摘要
目的探究解毒活血汤调控ERK/p38 MAPK信号通路治疗Ⅲ型前列腺炎的作用机制。方法采用去势手术+苯甲酸雌二醇(EB)诱导慢性前列腺炎大鼠模型。36只SD大鼠随机分为空白组(生理盐水,4 mL·kg^(-1))、模型组(生理盐水,4 mL·kg^(-1))、阳性药物对照组(前列康片混悬液,4 mL·kg^(-1))、解毒活血汤低(4 mL·kg^(-1))、中(8mL·kg^(-1))、高剂量组(12 mL·kg^(-1)),每组6只,所有实验动物连续给药30 d。苏木精-伊红(HE)染色观察各组大鼠组织病理学变化;免疫组化法、RT-PCR、Western Blot技术检测相关炎症因子及蛋白表达水平。结果与正常对照组相比,慢性前列腺炎大鼠前列腺组织增生及水肿明显、炎症浸润增加,而阳性药物对照组及解毒活血汤各剂量组大鼠前列腺组织病变减轻或消失、炎症浸润减少,且与解毒活血汤剂量成正比;免疫组化表示模型组p38、P-p38、STAT3、P-STAT3表达较高,阳性药物对照组、不同剂量解毒活血汤组的p38、P-p38、STAT3、P-STAT3表达呈下降趋势,且均低于模型组。RT-PCR结果显示阳性药物对照组及解毒活血汤低、中、高剂量组均能降低大鼠前列腺组织中TNF-α、IL-2、IL-6的表达水平;Western Blot检测提示大鼠疾病发生进展过程中p38、P-p38、P-ERK1/2、STAT3、P-STAT3呈高表达状态,解毒活血汤能够降低其表达,从而降低相关炎症因子的过度激活。结论解毒活血汤能够抑制ERK/p38 MAPK信号通路的过度激活,从而降低IL-2、IL-6、TNF-α等炎症因子的表达,以改善前列腺组织炎症反应。
Objective To study the mechanism of Jiedu Huoxue Decoction(JDHXD)in treating typeⅢprostatitis through ERK/p38 MAPK signaling pathway.Methods The rat model of chronic prostatitis was established by testectomy and using estradiol benzoate(EB).Thirty-six SD rats were randomly divided into sham(normal saline,4 mL·kg^(-1)),model(normal saline,4 mL·kg^(-1)),positive drug control(Qianliekang tablet suspension,4 mL·kg^(-1)),and JDHXD low(4mL·kg^(-1)),medium(8mL·kg^(-1))and high dose(12mL·kg^(-1))groups,with 6 rats in each group.All animals were administered continuously for 30 days.The histopathological changes of rats in each group were observed by hematoxylin-eosin(HE)staining.The expression levels of related inflammatory factors and proteins were detected by immunohistochemistry,RT-PCR and Western Blot.Results Compared to the sham group,rats in model group had chronic prostatitis with an increase in hyperplasia,edema,and inflammatory infiltration.However,JDHXD at different doses resulted in a reduction or disappearance of hyperplasia,edema,and inflammatory infiltration.The results of immunohistochemistry showed that the expression of p38,P-p38,STAT3 and P-STAT3 was elevated in the model group,but decreased in the positive drug control group and JDHXD groups.RT-PCR results showed that Qianliekang Tablets and JDHXD down-regulated the expression levels of TNF-α,IL-2,IL-6 and other cytokines in prostate tissue of rats at mRNA level.The results of Western Blot showed that p38,P-p38,P-ERK1/2,STAT3 and P-STAT3 were highly expressed in the process of disease progression in rats,while JDHXD down-regulated their expression,thereby inhibiting the excessive activation of related inflammatory factors.Conclusion JDHXD inhibits the excessive activation of ERK/p38 MAPK signaling pathway,thereby down-regulating the expression of IL-2,IL-6,TNF-αand other inflammatory factors,to improve the prostate tissue inflammatory infiltration and improve the inflammatory reaction.
作者
严张仁
殷宏伟
潘俊卿
邓思巧
刘灿
张乃忻
YAN Zhangren;YIN Hongwei;PAN Junqing;DENG Siqiao;LIU Can;ZHANG Naixin(Affiliated Hospital of Jiangxi University of Chinese Medicine,Nanchang 330006,China;Graduate School,Jiangxi University of Chinese Medicine,Nanchang 330004,China)
出处
《云南中医药大学学报》
2024年第1期67-78,共12页
Journal of Yunnan University of Chinese Medicine
基金
国家自然科学基金项目(81960873)
江西省自然科学基金(20202ACBL206027)
江西中医药大学1050青年人才工程项目(5142001001)
江西中医药大学科技创新团队(CXTD22009)。
