OBJECTIVE To investigate th e intervention effect of Jinkui shenqi pills on renal fibrosis （RF）model rats and its mechanism based on transforming growth factor β1/Smads（TGF-β1/Smads）and TGF-β1/extracellular signal regulated kinase （ERK） signaling pathway. METHODS Male SD rats were given adenine suspension （250 mg/kg）to induce RF model. After modeling ， they were randomly divided into model group ，Colchicine tablet group （positive control ，0.45 mg/kg）and Jinkui shenqi pills low-dose，medium-dose and high-dose groups （0.5，1，2 g/kg），with 10 rats in each group. Other 10 healthy rats were selected as normal group. The rats in administration groups were given the corresponding drugs intragastrically ；normal group and model group were given 0.1％ sodium carboxymethyl cellulose solution ，once a day ，for consecutive 30 d. After last medication ，the serum levels of creatinine （Cr）and blood urea nitrogen （BUN），renal weight and body weight were detected. The ratio of BUN/Cr and renal coefficient were calculated. The pathological morphology of renal tissue in rats were observed. The protein and mRNA expressions of TGF-β1，Smad2，Smad3，ERK1 and ERK 2 were detected. RESULTS Compared with normal group ，serum levels of Cr and BUN and renal coefficient were all increased significantly in model group （P＜0.05），while the ratio of BUN/Cr was decreased significantly （P＜0.05）. The volume of the kidney was significantly increased ，and the surface was seriously granulated. Mesangial hyperplasia ，dilation or atrophy of renal tubules ，accompanied by large-area collagen deposition，could be found. Protein and mRNA expressions of TGF-β 1，Smad2，Smad3，ERK1 and ERK 2 were increased significantly in renal tissue （P＜0.05）. Compared with model group ，above indexes of Jinkui shenqi pills groups were all reversed significantly （P＜0.05）；dilation or atrophy of renal tubules was relieved ，and collagen deposition was reduced to different extents. CONCLUSIONS Jinkui shenqi pills can improve renal function of RF model rats ，the mechanism of which may be associated with inhibiting TGF-β1/Smads and TGF-β1/ERK signaling pathway.

ObjectiveTo study the intervention effect of Bixie Fenqingwan on hyperuricemia （HUA） rats by regulating urate transporters. MethodSixty healthy rats were randomly divided into normal， model， allopurinol （0.03 g·kg^-1）， and Bixie Fenqingwan low-， medium- and high-dose （0.8， 1.6， 3.2 g·kg^-1） groups， 10 in each group. Except the normal group， the other rats were given potassium oxonate 1.5 g·kg^-1 and adenine 0.1 g·kg^-1 for 28 consecutive days to establish the HUA rat model， and rats with increased serum uric acid （SUA） were considered successfully modeled. After modeling， corresponding drugs were given to the groups， once per day. Urine and blood was collected after 24 h of the final administration. The levels of urine uric acid （UUA）， SUA， blood urea nitrogen （BUN） and serum creatinine （SCr） were measured by enzymatic colorimetry. The rat kidneys were taken and weighed to calculate the kidney index. The pathological changes of kidney tissue were observed by haematoxylin-eosin （HE） staining. The protein and mRNA expressions of urate transporter 1 （URAT1）， glucose transporter 9 （GLUT9）， adenosine triphosphate-binding cassette transporter protein G2 （ABCG2）， organic anion transporter 1 （OAT1） and organic anion 3 transporter （OAT3） in kidney tissue were detected by immunohistochemistry and real-time quantitative polymerase chain reaction （Real-time PCR）， respectively. ResultCompared with the conditions in the normal group， the kidney index， levels of SUA， BUN and SCr， and protein and mRNA expressions of URAT1 and GLUT9 in kidney tissue were increased （P<0.05）， while the UUA level and protein and mRNA expressions of OAT1， OAT3 and ABCG2 were decreased in the model group （P<0.05）. In addition， there was compensatory dilatation with urate crystals and protein casts in renal tubules in the model group. Compared with the model group， the intervention groups had lowered kidney index （P<0.05）， reduced levels of SUA， BUN and SCr （P<0.05）， down-regulated protein and mRNA expressions of URAT1 and GLUT9 （P<0.05）， elevated UUA level （P<0.05） and up-regulated protein and mRNA expressions of OAT1， OAT3 and ABCG2 （P<0.05）， and the kidney tissue lesions were alleviated （P<0.05）. ConclusionBixie Fenqingwan has intervention effect on HUA， and its mechanism may be related to regulating urate transporters.

OBJECTIVE To investigate the improvement effects of Jinkui shenqi pills on polycystic ovary syndrome （PCOS） model rats and the mechanism. METHODS Totally 40 rats were given letrozole suspension instragastrically （1 mg/kg， once a day， for consecutive 21 d） to induce PCOS model. Model rats were divided into model group， ethinylestradiol and cyproterone acetate tablets （short for diane-35）+metformin group （diane-35 0.2 mg/kg + metformin 230 mg/kg， as positive control）， Jinkui shenqi pills low-dose， medium-dose and high-dose groups （0.5， 1.0， 2.0 g/kg）， with 10 rats in each group. Other 10 healthy rats were included in normal group. Each group was given the corresponding drugs， once a day， for consecutive 30 d. Twelve hours after the last administration， serum levels of blood glucose， insulin， estrogen （E2）， testosterone （T）， gonadotropin-releasing hormone （GnRH）， follicle-stimulating hormone （FSH） and luteinizing hormone （LH） were measured. The insulin resistance indexes were calculated， and the ovary coefficients of rats were calculated. The pathological changes of ovary were observed. The protein and mRNA expressions of liver kinase B1 （LKB1） and AMP-activated protein kinase （AMPK） in ovary tissue were detected. RESULTS Compared with normal group， the levels of blood glucose， insulin， insulin resistance index， serum levels of T， GnRH and LH and ovarian indexes were significantly increased （P＜0.05）， while serum levels of E2 and FSH as well as protein and mRNA expressions of LKB1 and AMPK in ovary tissue were decreased significantly （P＜0.05）； collagenization of ovarian cortex， increased number of atresia follicles and cystic follicles without cumulus， and follicular cystic lesions could be seen. Compared with model group， most of above indexes of Jinkui shenqi pills groups were reversed significantly （P＜0.05）； the number of follicle at each level was increased and no follicular cystic lesion was found in Jinkui shenqi pills medium-dose and high-dose groups. CONCLUSIONS Jinkui shenqi pills can significantly improve the abnormal level of sex hormones， insulin resistance and 222102310139） ovarian cystic changes， the mechanism of which may be related to up-regulating the activation of LKB1/AMPK signaling pathway.