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作 者:李梦俊 张晓荣 王婧 高艳萍(指导)[1] LI Meng-Jun;ZHANG Xiao-Rong;WANG Jing;GAO Yan-Ping(Fenyang College of Shanxi Medical University,Fenyang 032200,China)
出 处:《中国免疫学杂志》2021年第17期2065-2069,共5页Chinese Journal of Immunology
基 金:山西医科大学汾阳学院校内科研项目(No.2019D01)资助。
摘 要:目的:探讨幽门螺杆菌感染导致的IL-1β升高对C57BL小鼠骨骼肌的影响及机制。方法:将24只C57BL小鼠平均分为4组:对照组(M)、低浓度组(L)、中浓度组(I)、高浓度组(H),对照组用生理盐水处理,处理组分别用低浓度0.3 ml、中浓度0.6 ml、高浓度0.9 ml幽门螺杆菌悬液(菌液浓度调至1×10^(9) CFU/ml)处理。采用物理方法测量小鼠的握力。ELISA检测小鼠血清中的炎症因子。HE染色观察小鼠胃黏膜、小鼠腓肠肌组织、小鼠比目鱼肌组织的炎症浸润程度及小鼠骨骼肌的变化情况。免疫组化观察IL-1β、MYOG表达。分别用qPCR和Western blot检测pNF-κB、IL-1β、MYOD1、MYOG的mRNA和蛋白表达水平。结果:幽门螺杆菌感染激活NF-κB通路使IL-1β升高,导致C57BL小鼠骨骼肌衰减。与对照组相比,随幽门螺杆菌浓度的增加炎症浸润程度增强;pNF-κB、IL-1β的mRNA水平升高(P<0.05)MYOD1、MYOG表达降低(P<0.05);小鼠腓肠肌、比目鱼肌中pNF-κB、IL-1β等炎症相关蛋白表达增强(P<0.05),肌肉相关蛋白MYOD1、MYOG表达降低(P<0.05),骨骼肌组织出现衰减。结论:幽门螺杆菌感染C57BL小鼠激活NF-κB通路使IL-1β升高导致小鼠骨骼肌衰减。Objective:To investigate the effect and mechanism of elevated IL-1βlevels induced by Helicobacter pylori infection on skeletal muscle of C57BL mice.Methods:24 mice were equally divided into 4 groups:control group(M),low concentration group(L),medium concentration group(I),and high concentration group(H).Control group was treated with normal saline,while treatment group was treated with low concentration 0.3 ml,medium concentration 0.6 ml,and high concentration 0.9 ml Helicobacter pylori suspension(bacterial concentration was adjusted to 1×10^(9) CFU/ml).The grip strength of mice was measured by physical method.Inflammatory factors in serum were detected by ELISA.HE staining was used to observe the inflammatory infiltration degree of gastric mucosa,gastrocnemius tissue,soleus tissue and skeletal muscle changes in mice.Expressions of IL-1βand MYOG were observed by immunohistochemistry.qPCR and Western blot to measure the mRNA and protein levels of pNF-κB,IL-1β,MYOD1 and MYOG.Results:Helicobacter pylori infection activates the NF-κB pathway and elevates IL-1βthat leads to skeletal muscle attenuation in C57BL mice.Compared with control group,with the increase of Helicobacter pylori concentration,the inflammatory infiltration degree of issue was increased;mRNA levels of pNF-κB and IL-1βwere increased(P<0.05),and expressions of MYOD1 and MYOG were decreased(P<0.05);expression of inflammatory proteins such as pNF-κB、IL-1βwas increased(P<0.05),and expression of muscle tissue related proteins MYOD1 and MYOG was decreased(P<0.05),and the skeletal muscle tissue was attenuated.Conclusion:Activation of NF-κB pathway by Helicobacter pylori infection in C57BL mice increased IL-1βand led to skeletal muscle attenuation.
分 类 号:R337.1[医药卫生—人体生理学] R392.13[医药卫生—基础医学]
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