出 处:《中国临床药理学杂志》2020年第10期1347-1349,共3页The Chinese Journal of Clinical Pharmacology
摘 要:目的研究雷公藤多苷通过调节Janus激酶(JAKs)-信号转导子与转录激活子(STAT)信号通路对银屑病小鼠皮损炎症的作用。方法BALB/c小鼠用咪喹莫特诱导建立银屑病小鼠模型,并将银屑病模型小鼠随机分为模型组(n=25)、实验组(n=25)及对照组(n=25),另取25只小鼠背部涂抹适量凡士林作为空白组。实验组小鼠灌胃雷公藤多苷10 mg·kg^-1·d^-1,对照组小鼠灌胃地塞米松5 mg·kg^-1·d^-1,空白组与模型组灌胃等量生理盐水,连续干预7 d。用银屑病皮损面积和疾病严重程度(PASI)评分标准进行红斑、鳞屑及浸润程度的评分;用酶联免疫吸附(ELISA)法检测小鼠血清肿瘤坏死因子-α(TNF-α)、白细胞介素-17(IL-17)及白细胞介素-23(IL-23)水平。结果空白组、模型组、实验组及对照组小鼠PASI总评分分别为(1.05±0.46),(6.24±1.12),(3.83±0.76),(2.98±1.07)分;血清TNF-α水平分别为(118.23±2.96),(306.37±3.48),(184.92±6.43),(156.22±4.38)ng·L^-1;IL-17水平分别为(13.42±1.57),(52.27±6.14),(30.56±2.47),(24.61±2.05)ng·L^-1;IL-23水平分别为(12.52±5.93),(46.28±3.84),(25.23±4.21),(18.46±7.92)ng·L^-1。与空白组比较,模型组小鼠PASI总评分,血清TNF-α、IL-17、IL-23水平及背部受试区组织JAK1、STAT3蛋白阳性细胞百分比均显著升高,且实验组低于模型组,对照组低于实验组(均P<0.05)。结论雷公藤多苷可改善银屑病小鼠皮损病变,抑制皮损炎症,其机制可能与抑制JAKs-STAT通路信号转导相关。Objective To investigate the effects of tripterygium glycosides on skin lesion inflammation in psoriasis mice by regulating Janus kinase(JAKs)-signal transducer and transcriptional activator(STAT)signaling pathway.Methods BALB/c mice were induced by imiquimod to establish the psoriasis mice models,and the psoriasis model mice were randomly divided into model group(n=25),test group(n=25)and control group(n=25),another 25 mice were given the right amount of petrolatum as blank group.The mice in test group were gavage with tripterygium glycosides 10 mg·kg^-1·d^-1,and the mice in control group were gavage with dexamethasone 5 mg·kg^-1·d^-1,blank group and model group were gavage with the same amount of normal saline for 7 d.The erythema lesions and disease severity(PASI)scoring criteria were used to score erythema,scale and infiltration.Serum tumor necrosis factor-α(TNF-α),interleukin-17(IL-17)and interleukin-23(IL-23)levels were detected by enzyme-linked immunosorbent assay(ELISA).Results The total PASI scores of blank group,model group,test group and control group were(1.05±0.46),(6.24±1.12),(3.83±0.76)and(2.98±1.07)scores,serum TNF-αlevels were(118.23±2.96),(306.37±3.48),(184.92±6.43),(156.22±4.38)ng·L^-1;the IL-17 levels were(13.42±1.57),(52.27±6.14),(30.56±2.47)and(24.61±2.05)ng·L^-1;IL-23 levels were(12.52±5.93),(46.28±3.84),(25.23±4.21),(18.46±7.92)ng·L^-1.Compared with blank group,the total PASI score,serum TNF-α,IL-17,IL-23 levels and the percentage of JAK1 and STAT3 protein positive cells in the back test area tissues in model group were significantly increased,and test group were lower than model group,control group were lower than test group(all P<0.05).Conclusion Tripterygium glycosides can improve the lesions of psoriasis mice and inhibit the inflammation of the lesions,and its mechanism may be related to the inhibition of JAKs-STAT pathway signal transduction.
关 键 词:银屑病 雷公藤多苷 皮损炎症 信号转导子与转录激活子
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