欢迎访问《现代生物医学进展》编辑部！

目的：探讨外源精胺在柯萨奇B3病毒（Coxsackie virus B3, CVB3）诱导的乳鼠心肌细胞损伤中的保护作用及其调控机制。方法：CVB3 感染原代培养的乳鼠心肌细胞，将细胞随机分为3 组：对照（control）组；病毒感染（CVB3）组；精胺干预（CVB3+Sp）组。MTT 试剂检测细胞增殖；流式细胞术检测细胞凋亡；Western blot 检测Bcl-2、Bax、Caspase-3、Caspase-9、GRP78、CHOP、Caspase- 12、p-PERK、PERK、p-eIF2alpha和eIF2alpha 的蛋白表达。结果：与control 组相比，CVB3 组的细胞增殖率显著降低（P<0.05）；凋亡率显著增加（P<0.05）；Bcl-2 的表达下调，Bax、Caspase-3、Caspase-9 蛋白表达增加（P<0.05）；GRP78、CHOP 和Caspase-12 的表达显著上调（P<0.05）；p-PERK 和p-eIF2alpha的表达显著上调（P<0.05）。与CVB3组相比，CVB3+Sp 组的细胞增殖率显著上升（P<0.05）；凋亡率显著下降（P<0.05）；Bcl-2 的表达上调，Bax、Caspase-3、Caspase-9 蛋白表达下调（P<0.05）；GRP78、CHOP 和Caspase-12 的表达显著下调（P<0.05）；p-PERK和p-eIF2alpha的表达显著下调（P<0.05）。结论：外源精胺可以缓解CVB3 诱导的乳鼠心肌细胞增殖降低和细胞凋亡增多等损伤，这可能与精胺抑制PERK-eIF2-alpha信号通路介导的内质网应激有关。

英文摘要:

Objective:To investigate the protective effect of exogenous spermine on Coxsackie virus B3 (CVB3)-induced neonatal rat cardiomyocytes injury and its regulatory mechanism.Methods:The primary neonatal rat cardiomyocytes were infected with CVB3, and the cells were randomly divided into 3 groups, control group, CVB3 group, CVB3 + Sp group. The cell proliferation was measured by MTT assay. The cell apoptosis was detected by flow cytometry. The protein expression levels of Bcl-2, Bax, Caspase-3, Caspase-9, GRP78, CHOP, Caspase-12, p-PERK, PERK, p-eIF2-alpha and eIF2-alpha were detected by western blot assay.Results:Compared with the control group, the cell proliferation rate was significantly reduced (P<0.05); the apoptosis rate was increased (P<0.05); the protein expression level of Bcl-2 was down-regulated, the expression levels of Bax, Caspase-3, Caspase-9 were increased (P<0.05); the expression levels of GRP78, CHOP and Caspase-12 were significantly up-regulated (P <0.05); the protein expression levels of p-PERK and p-eIF2琢 were dramatically up-regulated (P<0.05) in the CVB3 group. Compared with the CVB3 group, the cell proliferation rate was significantly increased (P<0.05); the apoptosis rate was decreased significantly (P<0.05); the protein expression of Bcl-2 was up-regulated, the expression levels of Bax, Caspase-3, Caspase-9 were down-regulated (P<0.05); the expression levels of GRP78, CHOP and Caspase-12 expression were significantly lower (P<0.05); the protein expression of p-PERK and p-eIF2-alpha expression were significantly lower (P<0.05) in the CVB3 + Sp group.Conclusion:Exogenous spermine may alleviate CVB3-induced proliferation reduction and apoptosis in neonatal rat cardiomyocytes, which may be related with the inhibition of PERK-eIF2alpha signaling pathway-mediated endoplasmic reticulumstress.

View Full Text View/Add Comment Download reader