Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases · 2015
[The effect of dexmedetomidine on autophagy and apoptosis in intestinal ischemia reperfusion-induced lung injury].
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Xie Chunyan, Li Yunfeng, Liang Jiangshui, Xiao Jinfang, Zhao Zhenlong, Li Tao
Аннотация
OBJECTIVE: To investigate the protective effects of dexmedetomidine against autophagy and apoptosis in intestinal ischemia reperfusion (I/R)-induced lung injury.
METHODS: Twenty-four SD rats were randomly and equally divided into 4 groups according to the random number table: control group, I/R group, small dose of dexmedetomidine (D1) group and large dose of dexmedetomidine (D2) group. The model of lung injury was induced by occlusion of the superior mesenteric artery for 60 min followed by 12 h reperfusion. Rats in D1 and D2 groups received intravenous injection of dexmedetomidine at dose of 1 µg/kg and 5 µg/kg respectively. Rats in control and I/R groups were given same volume of normal saline. Pathological changes were detected by hematoxylin-eosin (HE) staining. The microtubule-associated protein 1 light chain 3(LC3)II/I ratio, Beclin-1, Bax and Bcl-2 expression were measured by Western blot. Cell apoptosis was assayed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), while caspase-3 activity was evaluated by immunohistochemistry.
RESULTS: Significant infiltration of neutrophils and thickened alveolar walls were observed in the I/R group compared to the control group, which were improved by dexmedetomidine (5 µg/kg) treatment. Compared to the control group, the apoptosis cells [(69 ± 8) cells/field], LC3 II/I ratio(57 ± 8), Beclin-1(487%± 45%) and Bax (358% ± 37%) expression were markedly increased (P<0.05), while Bcl-2 (39% ± 5%) expression was decreased (P<0.05) in the I/R group. Compared to the I/R group, the apoptosis cells [(32 ± 5) cells/field], LC3 II/I ratio(27 ± 4), Beclin-1 (285%± 41%) and Bax (181% ± 25%) expression were markedly reduced (P<0.05), while Bcl-2 (91% ± 9%) expression was increased (P<0.05) in the D2 group.
CONCLUSIONS: Autophagy and apoptosis were activated in intestinal I/R-induced lung injury. Dexmedetomidine ameliorated intestinal I/R-induced lung injury via reducing autophagy and apoptosis.
METHODS: Twenty-four SD rats were randomly and equally divided into 4 groups according to the random number table: control group, I/R group, small dose of dexmedetomidine (D1) group and large dose of dexmedetomidine (D2) group. The model of lung injury was induced by occlusion of the superior mesenteric artery for 60 min followed by 12 h reperfusion. Rats in D1 and D2 groups received intravenous injection of dexmedetomidine at dose of 1 µg/kg and 5 µg/kg respectively. Rats in control and I/R groups were given same volume of normal saline. Pathological changes were detected by hematoxylin-eosin (HE) staining. The microtubule-associated protein 1 light chain 3(LC3)II/I ratio, Beclin-1, Bax and Bcl-2 expression were measured by Western blot. Cell apoptosis was assayed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), while caspase-3 activity was evaluated by immunohistochemistry.
RESULTS: Significant infiltration of neutrophils and thickened alveolar walls were observed in the I/R group compared to the control group, which were improved by dexmedetomidine (5 µg/kg) treatment. Compared to the control group, the apoptosis cells [(69 ± 8) cells/field], LC3 II/I ratio(57 ± 8), Beclin-1(487%± 45%) and Bax (358% ± 37%) expression were markedly increased (P<0.05), while Bcl-2 (39% ± 5%) expression was decreased (P<0.05) in the I/R group. Compared to the I/R group, the apoptosis cells [(32 ± 5) cells/field], LC3 II/I ratio(27 ± 4), Beclin-1 (285%± 41%) and Bax (181% ± 25%) expression were markedly reduced (P<0.05), while Bcl-2 (91% ± 9%) expression was increased (P<0.05) in the D2 group.
CONCLUSIONS: Autophagy and apoptosis were activated in intestinal I/R-induced lung injury. Dexmedetomidine ameliorated intestinal I/R-induced lung injury via reducing autophagy and apoptosis.