玉屏风总多糖对急性肝损伤的保护作用及部分机制研究
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摘要
本课题采用四氯化碳、D-氨基半乳糖致急性化学性肝损伤小鼠模型,卡介苗加脂多糖致急性免疫性肝损伤小鼠模型,研究玉屏风总多糖(polysaccharides fromYu-Ping-Feng Powder,YPF-P)对急性肝损伤的保护作用并研究其对急性肝损伤小鼠某些细胞因子、炎性介质等的影响,初步探讨玉屏风总多糖对实验性肝损伤的作用机制。
研究内容包括以下三部分:
1.玉屏风总多糖对CCl_4致小鼠急性化学性肝损伤的影响及部分机制研究YPF-P(200 mg·kg~(-1),ig)能显著降低CCl_4(0.1%CCl4,10ml·kg~(-1),ip)致急性化学性肝损伤小鼠的肝指数,降低血清中升高的ALT、AST水平:YPF-P(100,200 mg·kg~(-1),ig)可显著降低小鼠肝匀浆中升高的MDA含量,增高肝匀浆中已降低的SOD的活性及GSH的水平。提示,YPF-P对CCl_4诱导的急性化学性肝损伤具有一定的保护作用,可能与其清除自由基,抑制脂质过氧化,增强机体抗氧化能力有关。
2.玉屏风总多糖对D-Gal诱导小鼠急性化学性肝损伤的影响
YPF-P(200 mg·kg~(-1),ig)能显著降低D-Gal(800 mg·kg~(-1),ip)致急性化学性肝损伤小鼠的肝脏指数,降低血清中升高的ALT、AST水平:YPF-P(100,200 mg·kg~(-1))ig给药可显著降低小鼠肝匀浆中升高的MDA含量,增强肝匀浆中已降低的SOD的活性及GSH的水平。提示,YPF-P对D-Gal诱导的急性化学性肝损伤具有一定的保护作用,其保护机制可能与抑制脂质过氧化有关。
3.玉屏风总多糖对卡介苗加脂多糖致小鼠免疫性肝损伤的影响及部分机制研究
YPF-P(100、200 mg·kg~(-1),ig)能显著降低免疫性肝损伤小鼠的肝脏、脾脏指数,降低升高的血清ALT、AST水平及肝匀浆中MDA、NO含量,提高肝匀浆中已降低的SOD的活性,并显著降低TNF-αmRNA在肝组织中的表达;小鼠肝组织iNOS、TNF-α在模型组高表达,YPF-P(50、100、200 mg·kg~(-1),ig)治疗后,免疫组化结果提示,随剂量增加,表达逐渐减弱:图象分析结果提示YPF-P(100、200mg·k~(-1),ig)治疗组iNOS、TNF-α较模型组有显著性差异(P＜0.05)。提示YPF-P对卡介苗加脂多糖致免疫性肝损伤小鼠具有一定的保护作用,可能与它清除自由基,增强机体抗脂质过氧化能力及降低炎性细胞因子的表达有关。
The acute chemical and immunological liver injury models were established,We investigate its protective effects and explore partly mechanisms of total polysaccharides from Yu-Ping-Feng Powder(YPF-P) in acute liver injury mice.The main results are as follows:
1.Protective effects of YPF-P on CCl4-induced chemical liver injury mice and its partly mechanisms.
YPF-P(200 mg·kg~~(-1),ig)could significantly reduce the liver index and the elevated ALT,AST activities in serum;YPF-P(100,200 mg·kg~(-1),ig) could decrease MDA contents in liver homogenates,enhance activities of SOD and GSH.All of these suggest that YPF-P has protective effects on CCl_(4)-induced chemical liver injury.It is possibly related to the reduction of cytokines and inhibition of lipid peroxidation.
2.Protective effects of YPF-P on D-Gal-induced chemical liver injury mice and its partly mechanisms.
YPF-P(200 mg·kg~(-1),ig) could significantly reduce the elevated ALT,AST activities in serum and MDA contents of liver homogenates,enhance activities of SOD and GSH in liver of D-Gal(800 mg·kg~(-1),ip)-induced chemical liver injury mice.The pathology results of liver also show that YPF-P has liver protection to a certain extent. These results suggest that YPF-P has protective effects on D-Gal -induced chemical liver injury.It was possibly related to the inhibition of lipid peroxidation.
3.Protective effects of YPF-P on acute immunological liver injury mice and its partly mechanisms.
YPF-P(100、200 mg·kg~(-1),ig) could significantly reduce the elevated ALT,AST activities in serum and MDA、NO contents of liver homogenates,enhance activities of SOD,GSH,and inhibit production ofTNF-α,iNOS,TNF-αmRNA in liver of acute immunological liver injury mice.The dimensions of hepatic damage in the histopathology had reduced.These results suggest that YPF-P has protective effects on acute immunological liver injury.It is possibly related to removing free radicals, enhancing the antioxidant capacity of lipid peroxidation and reducing the expression of inflammatory cytokine.
