摘要
目的:探讨黄连解毒汤对小鼠动脉粥样硬化(AS)模型NLRP3炎症小体的调控作用。方法:将ApoE-/-小鼠随机分成空白组、模型组、治疗大剂量组(20 g/kg)、中剂量组(10 g/kg)、小剂量组(5 g/kg)和阳性组(20 mg/kg吡格列酮),每组6只。除空白组外,其他各组均构建AS模型,造模后连续给药6周,检测血清TC、TG、LDL-C、HDL-C含量;HE染色观察主动脉形态学变化;油红O染色评估AS斑块的形态和大小;免疫组织化学技术检测主动脉中NLRP3的含量;ELISA检测血清中TNF-α、IL-18和IL-1β的表达;RT-qPCR检测主动脉组织中IL-1β、Caspase-1、NLRP3、TNF-αmRNA的表达。结果:与模型组比较,用药组小鼠体重明显下降(P<0.05);黄连解毒汤小剂量组和中剂量组主动脉斑块面积显著减少(P<0.05);各剂量组小鼠血清LDL-C、TC、TG和TNF-α、IL-18、IL-1β水平均降低(P<0.05);中剂量组HDL-C含量上调(P<0.05);黄连解毒汤中、大剂量干预后,小鼠主动脉组织中IL-1β、Caspase-1、NLRP3、TNF-αmRNA表达明显下降(P<0.05)。结论:黄连解毒汤可通过调控NLRP3炎症小体的表达,降低小鼠AS模型炎症因子水平,从而发挥抗AS作用。
Objective:To investigate the regulation of Huanglian Jiedu Decoction(HJD)on NLRP3 inflammasome in a mouse model of atherosclerosis(AS).Methods:ApoE-/-mice were randomly divided into control group,model group,high-dose group(20 g/kg),medium-dose group(10 g/kg),low-dose group(5 g/kg),and positive group(20 mg/kg pioglitazone),6 cases in each group.Except for the control group,the AS model was constructed in all other groups.After the model was administered for 6 weeks,the serum levels of TC,TG,LDL-C and HDL-C were measured.HE staining was used to observe the morphological changes of the aorta.Oil red O staining to assess the morphology and size of AS plaques.Immunohistochemical technique for detection of NLRP3 in the aorta.The expression of TNF-α,IL-18 and IL-1βin serum was detected by ELISA.RT-qPCR was used to detect the expression of IL-1β,Caspase-1,NLRP3 and TNF-αmRNA in aortic tissues.Results:Compared with the model group,the body weight of the mice in the treatment group decreased significantly(P<0.05).The area of aortic plaque in the low-dose and middle-dose groups of HJD was significantly reduced(P<0.05).The levels of serum LDL-C,TC,TG and TNF-α,IL-18 and IL-1βin each dose group were decreased(P<0.05).The HDL-C content in the middle dose group was up-regulated(P<0.05).The expression of IL-1β,Caspase-1,NLRP3 and TNF-αmRNA in the aorta of mice was significantly decreased after HJD medium dose and high dose intervention(P<0.05).Conclusion:HJD can reduce the levels of inflammatory factors in mouse AS model by regulating the expression of NLRP3 inflammasome,thereby exerting anti-AS effect.
作者
许丽婷
于红红
许滔
喻旭梅
徐彬人
田维毅(指导)
俞琦(指导)
XU Li-Ting;YU Hong-Hong;XU Tao;YU Xu-Mei;XU Bin-Ren;TIAN Wei-Yi;YU Qi(Guizhou University of Traditional Chinese Medicine,Guiyang 550025,China)
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2020年第7期815-820,共6页
Chinese Journal of Immunology
基金
地区科学基金项目(No.81860776,81760790)
贵州省科学技术基金项目(No.黔科合基础[2017]1010号)
贵州省中医药管理局中医药
民族医药科学技术研究项目(No.QZYY-2016-002)
贵阳中医学院博士(硕士)启动基金项目。
