ObjectiveTo investigate the uric acid-lowering effects and mechanisms of acacetin on hyperuricemia （HUA） in mice. MethodsOteracil potassium and adenine were used to establish the mouse model of HUA. Male Kunming mice （n=48） were randomized into six groups： control， model， low-dose （12.5 mg·kg^-1） acacetin， medium-dose （25 mg·kg^-1） acacetin， high-dose （50 mg·kg^-1） acacetin， and allopurinol （10 mg·kg^-1）. Each group received continuous gavage administration for 21 days. An automatic biochemical analyzer was used to measure the levels of uric acid （UA）， creatinine （Cr）， urea nitrogen （BUN）， alanine aminotransferase （ALT） and aspartate aminotransferase （AST）. Additionally， the activity of xanthine oxidase （XOD） in the liver and the levels of tumor necrosis factor （TNF）-α， interleukin （IL）-1β， and IL-18 in the serum were measured by enzyme-linked immunosorbent assay （ELISA）. Pathological changes in the renal tissue were observed by hematoxylin-eosin （HE） staining. Western blot was employed to determine the levels of glucose transporter 9 （GLUT9）， urate transporter 1 （URAT1）， phospho-NF-κB p65 （p-NF-κB p65）， and nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3 （NLRP3） in the renal tissue. ResultsCompared with the control group， the model group showed elevated levels of UA， Cr， BUN， ALT， and AST， increased activity of XOD in the liver（P<0.01）， raised levels of TNF-α， IL-1β and IL-18 in the serum（P<0.01）， and significantly up-regulated expression of GLUT9， URAT1， p-NF-κB p65， and NLRP3 in the renal tissue（P<0.01）. Compared with the model group， acacetin reduced the UA level in a dose-dependent manner， significantly improved liver and kidney functions， decreased the XOD activity in the liver， ameliorated the pathological changes in the renal tissue， down-regulated the expression of GLUT9， URAT1， p-NF-κB p65 and NLRP3 in the renal tissue（P<0.01）， and lowered the levels of TNF-α， IL-1β， and IL-18 in the serum（P<0.01）. ConclusionAcacetin can ameliorate HUA by decreasing uric acid production， increasing uric acid excretion， and inhibiting the NF-κB/NLRP3 signaling pathway. Therefore， acacetin may be a potential drug for the treatment of HUA.

Objective To investigate the protective effects of soybean isoflavone(SI) on genetic toxicity induced by di-n-butul phthalate(DBP) in mice.Method(1) Micronucleus test:40 male 7 w old Kunming mice were randomized into 4 groups:High and low dose SI intervention groups,DBP model group,and solvent control group.SI intervention groups were given different doses of SI(50,100mg/kg) for 30 d,meanwhile,the DBP group and solvent group were given 0.5% sodium carboxymethyl cellulose.Then all groups were treated by 0.5g/kg DBP for 5d except solvent group.Mice were sacrificed 6 hour after last treatment,and then counting micronucleated cells in bone marrow.(2) Sperm malformation test:40 male 6w old Kunming mice were grouped and treated the same as micronucleus test.Mice were sacrificed at 35 day after the first treatment,and then sperm quantity,motility,viability and abnormality rate were calculated.Result Micronucleus rate and sperm abnormality rate of SI intervention group were lower than DBP model group,while sperm motility and viability were higher than DBP model group.Conclusion SI can relieve the genetic toxicity induced by DBP in mice.