Variation of fas/fasl pathway in limb ischemia-reperfusion lung injury rats after etomidate post-treatment
10.3969/j.issn.2095-4344.2865
- Author:
Haibo ZOU
1
Author Information
1. Affiliated Central Hospital, Shenyang Medical College
- Publication Type:Journal Article
- Keywords:
Apoptotic index;
Etomidate;
Fas;
FasL;
Interleukin-1β;
Ischemia-reperfusion;
Lung;
PaO2;
Post-treatment;
Rat;
Tumor necrosis factor-α
- From:
Chinese Journal of Tissue Engineering Research
2020;24(32):5162-5167
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: To date, it has been confirmed that etomidate pre-treatment can reduce the damage of remote organs caused by limb ischemia-reperfusion, but whether etomidate post-treatment has protective effect on remote organs and its mechanism has been rarely reported. OBJECTIVE: To investigate the influence of etomidate post-treatment on limb ischemia-reperfusion lung injury. METHODS: A rat model of limb ischemia-reperfusion lung injury was prepared by clamping the bilateral femoral arteries for 2 hours and reperfusion for 3 hours. After 2 hours of limb ischemia, I/R group experienced the process of limb ischemia-reperfusion; I/R+ETO group, I/R+Dex 0.2 group, I/R+Dex 0.5 group and I/R+Dex 1.0 group, besides the model of limb ischemia-reperfusion, were injected with etomidate 1.0 mg/kg and dexamethasone 0.2, 0.5 and 1.0 mg/kg respectively through tail vein. At 3 hours of reperfusion, blood samples were extracted from the carotid artery, blood gas analysis was performed and the partial pressure of blood oxygen (PaO2) was recorded. The pathological changes were detected by immunohistochemistry. Apoptotic index was detected by Hoechst 33258 staining and wet/dry weight ratio was detected. Fas protein and Fasl mRNA of lung tissue were detected by western blot and RT-PCR respectively. Tumor necrosis factor-α and interleukin-1β levels were detected by ELISA. RESULTS AND CONCLUSION: Compared with the I/R group, PaO2 increased (P < 0.05), Apoptotic index, wet/dry weight ratio, Fas and FasL mRNA, tumor necrosis factor-α and interleukin-1β decreased in the I/R+ETO group, and the number of apoptotic lesions decreased in the I/R+ETO group (P < 0.05). Compared with the I/R+ETO group, the change of each index was not statistically significant in the I/R+Dex 0.5 group (P > 0.05). To conclude, etomidate post-treatment can reduce lung injury caused by limb ischemia-reperfusion in rats, and its mechanism may be related to the down-regulation of Fas/FasL. In the statistical point of view, etomidate 1.0 mg/kg has the potency intensity of reducing lung injury, almost equivalent to dexamethasone 0.5 mg/kg.
