OBJECTIVE: To investigate the effects of artemisinin against proteinuria and glomerular filtration barrier damage in rats with adriamycin-induced nephropathy, and the potential mechanism underpinned the action. METHODS: Forty adriamycin rats were randomly divided into two groups with the ratio of 1 : 3; the small-number group served as control group (n = 10), and the rats in the large-number group were treated with adriamycin to induce nephropathy; then they were further randomly assigned into 3 subgroups: benazepril group (n = 10), artemisinin group (n = 10), and adriamycin group (n = 10). The benazepril group and artemisinin group were treated with benazepril suspl (5.0 mg/kg daily) and artemisinin suspl (150 mg/kg daily) respectively after being modeled; those in the control group and adriamycin group were intragastrically administered an equivalent volume of distilled water every day. The treatment after model establishment lasted for a total of 4 weeks. The 24 h uric protein, blood biochemicals, renal pathological changes, renal ultrastrutural changes, Nephrin and Podocin proteins and gene expressions were measured by Coomassie brilliant blue assay, completely automatic biochemical analyzer, light microscope, electron microscopy, Western blot and reverse transcription polymerase chain reaction, respectively. RESULTS: The rats in adriamycin group showed a significant increase in 24 h uric protein excretion, serum total cholesterol (TC), triglyceride (TG), blood urea nitrogen (BUN), serum creatinine (Scr) and decrease in albumin (Alb) (P < 0.05 or P < 0.01). Compared with adriamycin group, artemisinin could reduce uric protein excretion, decrease the serum TC, TG elevation, increase the serum Alb level, up-regulate the expressions of Nephrin and Podocin (P < 0.05 or P < 0.01), but no statistical significance effects on the levels of BUN, Scr in artemisinin group (P > 0.05). The renal pathological and ultrastrutural observation indicate that artemisinin could attenuate the severity of foot process effacement and fusion in the nephropathic rats. CONCLUSION: Artemisinin might have an effect on the nephropathy in rats caused by adriamycin, which may be at least partly correlated with attenu- ation of the severity of foot process effacement and fusion, up-regulation of the expressions of Nephrin and Podocin in the glomeruli in the rats.
OBJECTIVE: To investigate the effects of artemisinin against proteinuria and glomerular filtration barrier damage in rats with adriamycin-induced nephropathy, and the potential mechanism underpinned the action. METHODS: Forty adriamycinrats were randomly divided into two groups with the ratio of 1 : 3; the small-number group served as control group (n = 10), and the rats in the large-number group were treated with adriamycin to induce nephropathy; then they were further randomly assigned into 3 subgroups: benazepril group (n = 10), artemisinin group (n = 10), and adriamycin group (n = 10). The benazepril group and artemisinin group were treated with benazepril suspl (5.0 mg/kg daily) and artemisinin suspl (150 mg/kg daily) respectively after being modeled; those in the control group and adriamycin group were intragastrically administered an equivalent volume of distilled water every day. The treatment after model establishment lasted for a total of 4 weeks. The 24 h uric protein, blood biochemicals, renal pathological changes, renal ultrastrutural changes, Nephrin and Podocin proteins and gene expressions were measured by Coomassie brilliant blue assay, completely automatic biochemical analyzer, light microscope, electron microscopy, Western blot and reverse transcription polymerase chain reaction, respectively. RESULTS: The rats in adriamycin group showed a significant increase in 24 h uric protein excretion, serum total cholesterol (TC), triglyceride (TG), blood ureanitrogen (BUN), serum creatinine (Scr) and decrease in albumin (Alb) (P < 0.05 or P < 0.01). Compared with adriamycin group, artemisinin could reduce uric protein excretion, decrease the serum TC, TG elevation, increase the serum Alb level, up-regulate the expressions of Nephrin and Podocin (P < 0.05 or P < 0.01), but no statistical significance effects on the levels of BUN, Scr in artemisinin group (P > 0.05). The renal pathological and ultrastrutural observation indicate that artemisinin could attenuate the severity of foot process effacement and fusion in the nephropathicrats. CONCLUSION:Artemisinin might have an effect on the nephropathy in rats caused by adriamycin, which may be at least partly correlated with attenu- ation of the severity of foot process effacement and fusion, up-regulation of the expressions of Nephrin and Podocin in the glomeruli in the rats.