热应激加剧雄性 C57 小鼠小脑的氧化应激、细胞凋亡和内质网应激。

Heat stress aggravates oxidative stress, apoptosis, and endoplasmic reticulum stress in the cerebellum of male C57 mice.

机构信息

Neurosciences Research Center, Tabriz University of Medical Sciences, 51666-14756, Tabriz, Iran.

Deptartment of Physiology, Tabriz University of Medical Sciences, Tabriz, Iran.

出版信息

Mol Biol Rep. 2021 Aug;48(8):5881-5887. doi: 10.1007/s11033-021-06582-9. Epub 2021 Aug 2.

DOI:10.1007/s11033-021-06582-9

PMID:34338963

Abstract

BACKGROUND

The current study was set to assess the effect of heat stress exposure on oxidative stress, apoptosis, and endoplasmic reticulum stress markers in the cerebellum of male mice.

METHODS

Fifty male C57BL/6 mice were assigned to five groups of (I) control, (II) heat stress (HS)7, (III) HS14, (IV) HS21, and (V) HS42 groups. Animals in the control group were not exposed to HS. Mice in the II-V groups were exposed to HS once a day over 7, 14, 21, and 42 days, respectively. Cerebellar reactive oxygen species (ROS) levels, expression of heat shock protein (HSP)70 and caspase 3 as well as endoplasmic reticulum stress-related proteins (PERK, p-PERK, CHOP, and Full-length ATF-6) expression were determined on the 7th, 14th, 21st, and 42nd days.

RESULTS

ROS levels and HSP70 expression increased following HS on the 14th, 21st, and 42nd days and the 7th, and 14th days with a peak level of expression on the 14th day following HS. HSP70 levels decreased afterward on the 21st and 42nd days compared with the control group. Besides, exposure to HS for 14, 21, and 42 days resulted in a significant increase in the CHOP and p-PERK levels in the cerebellum compared with the control group. Heat exposure also increased protein expression of cleaved caspase 3 and active ATF-6/Full-length ATF-6 on the 21st and 42nd days in the cerebellum compared with the control animals.

CONCLUSION

These findings indicated that chronic HS augmented oxidative stress, endoplasmic reticulum stress, and apoptosis pathways in the cerebellum of mice.

摘要

背景

本研究旨在评估热应激暴露对雄性小鼠小脑组织中氧化应激、细胞凋亡和内质网应激标志物的影响。

方法

将 50 只雄性 C57BL/6 小鼠分为五组：（I）对照组，（II）热应激（HS）7 组，（III）HS14 组，（IV）HS21 组和（V）HS42 组。对照组动物未暴露于 HS。II-V 组动物每天暴露于 HS 一次，分别持续 7、14、21 和 42 天。第 7、14、21 和 42 天测定小脑组织中活性氧（ROS）水平、热休克蛋白（HSP）70 和半胱氨酸天冬氨酸蛋白酶 3（caspase 3）的表达，以及内质网应激相关蛋白（PERK、p-PERK、CHOP 和全长 ATF-6）的表达。

结果

HS 后第 14、21 和 42 天以及第 7 和 14 天，ROS 水平和 HSP70 表达增加，第 14 天表达水平达到峰值。之后，第 21 和 42 天与对照组相比，HSP70 水平下降。此外，与对照组相比，HS 暴露 14、21 和 42 天导致小脑组织中 CHOP 和 p-PERK 水平显著升高。热暴露还导致小脑组织中 cleaved caspase 3 和 active ATF-6/Full-length ATF-6 的蛋白表达在第 21 和 42 天增加。