人参皂苷联合地塞米松对刀豆蛋白所致肝损伤模型大鼠肝功能保护作用及相关机制研究

发布时间：2018-03-06 06:39

本文选题：人参皂苷　切入点：地塞米松　出处：《东南大学学报(医学版)》2016年01期 　论文类型：期刊论文

【摘要】：目的:探讨人参皂苷(GS)联合地塞米松(Dex)对刀豆蛋白所致肝损伤模型大鼠肝功能的保护作用,并分析其相关机制。方法:将Wistar大鼠40只按随机数字表法分为5组(每组8只):模型组、GS组、Dex组、GS+Dex组及对照组。模型组即建立刀豆蛋白诱导肝损伤模型;GS组、Dex组即分别给药Dex和GS;GS+Dex组则使用Dex和GS联合给药;对照组不给予任何干预。观察记录血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、脂质过氧化物丙二醛(MDA)和超氧化物歧化酶(SOD)水平,肝组织中核转录因子kappa B(NF-κB)P65的表达及肿瘤坏死因子-α(TNF-α)和γ-干扰素(IFN-γ)含量变化。并进行肝组织病理学检查。结果:模型组的ALT和AST水平与对照组比较显著上升(t=4.570、4.513,P0.01);GS和Dex单独及联合给药组的ALT和AST水平与模型组比较均明显降低(P0.05);GS+Dex组ALT水平降低程度显著大于GS组和Dex组(t=2.263、3.072,P0.05),AST水平也如此(t=2.829、2.765,P0.05)。模型组大鼠肝匀浆中的MDA水平与对照组相比上升,而SOD活性显著降低(t=7.515、8.514,P0.01),GS组的MDA水平、SOD活性与模型组比较差异无统计学意义(P0.05),GS+Dex组MDA水平降低和SOD活性升高程度显著大于Dex组(t=2.287、2.722,P0.05)。GS+Dex组大鼠体重显著高于模型组及GS组(t=2.942、2.327,P0.05)。模型组的NF-κB P65的蛋白表达与对照组比较显著上调(t=9.428,P0.01),GS+Dex组下调NF-κB P65蛋白表达的程度明显大于GS组和Dex组(t=6.428、5.246,P0.05)。模型组的TNF-α和IFN-γ水平与对照组比较显著上升(t=19.235、25.171,P0.01),GS+Dex组TNF-α水平降低程度显著大于GS组和Dex组(t=2.313、9.053,P0.05),GS+Dex组IFN-γ水平降低程度亦显著大于GS组和Dex组(t=5.171、8.933,P0.05)。结论:GS联合Dex可有效保护刀豆蛋白所致肝损伤模型大鼠的肝功能,其机制可能与抑制氧化应激、抑制NF-κB P65活性、下调TNF-α含量、调节免疫作用有关。
[Abstract]:Objective: to investigate the protective effect of ginsenoside GSH combined with dexamethasone Dexon on liver function in rat model of liver injury induced by concanavalin. Methods: forty Wistar rats were randomly divided into 5 groups (8 rats in each group: model group, GS group, Dex group, GS Dex group and control group). The model group established concanavalin induced liver injury model. Dex and GSG GS Dex group were treated with Dex and GS respectively. The levels of serum alanine aminotransferase (alt), aspartate aminotransferase (AST), lipid peroxide malondialdehyde (MDA) and superoxide dismutase (SOD) were observed and recorded in the control group. The expression of nuclear transcription factor kappa Bu NF- 魏 B p65 and the contents of tumor necrosis factor- 伪 (TNF- 伪) and interferon- 纬 (IFN- 纬) in liver tissue were also detected. Results: the levels of ALT and AST in the model group were significantly higher than those in the control group, and the levels of ALT and AST in the model group were significantly higher than those in the control group. Compared with the model group, the levels of ALT and AST in the single and combined administration groups were significantly lower than those in the model group. The level of ALT in the Dex group was significantly higher than that in the GS group and the Dex group. The same was true of the ALT level in the liver homogenate of the model group and the control group. The level of MDA in the liver homogenate of the model group was higher than that of the control group, and the level of ALT in the liver homogenate of the model group was higher than that of the control group. However, the activity of SOD decreased significantly in the GS group (7.515) and the MDA level in the GS group. There was no significant difference between the model group and the model group. The decrease of MDA level and the increase of SOD activity in the Dex group were significantly higher than those in the Dex group (2.2872.722), P0.05.GS Dex group was significantly higher than that in the model group and GS group, the body weight of the rats in the GS group was significantly higher than that in the model group and GS group. The protein expression of NF- 魏 B p65 in the model group was significantly up-regulated than that in the control group. The down-regulation of NF- 魏 B p65 protein expression in the GS Dex group was significantly higher than that in the GS group and the Dex group. The levels of TNF- 伪 and IFN- 纬 in the model group were significantly higher than those in the control group, and the levels of TNF- 伪 and IFN- 纬 in the GS Dex group were significantly higher than those in the GS Dex group. The level of IFN- 纬 in Dex group was significantly higher than that in GS group and Dex group. Conclusion the level of IFN- 纬 in GS group and Dex group was significantly higher than that in GS group and Dex group. Conclusion the liver function of rats with liver injury induced by concanavalin can be effectively protected by combining with Dex. The mechanism may be related to inhibition of oxidative stress, inhibition of NF- 魏 B p65 activity, down-regulation of TNF- 伪 content and regulation of immune function.
【作者单位】：上海市第七人民医院药学部;
【基金】：上海市第七人民医院“七院新星”人才培养项目(XX2012-026)
【分类号】：R575

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