红景天苷对大鼠肾脏缺血再灌注损伤的预防保护时限

目的：探讨红景天苷对大鼠肾脏缺血再灌注损伤预防保护时限，阐明其可能机制。方法：54只健康成年SD大鼠随机分成9组，分别为空白对照组、缺血再灌注夹闭15、30、45和60 min组、腹腔注射红景天苷水溶液夹闭15、30、45和60 min组，每组6只。缺血再灌注组和红景天苷组大鼠分别制作肾脏缺血再灌注模型,红景天苷组大鼠实验前采用红景天苷水溶液预处理。检测各组血清肌酐(Scr)水平；切除右肾，夹闭左肾蒂相应时间后取左肾组织HE染色，用光镜观察肾组织病理改变，蛋白质印迹法和免疫组织化学法分别检测肾组织中热休克蛋白72(HSP72)和核转录因子κB(NF-κB)的表达。结果：与缺血再灌注各组比较，红景天苷夹闭15、30和45 min组大鼠Scr水平明显下降(P<0.01），病理损伤明显减轻，肾脏组织中HSP72和NF-κB表达也明显减少。与空白对照组比较，红景天苷各组大鼠血清Scr水平有所上升，其中夹闭60 min明显上升(P<0.05），夹闭15、30和45 min时病理损伤变化不明显。结论：应用红景天苷后，大鼠肾脏缺血再灌注损伤明显减轻，其机制可能是通过抑制肾组织中Hsp72和NF-κB的表达，增强肾脏抗氧化能力，从而减轻肾脏组织炎性细胞浸润和细胞凋亡。

Protective effect of salidroside on renal ischemia-reperfusion injury in rats

Objective To study the effect of salidroside on rat renal ischemia reperfusion injury,and to clarify its mechanism of action.Methods 54 healthy SD rats were randomly divided into nine groups:control group,ischemia-reperfusion groups by clamping 15,30,45 and 60 min,intraperitoneal injection of salidroside solution groups by clamping 15,30,45 and 60 min.The serum creatinine(Scr) in various groups were detected.The pathological changes of rat kidney tissues were observed by light microscope.The expressions of HSP72 and NF-κB in kidney tissue were determined by Western blotting and immunohistochemistry.Results Compared with ischemia-reperfusion groups,the levels of Scr in salidroside solution groups(clamping 15,30 and 45 min) were significantly decreased(P<0.01),the pathological damage was significantly reduced,and the expressions of HSP72 and NF-κB in kidney tissue were also decreased significantly.Compared with control group,the Scr levels in salidroside groups were increased slightly,especially in clamping 60 min group,it was increased significantly(P<0.01),but in clamping 15,30 and 45 min groups,the changes were not obvious.Conclusion Application of salidroside can significantly reduce renal ischemia-reperfusion injury in kidney tissue,the mechanisms may be related to enhancing the antioxidant capacity of the kidneys,reducing inflammatory cell infiltration and apoptosis in kidney tissue and inhibiting the HSP72 and NF-κB expressions in kidney tissue.