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作 者:刘成虎[1] 高尚先[1] 张利宁[1] 李娜[1] 王群[1] 高立芬[1] 刘兴田[1] 张蘋[1] 高飞[1]
出 处:《药物分析杂志》2006年第7期981-985,共5页Chinese Journal of Pharmaceutical Analysis
摘 要:目的:研究低剂量无细胞短棒状杆菌纳米级制剂(NCPP)对刀豆蛋白 A(Con A)诱导的小鼠急性肝损伤的保护作用及机理。方法:BALB/c 小鼠腹腔注射 NCPP(0.01 mg·只)后第7 d 以 Con A(25μg·g^(-1))尾静脉注射诱导小鼠急性肝损伤模型。测定血清转氨酶(ALT/AST)及肝脏内的病理变化。同时设置 PBS 预处理对照组和 Con A 模型对照组,每组8只小鼠。用流式细胞仪检测肝脏内自然杀伤细胞(NK 细胞)的数量变化和 CD4~4T 淋巴细胞的活化情况。结果:与 Con A 模型组相比,NCPP 预处理组小鼠血清转氨酶明显降低[ALT 水平从(328±14)U·L^(-1)下降到(104±41)U·L^(-1),AST 水平从(141±9)U·L^(-1)下降到(98±17)U·L^(-1)],肝脏组织 HE 染色显示肝脏病理损伤明显减轻,同时流式细胞术的分析结果显示:与 Con A 模型组相比,小鼠肝脏 NK 细胞数量降低,且 CD4^+T 淋巴细胞的活化受到了明显抑制。结论:NCPP 对 Con A 诱导的小鼠急性肝损伤具有保护作用。其机理可能与抑制 CD4^+T 淋巴细胞活化和拮抗肝脏内 NK 细胞的回流有关。Objective :To investigate the effect and mechanism of pretreatment with a low dose of NCPP on concanavalin A( Con A) -induced severe liver injury. Method:On the seventh day after NCPP(0.01 mg per mouse) was injected into the peritoneal cavity of mice,Con A(25 μg ·g^-1 )was administrated intravenously to provoke severe liver injury models. The degree of liver injury was estimated by serum transaminase analysis and heptatic histopathology. At the same time, set up PBS pretreatment group as negative control, 8 mice per group. The number of hepatic NK cells and activation of CD4^+T lymphocytes were analyzed by flow cytometry. Result:Pretreatment with a low dose of NCPP significantly protected mice from Con A - induced severe liver injury, which were approved by the level of serum transaminase and alteration of hepatic histopathology. Accordingly, activation of hepatic CD4^+ T lymphocytes was dramatically inhibited and the number of hepatic NK cells was also decreased evidently. Conclusion: Pretreatment with a low dose of NCPP protected mice from Con A - induced severe liver injury, which mainly resulted from inhibiting the recruitment of hepatic NK cells and the activation of CD4^+T lymphocytes.
关 键 词:NCPP 刀豆蛋白A(Con A) CD4^+T淋巴细胞 NK细胞 血清转氨酶
分 类 号:R917[医药卫生—药物分析学]
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