XU Bo, WU Wei-nan, LI Chuan-jia, et al. Protection Mechanism of Total Flavones from Hemerocallis Fulva on Alcohol-induced Liver Injury in Mice[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(23): 139-143. DOI： 10.13422/j.cnki.syfjx.2016230139.

摘要

目的：观察萱草花总黄酮对小鼠急性酒精性肝损伤的保护作用，并探讨其可能的作用机制。方法： 60只小鼠随机分为正常组、模型组、联苯双酯组和萱草花总黄酮低、中、高剂量组。采用一次性灌胃乙醇的方法建立急性酒精性肝损伤模型。观察萱草花总黄酮对各组血清丙氨酸氨基转移酶（ALT）和天门冬氨酸氨基转移酶（AST）活性以及肝组织超氧化物歧化酶（SOD），丙二醛（MDA），谷胱甘肽过氧化物酶（GPX）以及还原型谷胱甘肽（GSH）水平的影响，并观察肝组织病理改变；蛋白质免疫印迹法（Western blot）检测肝细胞B淋巴细胞瘤-2（Bcl-2），Bcl-2相关X蛋白（Bax）蛋白的表达。结果：与模型组比较，萱草花总黄酮可明显降低血清ALT，AST活性（P<0.05）；降低肝组织中MDA含量，提高SOD，GPX，GSH活性（P<0.05，P<0.01）。病理学检查可见，与模型组比较，萱草花总黄酮中、高剂量组可明显减轻肝细胞变性和坏死的程度，改善肝组织的病理学改变。Western blot结果可见萱草花总黄酮组Bcl-2蛋白表达增加（P<0.05，P<0.01）；Bax蛋白表达减少，Bax/Bcl-2降低（P<0.05，P<0.01）。结论：萱草花总黄酮对乙醇所致小鼠急性酒精性肝损伤具有明显的保护作用，其作用机制可能与其抗氧化作用及调节凋亡相关蛋白Bcl-2，Bax的表达有一定关联。

Abstract

Objective: To study the protection effect of total flavones from the hemerocallis fulva (TFHF) on alcohol-induced liver injury in mice and explore their possible pharmacological mechanisms. Method: A total of 60 mice were randomly divided into normal group

model group

bifendate group and TFHF low dose

middle dose

and high dose groups. Acute hepatic injury models were established by once gavage administration of alcohol. Levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum

as well as sup eroxide dismutase (SOD)

malondialdehyde (MDA)

glutathione peroxidase (GPX) and glutathione (GSH) levels in liver tissues were assayed and compared. The pathological changes in liver tissues were observed

and the expression levels of Bcl-2 and Bax were detected by Western blot. Result: As compared with the model group

TFHF could significantly reduce serum ALT and AST levels (P<0.05)

decrease the MDA content in liver tissues and increase the activities of SOD

GSH and GPX(P<0.05

P<0.01). Pathological examination showed that as compared with the model group

TFHF middle dose group and high dose group could significantly alleviate the liver cell degeneration and necrosis

and improve the pathological changes of hepatic tissues. Western blot results showed that the protein expression level of Bcl-2 was significantly increased in TFHF groups (P<0.05

P<0.01)

whereas the protein expression of Bax was decreased and Bax/Bcl-2 was also decreased (P<0.05

P<0.01). Conclusion: TFHF may have a significant protection effect on alcohol-induced liver injury in mice

and the mechanism may be associated with its antioxidation effect and regulating the expression levels of Bcl-2 and Bax.

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