当归多糖对D―半乳糖致小鼠肾脏亚急性损伤保护作用及机制.docVIP

当归多糖对D―半乳糖致小鼠肾脏亚急性损伤保护作用及机制 　　[摘要] 探讨当归多糖（ASP）对D-半乳糖诱导致小鼠肾脏亚急性损伤的保护作用及机制。雄性C57BL/6J小鼠随机分为3组，每组10只。模型组：小鼠皮下注射D-半乳糖（120 mg?kg-1），qd×42；ASP组：从D-半乳糖模型复制的第8天起，腹腔注射ASP（100 mg?kg-1），qd×35；正常对照组：小鼠皮下注射等时与等量生理盐水。药物注射完成第2天，采外周血检测尿素氮（BUN）、肌酐（Crea）、尿酸（UA）、胱抑素C（Cys-C）含量；取肾脏制备石蜡切片，HE染色观察肾脏组织形态学，衰老相关β-半乳糖苷酶（SA-β-Gal）染色观察肾组织中染色阳性细胞相对光密度（ROD），透射电镜观察肾脏超微结构变化；制备肾脏组织匀浆检测超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-PX）活性和丙二醛（MDA）的含量；ELISA方法检测肾脏晚期糖基化终产物（AGEs）和8-羟基脱氧鸟苷（8-OH-dG）的含量。结果表明与模型组相比较，ASP组小鼠血清中BUN，Crea，UA，Cys-C，AGEs和8-OH-dG含量显著下降；肾小球数目增多，硬化肾小球减少，肾小囊腔与肾小管管腔扩张不明显；SA-β-Gal染色阳性细胞的相对光密度降低且颗粒小；超微病理呈现肾小球系膜细胞减少，基底膜变薄，足细胞核糖体和粗面内质网明显增多，足细胞次级突起融合减少；SOD与GSH-PX活性显著增加；MDA含量下降。综上所述，当归多糖能拮抗D-半乳糖致小鼠肾脏亚急性损伤，其保护肾脏机制可能与抑制氧化应激损伤有关。 　　[关键词] 当归多糖；D-半乳糖；肾损伤；保护机制 　　[Abstract] To explore the protective effect of Angelica sinensis polysaccharides（ASP） on subacute renal damages induced by D-galactose in mice and its mechanism. Male C57BL/6J mice were randomly divided into 3 groups， with 10 mice in each group. The D-galactose model group was subcutaneously injected with D-galactose （120 mg?kg-1）， qd×42； the ASP+D-galactose model group was intraperitoneally injected with ASP since the 8th day of the replication of the D-galactose model， qd×35； and the normal control group was subcutaneously injected with saline at the same dose and time. On the 2nd day of after the injection， the peripheral blood was collected to measure the content of BUN， Crea， UA， Cys-C； paraffin sections were made to observe the renal histomorphology by HE staining； senescence-associated β-g-alactosidase （SA-β-Gal） stain was used to observe the relative optical density （ROD） in renal tissues； transmission electron microscopy was assayed to observe the renal ultrastructure； the renal tissue homogenate was prepared to measure the content of SOD， GSH-PX， MDA； the content of AGEs and 8-OH-dG were measured by ELISA. According to the result， compared with the D-galactose model group， the ASP+D-galactose model group showed obviously decreases in the content of