EB病毒抑制小肠上皮细胞增殖的ERK1/2途径分析
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摘要
目的分析EB病毒(EB virus,EBV)抑制小肠上皮细胞增殖的机理,初步探讨EBV导致腹泻的病理机制。方法应用EBV作用于小肠上皮细胞,作用后0、12、24、36和48 h,采用MTT法检测细胞的增殖情况,Western blot法检测细胞MAPK(磷酸化的ERK1/2、JNK、p38)通路的表达情况。结果经EBV作用36及48 h的小肠上皮细胞存活率较24及12 h显著降低,并显著低于0 h(P <0. 05);磷酸化ERK1/2的表达在36和48 h最低,显著低于其他3个时间点(P <0. 05)。结论 EBV可抑制小肠上皮细胞的增殖,且通过抑制ERK1/2磷酸化途径实现。本实验为进一步研究EBV导致腹泻的发病机理提供了参考。
Objective To analyze the mechanism of EB virus(EBV)in inhibiting the proliferation of intestinal epithelial cells and causing diarrhea. Methods Intestinal epithelial cells were inoculated with EBV for 0,12,24,36 and 48 h,and determined for proliferation by MTT assay. The expression of MAPK(phosphorylated ERK1/2,phosphorylated JNK and phosphorylated p38) pathway was determined by Western blot. Results The survival rates of intestinal epithelial cells 36 and 48 h were significantly lower than those 12 and 24 h after inoculation with EBV as well as that before inoculation(0 h,P < 0. 05). However,the expression levels of phosphorylated ERK1/2(p-ERK1/2) 36 and 48 h were significantly lower than those at the other three time points after inoculation(P < 0. 05). Conclusion EBV inhibited the proliferation of intestinal epithelial cells via ERK1/2 pathway. It laid a foundation of further study on the pathological mechanism of diarrhea caused by EBV.
Objective To analyze the mechanism of EB virus(EBV)in inhibiting the proliferation of intestinal epithelial cells and causing diarrhea. Methods Intestinal epithelial cells were inoculated with EBV for 0,12,24,36 and 48 h,and determined for proliferation by MTT assay. The expression of MAPK(phosphorylated ERK1/2,phosphorylated JNK and phosphorylated p38) pathway was determined by Western blot. Results The survival rates of intestinal epithelial cells 36 and 48 h were significantly lower than those 12 and 24 h after inoculation with EBV as well as that before inoculation(0 h,P < 0. 05). However,the expression levels of phosphorylated ERK1/2(p-ERK1/2) 36 and 48 h were significantly lower than those at the other three time points after inoculation(P < 0. 05). Conclusion EBV inhibited the proliferation of intestinal epithelial cells via ERK1/2 pathway. It laid a foundation of further study on the pathological mechanism of diarrhea caused by EBV.
引文
[1]刘厚昌,杨必清.儿童EB病毒(EBV)感染的临床资料探究[J].临床医药文献杂志,2017,4(52):10132-10133.
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[8]GEARY L,LABONNE C.FGF mediated MAPK and PI3K/Akt Signals make distinct contributions to pluripotency and the establishment of Neural Crest[J].Elife,2018,7.pii:e33845.doi:10.7554/e Life.33845.
[9]XU J,YUAN C,WANG G,et al.Urolithins attenuate LPS-induced neuroinflammation in BV2Microglia via MAPK,Akt,and NF-κB signaling pathways[J].J Agric Food Chem,201866(3):571-580.(in Chinese)
[10]DING Y,SHI C,CHEN L,et al.Effects of andrographolide on postoperative cognitive dysfunction and the association with NF-κB/MAPK pathway[J].Oncol Lett,2017,14(6):7367-7373.
[2]罗燕,王春如,毛玮.儿童EB病毒感染相关疾病临床分析[J].中国现代医生,2009,47(34):25-26.
[3]陈春琼.小儿EB病毒与相关疾病的分析研究[J].中国社区医师,2013,15(4):148-149.
[4]王义渠,李杰.巨细胞病毒并EB病毒感染致长期发热、腹泻1例[J].山东医药,2001,41(17):76.
[5]OKA S,NOHGAWA M.EB virus reactivation triggers thrombotic thrombocytopenic purpura in a healthy adult[J].Leuk Res Rep,2017,8:1-3.
[6]OONISHI A,KARIYAMA K.EB virus[J].Nihon Rinsho,2015,73(Suppl 9):654-657.
[7]WANG Y,ZHANG L P,WU J,et al.A case report of giardia lamblia and EB virus associated hemophagocytic syndrome[J].Chin J Contemp Pediatr,2014,16(12):1281-1282.(in Chinese)王毓,张乐萍,吴珺,等.蓝氏贾第鞭毛虫合并EB病毒相关性噬血细胞综合征1例[J].中国当代儿科杂志,2014,16(12):1281-1282.
[8]GEARY L,LABONNE C.FGF mediated MAPK and PI3K/Akt Signals make distinct contributions to pluripotency and the establishment of Neural Crest[J].Elife,2018,7.pii:e33845.doi:10.7554/e Life.33845.
[9]XU J,YUAN C,WANG G,et al.Urolithins attenuate LPS-induced neuroinflammation in BV2Microglia via MAPK,Akt,and NF-κB signaling pathways[J].J Agric Food Chem,201866(3):571-580.(in Chinese)
[10]DING Y,SHI C,CHEN L,et al.Effects of andrographolide on postoperative cognitive dysfunction and the association with NF-κB/MAPK pathway[J].Oncol Lett,2017,14(6):7367-7373.