双氢青蒿素对CNP模型大鼠的治疗作用及对炎症小体NLRP3信号通路的影响

Treatment of dihydroartemisinin on CNP model rats and its effect on inflammasome NLRP3 signaling pathway

目的:探究双氢青蒿素(DHA)对慢性前列腺炎(CNP)模型大鼠的治疗作用及对炎症小体NLRP3信号通路的影响。方法:6周龄健康雄性SPF级SD大鼠分为5组:对照组、模型组、DHA低、高剂量组和前列康组,每组6只。除对照组外,其余组大鼠均建立CNP模型。对照组和模型组不采取治疗,DHA高、低剂量组每天灌胃给予40、20 mg/kg DHA,前列康组每天灌胃给予0.5 g/kg前列康片,连续治疗1个月。von Frey法检测大鼠痛觉敏感性,统计大鼠体质量和前列腺重量,HE染色观察大鼠前列腺组织病理损伤,ELISA检测大鼠前列腺组织TNF-α、IL-6和IL-10表达,Western blot检测大鼠前列腺组织NLRP3、caspase-1、IL-1β蛋白表达。结果:高、低剂量DHA和前列康片均显著降低了CNP大鼠痛觉敏感性和前列腺指数,增加了体质量,改善了前列腺组织病理损伤,并显著降低了前列腺组织TNF-α和IL-6含量,增加了IL-10含量,高剂量DHA和前列康片治疗效果优于低剂量DHA。高、低剂量DHA均显著降低了大鼠前列腺组织NLRP3、caspase-1、IL-1β蛋白表达。结论:DHA通过抑制NLRP3炎症小体通路减弱CNP大鼠炎症反应。

Objective:To investigate therapeutic effect of dihydroartemisinin(DHA)on chronic prostatitis(CNP)model rats and its effect on NLRP3 inflammasome pathway.Methods:Six-week-old healthy SPF grade SD male rats were divided into 5 groups:control group,model group,low-DNA group,high-DNA group and QLK group,with 6 rats in each group.Except for control group,other groups were constructed CNP model.No treatment was given for control and model groups.High-DHA and low-DHA groups were respectively given 40 and 20 mg/kg DHA by gavage every day for 1 month,while QLK group was given 0.5 g/kg QLK for 1 month.Pain sensitivity was tested by von Frey method,and body weight and prostate weight were counted.Pathological damage of prostate tissues was observed by HE staining.TNF-α,IL-6 and IL-10 expressions in prostate tissues were detected by ELISA,and expressions of NLRP3,caspase-1 and IL-1βproteins in prostate tissues were detected by Western blot.Results:High-DHA,low-DHA and QLK all significantly reduced pain sensitivity and prostate index,increased body weight,improved pathological injury of prostate tissue,and reduced TNF-αand IL-6 contents and increased IL-10 content in prostate tissue.Therapeutic effect of high-DHA and QLK were better than low-DHA.High-DHA and low-DHA significantly reduced expressions of NLRP3,caspase-1 and IL-1βin prostate tissues.Conclusion:DHA attenuates inflammatory response in CNP rats by inhibiting NLRP3 inflammatome pathway.