Protective effect of panax notoginseng saponins against femoral fracture- induced apoptosis in the superficial cells of rat renal cortex
- VernacularTitle:大鼠股骨骨折对肾皮质浅层细胞凋亡的影响及三七总皂苷的保护作用
- Author:
Anmin GAO
1
;
Ying FENG
;
Feng ZENG
;
Xiaomei WANG
;
Fang WANG
;
Lansheng YANG
;
Shaohua SUN
Author Information
1. 兰州大学第一医院病理研究所
- Keywords:
panax notoginseng saponins;
fracture;
renal cortex;
apoptosis
- From:
Journal of Southern Medical University
2013;(11):1692-1695
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the protective effect of panax notoginseng saponins (PNS) against apoptosis of the superficial cells of rat renal cortex following femoral fracture in rats. Methods Ninety Wistar rats were randomized into 3 groups, namely the fracture group (n=36), fracture with PNS treatment group (n=36), and normal control group (n=18). At 1, 6, 12, 24, 36, and 48 h after femoral fracture, 6 rats from first two groups and 3 from the control group were sacrificed to observe renal pathologies with HE-staining. Immunohistochemistry and in situ hybridization were used to detect Bcl-2 and Bax expression, and TUNEL staining was employed to detect the distribution of apoptotic cells. Results In the fracture group, the renal cortex showed telangiectasia and granular degeneration of proximal tubule, which were lessened in the PNS treatment group. Compared with the control group, the fracture group showed significantly increased Bcl-2 and Bcl-2 mRNA expressions in the renal cortex at 1-12 h (P<0.01) and increased Bax protein expression at 12-36 h (P<0.01) with increased Bax mRNA expression at 24-48 h (P<0.01). In PNS treatment group, Bcl-2 protein expression at 1 h and Bcl-2 mRNA expression at 12-48 h were significantly higher (P<0.01), but Bax protein and mRNA expressions at 24-48 h were significantly lower (P<0.01) than those in the fracture group. Conclusion Femoral fracture obviously affects Bcl-2 and Bax protein and mRNA expressions in the superficial cells of the renal cortex, PNS can suppress the cell apoptosis by down-regulating Bax expression and up-regulating Bcl-2 expression.
