作者
Cuiyan Liu,Youxi Kang,Xiuhong Zhou,Zhiming Yang,Jingang Gu,Chunyang Han
摘要
Rhizoma smilacis glabrae (RSG), which is mild-natured and tastes sweet or bland, has pharmacological action of eliminating dampness, detoxifying, and ensuring that joints were healthy and supple in traditional Chinese medicine. To discuss the protective effect of RSG on gentamicin (GM)-induced kidney injury in rats and its regulatory mechanisms of oxidative stress-induced apoptosis by inhibiting caspase-3 activation. A total of 40 Sprague–Dawley (SD) rats were randomly divided into 5 groups: control group, model group, and RSG low, middle, and high dose groups (0.75,1.5,3 g kg−1). Six hours after intramuscular GM injections, rats in the model group were given distilled water by intragastric administration, and rats in the 3 RSG intervention groups were given different dosages of RSG water-extracts. Twenty-four hours after the last administration, blood and kidney samples were collected to test for biochemical indexes of kidney injury, oxidative stress, histopathological defects, apoptosis rate, and caspase-3 protein expression to assess the protective effect of RSG water-extracts against GM-induced kidney injury. Compared with the model group, serum TP and ALB levels were significantly higher (P<0.05), and BUN, CRE, and UA levels were significantly lower (P<0.05) in the 3 RSG intervention groups. In kidney tissues, SOD, CAT, and GSH levels increased significantly (P<0.05), while MDA level decreased significantly (P<0.05). Total apoptosis rate dropped markedly (P<0.01), and the protein expressions of caspase-3 increased, while expressions of activated caspase-3 decreased. Histopathological analysis showed shrinkage of kidney cells reduced with appearance of complete kidney structure and decrease in activated caspase-3 expressions in impaired renal tubules decreased. Among the 3 RSG intervention groups, the middle dose group (1.5 g kg−1) showed the best protective effect. RSG water-extracts had protective effects against GM-induced kidney injury in rats, and its mechanism of action was related to oxidative stress-induced apoptosis by inhibiting caspase-3 activation.