本文選題：人參皂苷　切入點(diǎn)：地塞米松　出處：《東南大學(xué)學(xué)報(bào)(醫(yī)學(xué)版)》2016年01期 　論文類型：期刊論文

【摘要】：目的:探討人參皂苷(GS)聯(lián)合地塞米松(Dex)對(duì)刀豆蛋白所致肝損傷模型大鼠肝功能的保護(hù)作用,并分析其相關(guān)機(jī)制。方法:將Wistar大鼠40只按隨機(jī)數(shù)字表法分為5組(每組8只):模型組、GS組、Dex組、GS+Dex組及對(duì)照組。模型組即建立刀豆蛋白誘導(dǎo)肝損傷模型;GS組、Dex組即分別給藥Dex和GS;GS+Dex組則使用Dex和GS聯(lián)合給藥;對(duì)照組不給予任何干預(yù)。觀察記錄血清丙氨酸氨基轉(zhuǎn)移酶(ALT)、天門冬氨酸氨基轉(zhuǎn)移酶(AST)、脂質(zhì)過氧化物丙二醛(MDA)和超氧化物歧化酶(SOD)水平,肝組織中核轉(zhuǎn)錄因子kappa B(NF-κB)P65的表達(dá)及腫瘤壞死因子-α(TNF-α)和γ-干擾素(IFN-γ)含量變化。并進(jìn)行肝組織病理學(xué)檢查。結(jié)果:模型組的ALT和AST水平與對(duì)照組比較顯著上升(t=4.570、4.513,P0.01);GS和Dex單獨(dú)及聯(lián)合給藥組的ALT和AST水平與模型組比較均明顯降低(P0.05);GS+Dex組ALT水平降低程度顯著大于GS組和Dex組(t=2.263、3.072,P0.05),AST水平也如此(t=2.829、2.765,P0.05)。模型組大鼠肝勻漿中的MDA水平與對(duì)照組相比上升,而SOD活性顯著降低(t=7.515、8.514,P0.01),GS組的MDA水平、SOD活性與模型組比較差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05),GS+Dex組MDA水平降低和SOD活性升高程度顯著大于Dex組(t=2.287、2.722,P0.05)。GS+Dex組大鼠體重顯著高于模型組及GS組(t=2.942、2.327,P0.05)。模型組的NF-κB P65的蛋白表達(dá)與對(duì)照組比較顯著上調(diào)(t=9.428,P0.01),GS+Dex組下調(diào)NF-κB P65蛋白表達(dá)的程度明顯大于GS組和Dex組(t=6.428、5.246,P0.05)。模型組的TNF-α和IFN-γ水平與對(duì)照組比較顯著上升(t=19.235、25.171,P0.01),GS+Dex組TNF-α水平降低程度顯著大于GS組和Dex組(t=2.313、9.053,P0.05),GS+Dex組IFN-γ水平降低程度亦顯著大于GS組和Dex組(t=5.171、8.933,P0.05)。結(jié)論:GS聯(lián)合Dex可有效保護(hù)刀豆蛋白所致肝損傷模型大鼠的肝功能,其機(jī)制可能與抑制氧化應(yīng)激、抑制NF-κB P65活性、下調(diào)TNF-α含量、調(diào)節(jié)免疫作用有關(guān)。
[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- 偽 (TNF- 偽) and interferon- 緯 (IFN- 緯) 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- 偽 and IFN- 緯 in the model group were significantly higher than those in the control group, and the levels of TNF- 偽 and IFN- 緯 in the GS Dex group were significantly higher than those in the GS Dex group. The level of IFN- 緯 in Dex group was significantly higher than that in GS group and Dex group. Conclusion the level of IFN- 緯 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- 偽 content and regulation of immune function.
【作者單位】： 上海市第七人民醫(yī)院藥學(xué)部;
【基金】：上海市第七人民醫(yī)院“七院新星”人才培養(yǎng)項(xiàng)目(XX2012-026)
【分類號(hào)】：R575

【參考文獻(xiàn)】

相關(guān)期刊論文 前1條

1 王國(guó)華;劉風(fēng)玲;;人參皂甙Rg3抗腫瘤作用機(jī)制研究進(jìn)展[J];中國(guó)醫(yī)藥導(dǎo)刊;2015年03期

【二級(jí)參考文獻(xiàn)】

相關(guān)期刊論文 前10條

1 吳永娟;胡道珍;王敬忠;沈正林;;紫杉醇的抗腫瘤機(jī)制及研究進(jìn)展[J];中國(guó)醫(yī)藥導(dǎo)刊;2010年02期

2 齊平;靳穎華;張為革;宋宏銳;;分子靶點(diǎn)抗腫瘤藥物研究進(jìn)展[J];中國(guó)醫(yī)藥導(dǎo)刊;2014年02期

3 陳大富;莊永敬;黃建強(qiáng);;人參皂甙Rg3聯(lián)合FOLFOX 4方案治療直腸癌的療效觀察[J];臨床腫瘤學(xué)雜志;2013年02期

4 辛穎;姜新;崔俊生;倪勁松;;人參皂苷Rg3抑制B16黑色素瘤新生血管生成及其機(jī)制的探討[J];中華腫瘤防治雜志;2010年08期

5 于學(xué)濤;王淑萍;;人參皂苷Rg3聯(lián)合化療治療對(duì)胃癌術(shù)后患者的臨床觀察[J];中華腫瘤防治雜志;2010年10期

6 安寧;朱文;;人參皂苷Rg3抗腫瘤作用機(jī)制研究進(jìn)展[J];現(xiàn)代腫瘤醫(yī)學(xué);2008年04期

7 許霞輝;賀兼斌;張平;;人參皂苷Rg3聯(lián)合蘇拉明對(duì)小鼠肺癌生長(zhǎng)影響及其機(jī)制的探討[J];中華腫瘤防治雜志;2013年02期

8 李雪甫;劉艷文;王永實(shí);;人參皂甙Rh2聯(lián)合順鉑對(duì)食管癌細(xì)胞的殺傷作用[J];現(xiàn)代腫瘤醫(yī)學(xué);2014年03期

9 陳曦;陳魯;;人參皂苷Rg3的抗腫瘤作用研究進(jìn)展[J];中國(guó)當(dāng)代醫(yī)藥;2011年36期

10 侯俊杰;宋艷秋;康麗花;趙玲玲;單既英;韓倩;;20(R)-人參皂甙Rg3對(duì)老年腫瘤患者放、化療后的輔助治療效果[J];中國(guó)老年學(xué)雜志;2011年20期

相關(guān)博士學(xué)位論文 前1條

1 魯培;人參皂甙Rg3治療食管癌分子機(jī)制的實(shí)驗(yàn)性研究[D];鄭州大學(xué);2013年

相關(guān)碩士學(xué)位論文 前4條

1 錢伶凌;人參皂甙Rg3對(duì)乳腺癌細(xì)胞系的抑制作用[D];浙江工業(yè)大學(xué);2010年

2 王小燕;人參皂甙Rg3聯(lián)合小劑量化療對(duì)乳腺癌抗血管作用的實(shí)驗(yàn)研究[D];大連醫(yī)科大學(xué);2010年

3 馬利軍;人參皂甙Rg3上調(diào)Fas蛋白誘導(dǎo)乳腺癌MCF-7細(xì)胞的凋亡[D];山西醫(yī)科大學(xué);2010年

4 章馨允;人參皂甙Rh2聯(lián)合化療對(duì)T細(xì)胞淋巴瘤協(xié)同增效的分子機(jī)制[D];天津醫(yī)科大學(xué);2013年

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