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作 者:刘蕊洁 杨先照 张嘉鑫 叶永安 LIU Rui-jie;YANG Xian-zhao;ZHANG Jia-xin;YE Yong-an(Beijing Tongren hospital affiliated to capital medical university,Beijing,100730,China)
机构地区:[1]首都医科大学附属北京同仁医院肝病科,北京100730 [2]北京中医药大学东直门医院
出 处:《中西医结合肝病杂志》2021年第1期56-59,共4页Chinese Journal of Integrated Traditional and Western Medicine on Liver Diseases
基 金:国家自然科学基金资助项目(No.81603555);首都医科大学附属北京同仁医院科研基金资助课题(No.TRYY-KYJJ-2017-010、2018-YJJ-ZZL-003)。
摘 要:目的:观察益肝消癥方对二乙基亚硝胺诱导的大鼠肝癌前病变肝细胞凋亡因子Bcl-2、Bax mRNA及蛋白质表达的影响。方法:将40只Wistar雄性大鼠随机分为对照组10只、模型组15只和益肝消癥组15只,除对照组外,其余各组大鼠以二乙基亚硝胺腹腔注射诱导肝癌前病变模型,持续14周。第8周起,每天分别以生理盐水、益肝消癥颗粒的水溶剂给予相应组大鼠灌胃给药,第14周末给药后取材,检测大鼠0、7、14周体重,Bcl-2、Bax mRNA及蛋白质表达,观察肝脏病理情况。结果:益肝消癥方可改善肝癌前病变大鼠一般状况、肝脏病理,下调Bcl-2、Bax mRNA、Bax蛋白表达及Bax/Bcl-2比值。结论:益肝消癥方通过Bcl-2/Bax途径抑制肝细胞凋亡,减轻肝星状细胞增殖,从而对大鼠肝癌前病变具有一定改善作用。Objective:To observe the effect of Yigan Xiaozheng formula for rats with precancerous lesions of liver induced by diethylnitrosamine on the expression of hepatocyte apoptosis factor Bcl-2,Bax mRNA,and protein.Methods:Forty male rats were randomly divided into Yigan Xiaozheng group with 15 rats,model group with 15 rats,and control group with 10 rats.Except for the control group,the precancerous lesions of the liver in the other two groups were induced by intraperitoneal injection of diethylnitrosamine,once a week lasting for 14 weeks.Since the eighth week,the rats were given intragastric administration of normal saline or Yigan Xiaozheng granules in a water solvent.The rats'weight was measured at the 0 weeks,the seventh week,and the 14th week.The samples were taken after the end of the 14th-week administration to detect liver HE pathological staining,Bcl-2,Bax mRNA,and protein expression.Results:Yigan Xiaozheng formula improved the general condition and liver pathology of the rats with the precancerous lesions,down-regulated Bcl-2,Bax mRNA,Bax protein expression,and Bax/Bcl-2 ratio.Conclusion:Yigan Xiaozheng formula can improve rates with precancerous lesions of the liver by inhibiting hepatocyte apoptosis and reducing hepatic stellate cell proliferation through the Bcl-2/Bax pathway.
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