Yi Junfeng,He Genlin,Yang Ju,Yang Xuesen.Heat acclimation attenuates neuronal autophagy and apoptosis in heat stroke mice[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(11):1059-1063.
Yi Junfeng,He Genlin,Yang Ju,Yang Xuesen.Heat acclimation attenuates neuronal autophagy and apoptosis in heat stroke mice[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(11):1059-1063.DOI:
Western blot检测Caspase 3及LC3蛋白表达。 结果 在43 ℃环境中暴露120 min后,HA+HS组脑组织含水量为(78.54±0.25)%,显著低于HS组的(79.64±0.21)%,差异有统计学意义(P0.05);脑组织病理学显示HS组细胞肿胀,胞质疏松,染色质边集,核明显固缩、破裂、溶解,细胞空泡化明显,神经元变性和凋亡加剧,HA+HS组细胞损伤程度明显减轻,神经元变性和凋亡减轻,Caspase-3蛋白表达明显下降(P0.05);HA、HA+HS和HS组神经细胞自噬均明显增强,但与HS组相比,HA+HS组自噬程度下降,且LC3蛋白表达明显降低(P0.05)。 结论 热习服对热射病小鼠脑损伤具有保护作用,并可减轻热射病导致的中枢神经细胞自噬及凋亡。
Abstract
Objective To determine the effect of heat acclimation (HA) on the autophagy and apoptosis of cerebral neurons in mice after heat stroke (HS). Methods A total of 48 C57 male mice were randomly divided into control (CON) group
HA group
HS group and HA+HS group. After the establishment of HA and HS models
the brain water content was measured
pathological changes of the brain were observed by HE staining
neuronal degeneration was tested by Fluoro-Jade B (FJB) staining
neuronal apoptosis was detected by TUNEL staining and Western blotting
and the expression of Caspase 3 and LC3 was measured by immunofluorescence assay and Western blotting. The results were compared among the groups. Results After exposure to 43 ℃ for 120 min
the brain water content was significantly lower in HA+HS group than HS group [(78.54±0.25)% vs (79.64±0.21)%
and exacerbated neuronal degeneration and apoptosis in HS mice
but the damage degrees were milder in the HA+HS mice with remarkably attenuated neuronal degeneration and apoptosis and decreased expression of Caspase 3 (P0.05). Heat exposure elevated the autophagy in the HA
HA+HS and HS groups
but the autophagy and LC3 expression were attenuated after HA preconditioning when compared with HS mice. Conclusion HA plays protective role in brain injury in HS-induced mice
and down-regulates the neuronal autophagy and apoptosis.