穗花杉双黄酮对急性肝损伤大鼠炎症相关因子的影响

黄振青; 韦燕飞; 刘雪梅; 段雪琳; 赵铁建

doi:10.13422/j.cnki.syfjx.2014110147

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穗花杉双黄酮对急性肝损伤大鼠炎症相关因子的影响

药理 | 更新时间：2024-01-04

- 穗花杉双黄酮对急性肝损伤大鼠炎症相关因子的影响
- Effect of Amentoflavone on Inflammatory Factors in Rats with Acute Liver Injury
- 中国实验方剂学杂志 2014年20卷第11期页码：147-150
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.2014110147
  中图分类号： R285.5
- 纸质出版日期：2014
- 稿件说明：
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黄振青, 韦燕飞, 刘雪梅, 等. 穗花杉双黄酮对急性肝损伤大鼠炎症相关因子的影响[J]. 中国实验方剂学杂志, 2014,20(11):147-150.

HUANG Zhen-qing, WEI Yan-fei, LIU Xue-mei, et al. Effect of Amentoflavone on Inflammatory Factors in Rats with Acute Liver Injury[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(11): 147-150.
黄振青, 韦燕飞, 刘雪梅, 等. 穗花杉双黄酮对急性肝损伤大鼠炎症相关因子的影响[J]. 中国实验方剂学杂志, 2014,20(11):147-150. DOI： 10.13422/j.cnki.syfjx.2014110147.

HUANG Zhen-qing, WEI Yan-fei, LIU Xue-mei, et al. Effect of Amentoflavone on Inflammatory Factors in Rats with Acute Liver Injury[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(11): 147-150. DOI： 10.13422/j.cnki.syfjx.2014110147.

摘要

目的：研究穗花杉双黄酮（ATF）对四氯化碳（CCl4）诱导急性肝损伤大鼠炎症相关因子的影响。方法：将健康雄性SD大鼠随机分为正常对照组，损伤模型组，阳性对照组，穗花杉双黄酮低、中、高剂量组（15，30，60 mg·kg-1），连续给药7 d，末次灌胃给药1 h后，腹腔注射CCl4原液建立急性肝损伤大鼠模型，采用ELISA法分别检测各组大鼠血清肿瘤坏死因子-α（TNF-α），转化生长因子β1 （TGF-β1），白介素1β（IL-1β），白细胞介素6（IL-6）的含量和肝组织核因子-κB （NF-κB），磷酸化抑制蛋白（nuclear factor kappa B inhibitor protein，IκB-α）的水平，采用鲎试剂终点显色法检测大鼠血浆内毒素（LPS）水平，Real time PCR法检测肝组织TNF-α和诱导型一氧化氮合酶（iNOS）基因的表达。结果：与正常组比较，模型组大鼠血清TNF-α，TGF-β1，IL-1β，IL-6的含量显著升高（P<0.01），大鼠血浆内毒素水平明显提高（P<0.01），肝组织NF-kB和磷酸化IκB-α的水平也明显升高（P<0.01），肝组织TNF-α和iNOS基因的表达也显著上调（P<0.01）。与模型组比较，ATF能显著降低血清TNF-α，TGF-β1，IL-1β，IL-6的含量（P<0.05 或P<0.01），降低肝组织NF-κB和磷酸化IκB-α的水平，且能显著降低LPS水平，下调肝组织TNF-α和iNOS基因的表达（P<0.05或P<0.01）。结论：穗花杉双黄酮对四氯化碳致急性肝损伤大鼠具有明显的保护作用，其机制可能通过抑制内毒素引起的Kupffer细胞激活，进而抑制下游核因子NF-κB的激活，减少炎症细胞因子的释放。

Abstract

Objective:To investigate the effects of amentoflavone (ATF) on inflammatory factors in rats with acute liver injury. Method:The healthy adult male Sprague-Dawley(SD) rats were randomly divided into six groups

control group

model group

positive control group

ATF low-dose

middle-dose and high-dose group(15

60 mg·kg-1)

respectively. The experimental rats were administrated with drugs by ig for 7 days

one hours after the last administration

the experimental rats were injected carbon tetrachloride to copy the acute liver injury model except control group. The contents of tumor necrosis factor-α(TNF-α)

transforming growth factor beta(TGF-β1)

interleukin 1β(IL-1β)

interleukin-6(IL-6) were investigated by ELISA. The phosphor-IκB-α level and nuclear factor κB(NF-κB) nuclear translocation in hepatic tissue were measured by ELISA. The plasma endotoxin(LPS) level was measured by limulus amebocyte lysate(LAL)chromogenic endpoint assay. The expression of TNF-α mRNA and induced nitric oxide synthase(iNOS) mRNA in hepatical tissues in rats were detected by Real time PCR. Result:Compared with the normal control group

the contents of TNF-α

TGF-β1

IL-1β and IL-6 in the serum of the model group rats were obviously increased(P<0.01)

and the level of plasma endotoxin was obviously increased(P<0.01)

the phosphor-IκB-α level and NF-κB nuclear translocation were obviously increased

the expression of TNF-α mRNA and iNOS mRNA were up-regulated(both P<0.01). Compared with the model group

the contents of TNF-α

TGF-β1

IL-1β

IL-6 were obviously decreased(P<0.05 or P<0.01)

The phosphor-IκB-α level and NF-κB nuclear translocation were decreased(P<0.05 or P<0.01)

and the level of plasma endotoxin was obviously decreased

the expression of TNF-α mRNA and iNOS mRNA in hepatical tissues in rats were down-regulated(P<0.05 or P<0.01). Conclusion:ATF could protect the acute hepatic injury induced by CCl4 in rats

the mechanism may be related to decreasing endotoxin level and NF-κB nuclear translocation and attenuating the trigger of inflammation-related cascade amplification.

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