Study On The Anti-gout Effect And Mechanism Of Baicalin

Gout is a kind of metabolic diseases which sodium urate crystals deposite in the joints and soft tissues after hyperuricemia caused by the result of purine metabolic disorders.Epidemiological data show that the incidence of gout increases year by year,endangering people’s health.The first-line anti-gout drugs in clinic are colchicine which plays anti-inflammatory effect,allopurinol which inhibits production of uric acid,non-steroidal anti-inflammatory drugs and glucocorticoids.These drugs have many adverse reactions,so looking for new anti-gout drugs become a hot spot in anti-gout treatment.Baicalin(BA)is a flavonoid compound,with anti-inflammatory effect,anti-oxidation,inhibition of xanthine oxidase and other pharmacological effects.This study investigated the anti-gout effect of baicalin by studying the effect of baicalin on RAW264.7 cells induced by sodium urate crystals in vitro and on gouty arthritis of rats induced by sodiusm urate crystals in vivo.1.In vitro experiment investigated the effects of baicalin on the expression of NLRP3 inflammsome and some inflammatory factors in monosodium urate-induced RAW264.7 macrophage.Cultured murine macrophages RAW264.7 were divided into control group,experimental drug groups which pre-received different concentrations of baicalin which final concentration was 2.5、5、10 and 20μg/mL,respectively for one hour before induced by monosodium urate suspension which final concentration was 2 mg/mL and model group which were treated by monosodium urate suspension of final concentration 2 mg/mL.24 h later cells were collected and the mRNA expression of TNF-α,IL-1β,IL-18 and NLRP3 was determined by fluorescence quantitative PCR method and the level of TNF-α,IL-1β and IL-18 in cell supernatant was detected by ELISA.These results indicated that,compared with control group,the mRNA expression of NLRP3,TNF-α,IL-1β and IL-18 was significantly upregulated and the level of TNF-α,IL-1β and IL-18 was significantly increased by monosodium urate in model group,and compared with model group,the gene expression of TNF-α,IL-1β,IL-18 and NLRP3 and their contents were significantly inhibited in baicalin-treated groups.2.In vivo experiment investigated the effect of baicalin on acute gouty arthritis of rats.Wistar rats were randomly assigned to 6 groups,including normal group,model group,colchicine group(0.5mg/kg),and the low,medium,and high dose of baicalin groups(15、30 and 60mg/kg).All drugs were ig administrated once a day for 7 days consecutively.On the fifth day after drug administrated,model of gouty arthritis was induced by injection of monosodium urate solution except the normal group.Swelling dimension and gait profile score were tested at different time.On the seventh day,IL-1β,IL-18 and TNF-αlevels in rats’ serum were determined by using ELISA kits,ankle joints of rats were drawn for histopathological observation.The mice hot-plate test,writhing test and ear swelling method were used to observe the analgesic and nonspecific anti-inflammatory effects of baicalin.These results indicated that,compared with the model group,the joint swelling degree of baicalin-treated groups were significantly decreased(P<0.05 or P<0.01);and the levels of IL-1β and IL-18 in the high dose group of baicalin were decreased statistically(P<0.01);and degree of inflammatory cell infiltration was decreased in baicalin-treated groups and colchicine-treated group.Baicalin also had significantly analgesic and anti-inflammatory effects on mice.Above of all,in vitro,baicalin could inhibit the expression of NLRP3 mRNA,and reduce the secretion of inflammatory factors TNF-α,IL-1β and IL-18 and played an anti-inflammatory effect;In vivo,baicalin reduced synthesis and release of inflammatory cytokines in the serum,and decreasesd the degree of joint swelling in rats with gouty arthritis,and thus played a role in the treatment of acute gouty arthritis of rate.