Effects of rhynchophylline on adriamycin-induced renal injury in rats

AIM: To explore the effects of rhynchophylline (RHL) on rat renal injury induced by adriamycin. METHODS: Fifty-two female SD rats were randomly divided into normal saline group (NSG, n=10), model group (MG, n=14), low-dose RHL treatment group (RHL-LG, n=14) and high-dose RHL treatment group (RHL-HG, n=14). The animals in the latter 3 groups were injected with adriamycin at a dose of 5 mg/kg through the tail vein. The animals in RHL-LG and RHL-HG were treated with RHL at doses of 5 mg/kg and 15 mg/kg, respectively, by intraperitoneal injection for 8 weeks. The animals in NSG and MG were treated with normal saline only. Urine and blood samples were collected to detect the urine protein, blood urea nitrogen (BUN) and serum creatinine (SCr). The renal tissues of the animals were collected for detection of malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, pathological changes and mRNA expression of angiotension Ⅱreceptors 1,2 (AT_1,2-R), angiotensin-converting enzyme (ACE) and angiotensinogen (AGT). RESULTS: The urine protein, BUN and SCr in RHL-LG were significantly lower than those in MG, but higher than those in RHL-HG (P<0.05). The SOD activity in MG was significantly lower than that in RHL-LG in the renal tissues. The SOD activity in RHL-LG was significantly lower than that in RHL-HG (P<0.05), but the content of MDA was on the contrary. The renal pathological damages in RHL-LG were weaker than that in MG, and that in RHL-HG were weaker than that in RHL-LG. The mRNA expression of AT₁-R, ACE and AGT in MG was significantly higher than that in RHL-LG in the renal tissues, and that in RHL-LG was higher than that in RHL-HG (P<0.05). The mRNA expression of AT₂-R in MG was significantly lower than that in RHL-LG, and that in RHL-LG was significantly lower than that in RHL-HG (P<0.05). CONCLUSION: RHL reduces adriamycin-induced renal injury in rats by attenuating the injury of lipid peroxidation in renal tissue, regulating the mRNA expression of AT_{1, 2}-R, ACE and AGT, and increasing renal blood flow.