研究内容包括以下三部分:
1.玉屏风总多糖对CCl_4致小鼠急性化学性肝损伤的影响及部分机制研究YPF-P(200 mg·kg~(-1),ig)能显著降低CCl_4(0.1%CCl4,10ml·kg~(-1),ip)致急性化学性肝损伤小鼠的肝指数,降低血清中升高的ALT、AST水平:YPF-P(100,200 mg·kg~(-1),ig)可显著降低小鼠肝匀浆中升高的MDA含量,增高肝匀浆中已降低的SOD的活性及GSH的水平。提示,YPF-P对CCl_4诱导的急性化学性肝损伤具有一定的保护作用,可能与其清除自由基,抑制脂质过氧化,增强机体抗氧化能力有关。
2.玉屏风总多糖对D-Gal诱导小鼠急性化学性肝损伤的影响
YPF-P(200 mg·kg~(-1),ig)能显著降低D-Gal(800 mg·kg~(-1),ip)致急性化学性肝损伤小鼠的肝脏指数,降低血清中升高的ALT、AST水平:YPF-P(100,200 mg·kg~(-1))ig给药可显著降低小鼠肝匀浆中升高的MDA含量,增强肝匀浆中已降低的SOD的活性及GSH的水平。提示,YPF-P对D-Gal诱导的急性化学性肝损伤具有一定的保护作用,其保护机制可能与抑制脂质过氧化有关。
3.玉屏风总多糖对卡介苗加脂多糖致小鼠免疫性肝损伤的影响及部分机制研究
YPF-P(100、200 mg·kg~(-1),ig)能显著降低免疫性肝损伤小鼠的肝脏、脾脏指数,降低升高的血清ALT、AST水平及肝匀浆中MDA、NO含量,提高肝匀浆中已降低的SOD的活性,并显著降低TNF-αmRNA在肝组织中的表达;小鼠肝组织iNOS、TNF-α在模型组高表达,YPF-P(50、100、200 mg·kg~(-1),ig)治疗后,免疫组化结果提示,随剂量增加,表达逐渐减弱:图象分析结果提示YPF-P(100、200mg·k~(-1),ig)治疗组iNOS、TNF-α较模型组有显著性差异(P＜0.05)。提示YPF-P对卡介苗加脂多糖致免疫性肝损伤小鼠具有一定的保护作用,可能与它清除自由基,增强机体抗脂质过氧化能力及降低炎性细胞因子的表达有关。
The acute chemical and immunological liver injury models were established,We investigate its protective effects and explore partly mechanisms of total polysaccharides from Yu-Ping-Feng Powder(YPF-P) in acute liver injury mice.The main results are as follows:
1.Protective effects of YPF-P on CCl4-induced chemical liver injury mice and its partly mechanisms.
YPF-P(200 mg·kg~~(-1),ig)could significantly reduce the liver index and the elevated ALT,AST activities in serum;YPF-P(100,200 mg·kg~(-1),ig) could decrease MDA contents in liver homogenates,enhance activities of SOD and GSH.All of these suggest that YPF-P has protective effects on CCl_(4)-induced chemical liver injury.It is possibly related to the reduction of cytokines and inhibition of lipid peroxidation.
2.Protective effects of YPF-P on D-Gal-induced chemical liver injury mice and its partly mechanisms.
YPF-P(200 mg·kg~(-1),ig) could significantly reduce the elevated ALT,AST activities in serum and MDA contents of liver homogenates,enhance activities of SOD and GSH in liver of D-Gal(800 mg·kg~(-1),ip)-induced chemical liver injury mice.The pathology results of liver also show that YPF-P has liver protection to a certain extent. These results suggest that YPF-P has protective effects on D-Gal -induced chemical liver injury.It was possibly related to the inhibition of lipid peroxidation.
3.Protective effects of YPF-P on acute immunological liver injury mice and its partly mechanisms.
YPF-P(100、200 mg·kg~(-1),ig) could significantly reduce the elevated ALT,AST activities in serum and MDA、NO contents of liver homogenates,enhance activities of SOD,GSH,and inhibit production ofTNF-α,iNOS,TNF-αmRNA in liver of acute immunological liver injury mice.The dimensions of hepatic damage in the histopathology had reduced.These results suggest that YPF-P has protective effects on acute immunological liver injury.It is possibly related to removing free radicals, enhancing the antioxidant capacity of lipid peroxidation and reducing the expression of inflammatory cytokine.
引文
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