Effects of dexmedetomidine on hypoxia/reoxygenation injury-induced cell apoptosis and caspase-12 expression in A549 cells.
- Author:
Zi-Yin LUO
1
;
Bing-Qian XIANG
1
;
Hui GAO
1
;
Xiao-Xiao QIU
1
;
Mao-Lin HAO
2
;
Wan-Tie WANG
3
Author Information
1. Ischemia/Reperfusion Injury Research Institute of Wenzhou Medical University, Wenzhou 325035, China.
2. Ischemia/Reperfusion Injury Research Institute of Wenzhou Medical University, Wenzhou 325035, China. hml@wmu.edu.cn.
3. Ischemia/Reperfusion Injury Research Institute of Wenzhou Medical University, Wenzhou 325035, China. wwt@wmu.edu.cn.
- Publication Type:Journal Article
- From:
Acta Physiologica Sinica
2017;69(4):437-444
- CountryChina
- Language:Chinese
-
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.
