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槐定碱对内毒素肝损伤小鼠ERK和TNF-α表达的干预作用 被引量:3

Effect of sophoridine on endotoxin-induced acute liver injury in mice and its intervention action of the pERK and TNF-α expression
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摘要 目的观察槐定碱对急性内毒素肝损伤小鼠的干预效应及对磷酸化ERK(pERK)、TNF-α表达的影响。方法以内毒素肝损伤小鼠为实验对象,记录各组小鼠一般情况,肉眼及HE染色光镜观察小鼠肝组织病理改变,免疫组化检测肝组织中pERK的表达与分布,放射免疫法检测血清TNF-α。结果槐定碱3个剂量干预组小鼠一般情况改善,肝组织病理改变减轻,中、高剂量组肝组织中pERK核移位现象及pERK阳性细胞数较LPS组显著减少(P<0.01),与正常对照组比较差异无统计学意义(P>0.05);中、高剂量组小鼠血清TNF-α水平均显著低于LPS组(P<0.01),而与正常对照组的差异无统计学意义(P>0.05)。结论槐定碱干预对急性内毒素肝损伤小鼠具有明显保护作用,其机制与抑制肝组织中pERK及血清TNF-α的表达有关。 Objective To observe the effect of sophoridine on endotoxin-induced acute liver injury in mice and its intervention action of the protein expression levels of phosphorylated ERK(pERK) in liver and the level of TNF-α in serum.Method It was recorded that general situation of mice with acute liver injury due to endotoxin,and the pathological changes in liver tissue were observed by light microscope.pERK expression and distribution was detected by immunohistochemical method,as well as TNF-α levels in serum were assayed by radioimmunity method.Results The general situation was improved and the liver pathological change was reduced in three-dose Sophoridine groups of mice.Compared with LPS group,LPS induced pERK translocation from cytoplasm to nuclear and the positive cells with pERK in liver tissue were significantly reduced(P0.01) and the level of TNF-α in serum significantly lower(P0.01) in middle and high-dose group,while compared with the normal control group,they were no significant difference(P0.05).Conclusion The present study shows a significant protective effect of Sophoridine on endotoxin-induced acute liver injury in mice and its mechanism is related to inhibition against the protein expression levels of pERK in liver and the level of TNF-α in serum.
机构地区 宁夏医科大学
出处 《宁夏医学杂志》 CAS 2010年第5期391-392,F0003,共3页 Ningxia Medical Journal
基金 国家自然科学基金(30660227) 教育部新世纪优秀人才支持计划(NCET-06-0916) 宁夏自然科学基金(NZ0783)
关键词 槐定碱 内毒素 急性肝损伤 磷酸化ERK(pERK) TNF-Α Sophoridine Endotoxin Acute liver injury Phosphorylated ERK(pERK) TNF-α
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