摘要
目的研究天抗(TK)对脂多糖(LPS)诱导的小鼠炎症模型的抗炎作用及机制研究。方法将42只昆明小鼠随机分为正常对照(NC)组、模型对照(LPS)组、地塞米松(DXM)组、天抗低(TK-L)、中(TK-M)和高(TK-H)剂量组(0.2,0.8和3.2 g/kg)。各组分别灌胃给药7 d后,腹腔注射30 mg/kg的LPS诱导小鼠急性炎性模型,6 h后处死小鼠,检测小鼠脾脏指数,ELISA测定小鼠血清中IL-1β、IL-6和TNF-α的表达水平;生化法检测小鼠血清中SOD和MDA的表达;qRT-PCR检测小鼠脾脏TLR4、MyD88、TRAF6、p65、IL-1β、IL-6和TNF-αmRNA的表达水平;Western blot检测小鼠脾脏TLR4、MyD88、TRAF6、p-p65和p65蛋白表达水平。结果与LPS组相比,TK组小鼠的脾脏指数明显降低,血清和脾脏组织中IL-1β、IL-6、TNF-α和MDA水平显著下降,SOD水平明显升高,小鼠脾脏组织的TLR4、MyD88、TRAF6和p-p65等蛋白及mRNA表达水平均明显降低。结论天抗对LPS诱导的小鼠急性炎症模型具有抗炎作用,其作用机制可能是通过TLR4/MyD88/NF-κB(p-65)信号通路抑制炎症因子的释放。
To investigate the anti-inflammation effect of Tiankang(TK)on lipopolysaccharide(LPS)-induced mouse inflammatory model and its mechanism,total of 42 Kunming mice were recruited and randomly divided into negative control(NC)group,model control(LPS)group,dexamethasone(DXM)group,Tian Kang low(TK-L),medium(TK-M)and high(TK-H)dose group(0.2,0.8 and 3.2 g/kg).After 7 days of intragastric administration,30 mg/kg of LPS was injected into the abdominal cavity to induce acute inflammation in mice.Six hours later,the mice were sacrificed and the spleen index were analyzed.The expression levels of IL-1β,IL-6 and TNF-αof mouse blood serum were measured by ELISA;the expression levels of SOD and MDA of mouse blood serum were detected by biochemical methods.qRTPCR was used to detect the mRNA expression levels of TLR4,MyD88,TPAF6,p65,IL-1β,IL-6 and TNF-αof mouse spleen;Western blot was employed to detect the protein expression levels of TLR4,MyD88,TRAF6,p65,IL-1β,IL-6 and TNF-αof mouse spleen.Compared with the LPS group,the spleen index of the mice in the TK group was significantly reduced,while the levels of IL-1β,IL-6,TNF-αand MDA in the serum and spleen tissue were significantly decreased,and the level of SOD was significantly increased.In addition,the protein and mRNA expression levels of TLR4,MyD88,TRAF6 and p-p65 were significantly reduced in spleen tissue of the mice in TK group.Overall,TK has anti-inflammatory effects in mice with LPS-induced inflammation,and its mechanism may relate to the inhibition of inflammatory factors release via TLR4/MyD88/NF-κB(p-65)signaling pathway.
作者
曾鸿芳
李小丽
何起臣
周端方
程远芳
于晓萍
宋燚
刘旭
张欢
尹超
周维英
ZENG Hongfang;LI Xiaoli;HE Qichen;ZHOU Duanfang;CHENG Yuanfang;YU Xiaoping;SONG Yi;LIU Xu;ZHANG Huan;YIN Chao;ZHOU Weiying(Department of Pharmacology,College of Pharmacy,Chongqing Medical University,Chongqing 400016,China;Chongqing Key Laboratory of Drug Metabolism,Chongqing 400016,China;Key Laboratory for Biochemistry and Molecular Pharmacology of Chongqing,Chongqing 400016,China;Chengdu Grasswood Jinhua Technology Co.,Ltd.,Chengdu 611130,China)
出处
《免疫学杂志》
CAS
CSCD
北大核心
2021年第4期322-328,共7页
Immunological Journal
基金
国家自然科学基金(8187102395)
重庆市教育委员会科学技术研究项目(KJQN201800431)。
关键词
天抗
脂多糖
抗炎
TLR4
Tiankang
Lipopolysaccharide
Anti-inflammatory
TLR4
