Objective To investigate the protective effect of oxymatrine on acute lung injury induced by myocardial ischemia/reperfusion (I/R) in diabetic rats via autophagy pathway.
Methods Diabetic rat model was established by intraperitoneal injection of streptozotozin. Then, the left anterior descending artery was ligated. Acute lung injury was induced by ischemia for 30 min and reperfusion for 120 min. Rats were randomly divided into the following groups: control group, diabetes group, diabetes+sham group, diabetes+I/R group, diabetes+I/R+rapamycin group, diabetes+I/R+3-methyladenine group, diabetes+I/R+oxymatrine group (12.5 mg/kg, 25 mg/kg, 50 mg/kg). ELISA method was used to determine the level of CK-MB content in tissue homogenate. Autophagy-related proteins LC-3 Ⅱ/LC-3 Ⅰ, Beclin-1, Atg5 and P62 were detected by western blotting.
Results The results showed that myocardial I/R in diabetic rats caused a significant increase in CK-MB content, and it was 1 566.67±404.15 in control group, 3 566.67±1 401.19 in diabetic group, and 5 776.67±252.55 in diabetic+I/R group, respectively. HE staining showed alveolar and interstitial edema, hemorrhage and inflammatory cell infiltration. The lung tissue injury scores were 0.83±0.69 in control group, 1.00±0.58 in sham group, 2.00±0.58 in diabetic group and 3.88±0.37 in diabetic+I/R group, respectively. Lung function deteriorated significantly, the ratio of WET/DRY in lung tissue increased, the expressions of autophagy-related proteins LC-3 Ⅱ/LC-3 Ⅰ, Beclin-1, Atg5 were significantly up-regulated and P62 expression was down-regulated. OMT reversed myocardial I/R induced lung injury concentration dependently in diabetic rats.
Conclusion OMT can alleviate myocardial I/R induced lung injury in diabetic rats, which may be related to inhibition of autophagy.
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