Hong-fei Lin1, Zhi-rui Zhu, Zhi-yong Hu. 1. Department of Anesthesiology, Children's Hospital of Zhejiang University School of Medicine, Hangzhou 310003, China.
Abstract
OBJECTIVE: To investigate if sevoflurane preconditioning attenuate neuronal apoptosis induced by ischemia-reperfusion. METHODS: Thirty-six male SD rats weighing 250 - 300 g were randomly divided into three groups (n = 12 each): control group (group C), ischemia-reperfusion group (group IR) (rats were established cerebral artery clamped and reperfusion model), sevoflurane preconditioning group (group S) (rats were established cerebral artery clamped and reperfusion model after 1 h 2.4% sevoflurane preconditioning). Apoptosis neurons were observed by Hematoxylin and Eosin (HE) staining and transmission electron microscope, TdT mediated Dutp nick end labeling (TUNEL) method was used to count apoptosis neurons density, fresh ischemic brain tissue was taken out, while Caspase-3 zymogen and 20 000 segment were checked by Western blot. RESULTS: apoptosis neurons in group IR were more than ones in group S under HE staining and light microscope and transmission electron microscope, and apoptosis neurons density (cell number/0.1 mm(2)) by TUNEL staining: group C, 13.0 +/- 1.4; group IR, 189.8 +/- 6.8; group S, 110.5 +/- 4.3, the relative gray values of the contents of procaspase-3 and its 20 000 cleavage fragment were 16.72 +/- 3.0, 76.1 +/- 3.4, 51.2 +/- 3.1 and 8.2 +/- 2.3, 59.0 +/- 6.3, 31.2 +/- 5.4 respectively. CONCLUSIONS: Sevoflurane pretreatment can protect neuron on ischemia-reperfusion injury by attenuating neuronal apoptosis in rats.
OBJECTIVE: To investigate if sevoflurane preconditioning attenuate neuronal apoptosis induced by ischemia-reperfusion. METHODS: Thirty-six male SD rats weighing 250 - 300 g were randomly divided into three groups (n = 12 each): control group (group C), ischemia-reperfusion group (group IR) (rats were established cerebral artery clamped and reperfusion model), sevoflurane preconditioning group (group S) (rats were established cerebral artery clamped and reperfusion model after 1 h 2.4% sevoflurane preconditioning). Apoptosis neurons were observed by Hematoxylin and Eosin (HE) staining and transmission electron microscope, TdT mediated Dutp nick end labeling (TUNEL) method was used to count apoptosis neurons density, fresh ischemic brain tissue was taken out, while Caspase-3 zymogen and 20 000 segment were checked by Western blot. RESULTS: apoptosis neurons in group IR were more than ones in group S under HE staining and light microscope and transmission electron microscope, and apoptosis neurons density (cell number/0.1 mm(2)) by TUNEL staining: group C, 13.0 +/- 1.4; group IR, 189.8 +/- 6.8; group S, 110.5 +/- 4.3, the relative gray values of the contents of procaspase-3 and its 20 000 cleavage fragment were 16.72 +/- 3.0, 76.1 +/- 3.4, 51.2 +/- 3.1 and 8.2 +/- 2.3, 59.0 +/- 6.3, 31.2 +/- 5.4 respectively. CONCLUSIONS:Sevoflurane pretreatment can protect neuron on ischemia-reperfusion injury by attenuating neuronal apoptosis in rats.