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:
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.
Effect of Amentoflavone on Inflammatory Factors in Rats with Acute Liver Injury
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
30
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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