Fan Yan-ling, Xia Jie-yu, Jia Dao-yong, Zhang Meng-si, Zhang Yan-yan, Wang Lu, Huang Guo-ning, Wang Ya-ping
Zhongguo Zhong Yao Za Zhi. 2015 Nov;40(21):4229-33.
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 x kg(-1)), qd x 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 x 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 BUN, Crea, UA, Cysc, AGES, 8-OH-dG, the number of hardening renal corpuscle, renal capsular space and renal tubular lumen, ROD of SA-β-Gal staining positive kidney cells, mesangial cells, basement membrane thickness, podocyte secondary processes fusion and MDA and increases in the number of normal renal corpuscle, ribosome and rough endoplasmic reticulum in podocytes, the activity of SOD and GSH-PX. In Conclusion, A. sinensis polysaccharides can antagonize kidney subacute damages induced by D-galactose in mice. Its protective mechanism may be correlated with the inhibition of the oxidative stress injury.
探讨当归多糖(ASP)对D-半乳糖诱导的小鼠亚急性肾损伤的保护作用及其机制。将雄性C57BL/6J小鼠随机分为3组,每组10只。D-半乳糖模型组皮下注射D-半乳糖(120 mg·kg⁻¹),每日1次,共42天;ASP + D-半乳糖模型组自D-半乳糖模型复制第8天起腹腔注射ASP,每日1次,共35天;正常对照组在相同剂量和时间皮下注射生理盐水。注射后第2天,采集外周血检测尿素氮(BUN)、肌酐(Crea)、尿酸(UA)、胱抑素C(Cys-C)含量;制作石蜡切片,采用苏木精-伊红(HE)染色观察肾脏组织形态学;采用衰老相关β-半乳糖苷酶(SA-β-Gal)染色观察肾脏组织相对光密度(ROD);采用透射电子显微镜观察肾脏超微结构;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)、丙二醛(MDA)含量;采用酶联免疫吸附测定(ELISA)法检测晚期糖基化终末产物(AGEs)和8-羟基脱氧鸟苷(8-OH-dG)含量。结果显示,与D-半乳糖模型组相比,ASP + D-半乳糖模型组BUN、Crea、UA、Cys-C、AGEs、8-OH-dG含量,硬化肾小球、肾小囊腔和肾小管管腔数量,SA-β-Gal染色阳性肾细胞、系膜细胞的ROD,基底膜厚度,足细胞次级突起融合及MDA均明显降低,正常肾小球、足细胞核糖体和粗面内质网数量,SOD和GSH-PX活性均明显升高。结论:当归多糖可拮抗D-半乳糖诱导的小鼠肾脏亚急性损伤,其保护机制可能与抑制氧化应激损伤有关。