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Effects of dexmedetomidine on hypoxia/reoxygenation injury-induced cell apoptosis and caspase-12 expression in A549 cells

LUO Zi-Yin, XIANG Bing-Qian, GAO Hui, QIU Xiao-Xiao, HAO Mao-Lin, WANG Wan-Tie

Ischemia/Reperfusion Injury Research Institute of Wenzhou Medical University, Wenzhou 325035, China； Pathology Department of Hubei Provincial Hospital of Integrated Chinese &； Western Medicine, Wuhan 430015, China

Abstract

To investigate the effects of dexmedetomidine (DEX) on hypoxia/reoxygenation (H/R) injury-induced cell apoptosis and caspase-12 expression, A549 cells were randomly divided into 4 groups: control group, DEX group, H/R group and DEX+H/R group. Cells of control and DEX groups were cultured in the normoxic incubator for 30 h. Cells of H/R and DEX+ H/R groups were incubated in the anoxic cultivation for 6 h, followed by normoxic culture for 24 h, and DEX (1 nmol/L) was added into the culture medium in DEX and DEX+H/R groups. Morphological changes were observed under the inverted microscope. Cell viability was detected by CCK-8. The apoptosis index (AI) of A549 cells was detected by TUNEL method. The activity of caspase-3 enzyme in cells was detected by using caspase-3 kit. The expressions of GRP78, caspase-12 protein and mRNA were determined by Western blot and RT-PCR respectively. Compared with control group, the morphological changes of the cultured cells were observed: some of the cell fusion occurred and the shape of the cells was multilateral; the cell viability was decreased significantly (P < 0.01), the number of apoptotic cells and the AI value, caspase-3 activity, and the expressions of GRP78, caspase-12 protein/mRNA were significantly increased (P < 0.01) in H/R group. While the administration of DEX alleviated the H/R injury-induced cell damage, obviously increased the cell viability (P < 0.01), significantly decreased the increment of apoptotic cells and the AI value induced by H/R injury (P < 0.01), and also dramatically decreased the H/R injury-induced high level of caspase-3 activity (P < 0.01) as well as high expression of caspase-12 protein and mRNA (P < 0.01). Taken together, the results suggest that DEX can effectively protect A549 cells from the H/R injury, which may be mediated by down-regulating the expression of caspase-12 and inhibiting cell apoptosis.

Key words: dexmedetomidine; lung hypoxia/reoxygenation injury ; A549 cells ; cell apoptosis; caspase-12

Received: 2016-11-28　　Accepted: 2017-05-18

Corresponding author: 郝卯林,王万铁　　E-mail: wwt@wmu.edu.cn, hml@wmu.edu.cn

Citing This Article：

LUO Zi-Yin, XIANG Bing-Qian, GAO Hui, QIU Xiao-Xiao, HAO Mao-Lin, WANG Wan-Tie. Effects of dexmedetomidine on hypoxia/reoxygenation injury-induced cell apoptosis and caspase-12 expression in A549 cells. Acta Physiol Sin 2017; 69 (4): 437-444 (in Chinese with English abstract).