Objective:To explore the effects of Rhizoma Polygoni Cuspidati and Ramulus Cinnamomicompatibility(PR) on uric acid metabolism and the expression of urinary neutrophil gelatinase-associated lipocalin(NGAL) and kid...Objective:To explore the effects of Rhizoma Polygoni Cuspidati and Ramulus Cinnamomicompatibility(PR) on uric acid metabolism and the expression of urinary neutrophil gelatinase-associated lipocalin(NGAL) and kidney injury molecule-1(KIM-1) in rats with hyperuricemia. Methods:Seventy male Sprague Dawley(SD) rats were randomly divided into 7 groups with 10 rats per group, including the normal group, model group, allopurinol group, benzbromarone group and PR groups at 3 doses(3.5, 7, 14 g/kg). Except the normal group, rats of the other groups were intragastrically administered 100 mg/kg hypoxanthine and 250 mg/kg ethambutol, and subcutaneously injected with 200 mg/kg potassium oxonate. All rats were continuously modeled for 17 days, and gavaged with corresponding drugs. The rats of the normal and model groups were gavaged with saline, once a day, for 2 weeks. The levels of serum uric acid(SUA), blood urea nitrogen(BUN) and creatinine(Cr) were determined. In addition, the contents of NGAL and KIM-1 in urine and the m RNA and protein expressions of xanthine oxidase(XOD) in liver of hyperuricemia rats were measured by reverse transcription polymerase chain reaction(RT-PCR) and Western blot, respectively. Moreover, the pathological changes of kidney were analyzed by hematoxylin and eosin(HE) stain method. Results:Compared with the normal group, the levels of SUA, BUN, NGAL and KIM-1 and the expressions of hepatic XOD m RNA and protein in the hyperuricemia rats were increased significantly(P〈0.01). PR significantly decreased the levels of SUA, BUN, NGAL and KIM-1 and down-regulated the m RNA and protein expressions of hepatic XOD(P〈0.05 or P〈0.01). In addition, the pathological changes of kidney were significantly suppressed by oral administration of PR. Conclusions:PR ameliorated uric acid metabolism and protected renal function, the underlying mechanism was mediated by decreasing the levels of SUA, BUN, NGAL and KIM-1, inhibiting the expression of hepatic XOD and ameliorating the pathological change of kidney.展开更多
基金Supported by the National Natural Science Foundation of China(No.81173194)
文摘Objective:To explore the effects of Rhizoma Polygoni Cuspidati and Ramulus Cinnamomicompatibility(PR) on uric acid metabolism and the expression of urinary neutrophil gelatinase-associated lipocalin(NGAL) and kidney injury molecule-1(KIM-1) in rats with hyperuricemia. Methods:Seventy male Sprague Dawley(SD) rats were randomly divided into 7 groups with 10 rats per group, including the normal group, model group, allopurinol group, benzbromarone group and PR groups at 3 doses(3.5, 7, 14 g/kg). Except the normal group, rats of the other groups were intragastrically administered 100 mg/kg hypoxanthine and 250 mg/kg ethambutol, and subcutaneously injected with 200 mg/kg potassium oxonate. All rats were continuously modeled for 17 days, and gavaged with corresponding drugs. The rats of the normal and model groups were gavaged with saline, once a day, for 2 weeks. The levels of serum uric acid(SUA), blood urea nitrogen(BUN) and creatinine(Cr) were determined. In addition, the contents of NGAL and KIM-1 in urine and the m RNA and protein expressions of xanthine oxidase(XOD) in liver of hyperuricemia rats were measured by reverse transcription polymerase chain reaction(RT-PCR) and Western blot, respectively. Moreover, the pathological changes of kidney were analyzed by hematoxylin and eosin(HE) stain method. Results:Compared with the normal group, the levels of SUA, BUN, NGAL and KIM-1 and the expressions of hepatic XOD m RNA and protein in the hyperuricemia rats were increased significantly(P〈0.01). PR significantly decreased the levels of SUA, BUN, NGAL and KIM-1 and down-regulated the m RNA and protein expressions of hepatic XOD(P〈0.05 or P〈0.01). In addition, the pathological changes of kidney were significantly suppressed by oral administration of PR. Conclusions:PR ameliorated uric acid metabolism and protected renal function, the underlying mechanism was mediated by decreasing the levels of SUA, BUN, NGAL and KIM-1, inhibiting the expression of hepatic XOD and ameliorating the pathological change of kidney.