摘要
目的:探讨甲泼尼龙对蛋白酶R样内质网激酶(PERK)的调节机制,及其在机械通气相关性肺损伤(VILI)大鼠中的作用。方法:雄性SD大鼠40只,随机分五组(n=8):对照组(C),VILI模型组(V)以及VILI模型甲泼尼龙低、中、高剂量组(M1-M3)。检测各组大鼠p-PERK、p-e IF2α、ATF-4和CHOP蛋白表达水平及凋亡指数。结果:与C组相比,V组p-PERK、p-e IF2a、ATF-4和CHOP蛋白表达增高;M2、3组的表达水平较V组显著降低(p<0.05)且凋亡指标降低。结论:甲泼尼龙通过调节PERK/eIF2α通路活性,减轻VILI大鼠肺损伤。
Objective: To investigate the regulatory mechanism of methylprednisolone on protease R-like endoplasmic reticulum kinase(PERK) and its role in mechanical ventilation-associated lung injury(VILI) in rats.Methods: Forty male SD rats were randomly divided into five groups(n=8): control group(C), VILI model group(V) and VILI model methylprednisolone low, medium and high dose groups(M1-M3). P-PERK, p-eIF2α, ATF-4 and CHOP protein expression levels and apoptotic index were tested in each group of rats. Results: Compared with group C, the expression of p-PERK, p-eIF2 a, ATF-4 and CHOP protein in group V was increased, and the expression levels of M2 and 3 groups were significantly lower than those in group V(p<0.05). Conclusion: Methylprednisolone attenuates lung injury in VILI rats by regulating the activity of PERK/eIF2α pathway.
作者
李梦迪
杨秀娟
Li Mengdi;Yang Xiujuan(First Hospital Affiliated to Jiamusi University,Jiamusi 154003,China)
出处
《广东化工》
CAS
2020年第21期51-52,共2页
Guangdong Chemical Industry
关键词
甲泼尼龙
机械通气
内质网应激
PERK通路
细胞凋亡
methylprednisolone
mechanical ventilation
endoplasmic reticulum stress
PERK pathway
apoptosis
