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This study aimed to investigate the protective effect and the underlying mechanism of Ephedra sinica Stapf on renal injury in a murine model. Sixty rats were randomly divided into 5 groups with 12 animals per group as follows: control group, model group, high dose group of Ephedra (20 g/kg bw/day), middle dose group of Ephedra (10 g/kg bw/day), and low dose group of Ephedra (5 g/kg bw/day). Renal injury was induced in rats using a renal ischemia-reperfusion model. Blood urea nitrogen (BUN), serum creatinine (SCr) and malondialdehyde (MDA) in the model group increase significantly while superoxide dismutase (SOD), nitric oxide (NO), and endothelial nitric oxide synthase (eNOS) decrease significantly compared with the control group (p < 0.05). In Ephedra groups BUN, SCr, and MDA decrease and SOD, NO, and eNOS increase compared to the model group in a dose-dependent manner. The histo-pathological evaluation showed in the model group appears a renal tubular protein cast with inflammatory cell infiltration, renal interstitial congestion, and visible turbid swelling of renal tubular epithelial cells. The histo-pathological changes are significantly reducing or even disappearing after the treatment with Ephedra. The model group showed severe tissue damage and a large number of apoptotic cells, up-regulation of Bax protein and down-regulation of Bcl-2 protein expression compared to control group (p < 0.05). Tissue damage in the Ephedra treatment groups is minor, and only scattered apoptotic cells were seen. Bax protein expression in the Ephedra groups was significantly down-regulated and Bcl-2 protein expression was significantly up-regulated in a dose-dependent manner compared to the model group (p < 0.05). Ephedra can reduce renal injury and improve renal function by reducing oxidative damage, free radical generation, and inhibiting apoptosis.

THE PROTECTIVE EFFECT AND THE UNDERLYING MECHANISM OF EPHEDRA SINICA STAPF ON RENAL INJURY IN A MURINE MODEL