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Objective To investigate the relationship between rs1260326 polymorphism of glucokinase regulatory protein gene and hyperuricemia and primary gout in Enshi area populations.Methods One hundred and fifty-eight primary gout,190 hyperuricemia and 104 healthy controls (normal group) in total were collected.Hi-single nucleotide polymorphism (SNP) combined with multiplex polymerase chain reaction (PCR) with next generation sequencing techniques were used for gene polymorphism analysis,and the relationship between different alleles or genotypes and susceptibility to primary gout and hyperuricemia were analyzed.The measurement data and numeration data were statistically analyzed with t test and x2 test respectively.Logistic regression analysis was used to assess the relative risk of gout and hyperuricemia.Results The frequency of rs1260326 genotype CC,TC,TT was 8.8％(14/158),60.8％(96/158),30.4％(48/158) respectively in gout patients,15.8％ (30/190),54.7％ (104/190),29.5％ (56/190) in hyperuricemia patients,21.2％ (22/104),45.1％ (47/104),33.7％(35/104) in the normal group,the genotype distribution was significantly different in gout group and normal group (x2=9.895,P=0.007),and there was no difference between hyperuricemia group and normal group (x2=2.665,P=0.264).Allele C and T frequency was 39.2％(124/316) and 60.8％(192/316) in gout patients,43.2％(164/380) and 56.8％(216/380) in hyperuricemia patients,43.8％(91/208) and 56.2％(117/208) in the normal group.Allele T was the susceptible gene for gout.Logistic regression analysis showed that genotypes TC,TT,TC+TT increased the risk of gout.And Logistic regression analysis showed that rs1260326 single nucleotide polymorphism and hyperuricemia were no susceptibile.Conclusion Glucokinase regulatory protein (GCKR) rs1260326 sin-gle nucleotide polymorphism may be associated with primary gout risk in En Shi area,but has no significant correlation with hyperuricemia.
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Objective:To analyze the curative effect of tripterygium on NOD mice and the possible mechanisms.Methods:NOD mice were divided into 2 groups,Group A:tripterygium treatment(0.07 mg/kg,intraperitoneal injection,12 weeks);Group B:saline control.BALB/c mice were enrolled as control group( Group C).Results:After experiment,Group A had lower salivary flow rate than these of Group C,but higher than these of Group B at 12 and 20 weeks old( P<0.05).Group A had higher rate of inflammatory cells apoptosis than these of Group B and Group C(P<0.05).Group A mice had lower levels of TNF-α,IL-6 and IL-1βthan these of Group B(P<0.05),but higher than these of Group C(P<0.05).Group A mice had a higher level of SHIP-1 but a lower level of Mir-155 than these of Group B mice(P<0.05).Group A mice had a better neuroelectrophysiological outcomes than these of Group B mice ( P<0.05).Conclusion:Tripterygium can meliorate the sailoadentitis of NOD mice,which may though activating the SHIP-1/Mir-155 signaling pathway.