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CD38 deficiency activates ERK1/2-NF-κB signaling pathway in sepsis-associated renal injury

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摘要 CD38 is known to play roles in various inflammatory pathways.However,whether it has a protective or detrimental effect during bacterial septicemia remains disputed.Herein,this study aimed to determine the potential effect of CD38 on renal injury in septicemia.Escherichia coli(E.coli)was used to induce sepsis-associated renal injury in mice.WT and CD38-/-mice were stimulated with E.coli.After three hours,the serum was collected to detect renal function.Function mRNA expressions inflammatory cytokines in kidneys were quantified by real-time PCR.Hematoxylin and eosin staining were used to observe the histomorphology of kidney.The expression of TLR4,NF-κB,MAPK and cytokines were detected by Western Blot.Our results demonstrated that 3×10^(8) cfu/mL E.coli is the appropriate dose to induce sepsis mice model.Compared to WT sepsis mice,CD38-/-mice showed aggravated kidney injuries with impaired renal function,increased inflammation and apoptosis after E.coli stimulation.Interestingly,CD38 deficiency also led to elevated expression of TLR4 and increased phosphorylation of NF-κB p65/p105 and ERK1/2.To sum up,our results suggested that CD38 deficiency could aggravate E.coli-induced renal injury through activating ERK1/2-NF-κB signaling pathway.
作者 ZHANG Huiqing DU Yuna XIE Zhengyu WANG Zeyu LI Hua 李蓉 ZHANG Huiqing;DU Yuna;XIE Zhengyu;WANG Zeyu;LI Hua;LI Rong(Department of Clinical Laboratory,Jiangxi Provincial People's Hospital&The first Affiliated Hospital of Nanchang Medical College,Nanchang,China;Department of Clinical Laboratory,the Second Affiliated Hospital of Nanchang University&Jiangxi Provincial Key Laboratory for Laboratory Medicine,Nanchang,China)
出处 《实验与检验医学》 CAS 2022年第1期129-138,共10页 Experimental and Laboratory Medicine
基金 supported by the National Natural Sciences Foundation of China (NSFC) grant numbers [31960165&81760288]
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