养血解毒汤对银屑病模型小鼠JAKs-STAT信号通路及炎性因子的影响

Effects of yangxue jiedu tang on JAKs-STAT signaling pathway and inflammatory factors in psoriasis model mice

目的探讨养血解毒汤对银屑病模型小鼠Janus激酶(JAKs)-信号转导子与转录激活子(STAT)信号通路及炎性因子的影响。方法选择昆明种小鼠24只建立银屑病小鼠模型,根据随机数字法分为生理盐水组、养血解毒汤组、甲氨蝶呤组,每组8只。测定小鼠阴道上皮有丝分裂指数和尾部颗粒层片数,免疫组化法测定组织中STAT3、磷酸化(P)-STAT3、STAT5、P-STAT5表达,逆转录-聚合酶链反应(RT-PCR)测定组织中肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β、IL-6、干扰素(INF)-γmRNA表达。结果与生理盐水组比较,养血解毒汤组和甲氨蝶呤组小鼠阴道上皮有丝分裂指数降低、尾部颗粒层片数升高(P<0. 05),养血解毒汤组和甲氨蝶呤组阴道上皮和尾部皮肤中P-STAT3、P-STAT5光密度值降低(P<0. 05),阴道上皮和尾部组织中TNF-α、IL-1β、IL-6、INF-γmRNA降低(P<0. 05);养血解毒汤组和甲氨蝶呤组各指标比较差异统无计学意义(P> 0. 05)。结论养血解毒汤对银屑病具有治疗作用,其机制可能与养血解毒汤可抑制上皮细胞有丝分裂、促进表皮颗粒层生成、抑制STAT3和STAT5磷酸化,减少炎性因子水平有关。

Objective To investigate the effects of yangxue jiedu tang on JAKs-STAT signaling pathway and inflammatory factors in psoriasis model mice. Methods .24 cases Kunming mice were selected to establish psoriasis mouse model, and were randomly divided into saline, yangxie jiedu tang, methotrexate groups, 8 mice in each group. The mitotic index and the number of tail particles were measured. The signal transducers and transcriptional activators （STAT） 3, phosphorylation（P）-STAT3, STAT5 and P-STATS were detected by immunohis- tochemistry. The tumor necrosis factor（TNF）-α, interleukin （IL）-1β, IL-6 and interleukin （IFN）-γ were detected by reverse transcription- polymerase chain reaction （RT-PCR） . Results Compared with those of saline group, the mitotic index of the vaginal epithelium was decreased and the number of tail particles was increased （ P〈0.05 ）, the P-STAT3 and P-STATS densities of the vaginal epithelium and tail skin were decreased （P〈0.05）, the levels of TNF-, IL-1β, IL-6 and INF-γ mRNA in vaginal epithelium and tail tissue were decreased （P〈0.05）. There were no significant difference in the indexes of yangxie jiedu tang and methotrexate groups （ P〉0.05 ）. Conclusions Yangxue jiedu tang has therapeutic effect on psoriasis, and its mechanism might be related to inhibiting epithelial cell mitosis, promoting the epidermal granule formation, inhibiting STAT3 and STAT5 phosphorylation, and reducing the levels of inflammatory factors.