Berberine alleviates myocardial ischemia–reperfusion injury by inhibiting inflammatory response and oxidative stress: the key function of miR-26b-5p-mediated PTGS2/MAPK signal transduction

Context:Berberine has myocardial protective effects.

Objectives:The protective effects of berberine on heart ischemia-reperfusion (I/R) injury were explored.

Materials and methods:Human cardiomyocytes were divided into control group, oxygen-glucose deprivation/re-oxygen (OGD/R) (2 h OGD with 24 h reoxygenation) group, OGD/R + low group (5 μM berberine for 24 h) and OGD/R + high group (10 μM berberine for 24 h). Twenty-four Wistar rats were divided into sham group, I/R group (45 min occlusion with 2 h reperfusion), I/R + berberine group (50 mg/kg berberine 1 h before I/R surgery) and I/R + berberine + antagomir (intraperitoneally injected with miR-26b-5p antagomir). MicroRNA profile, effects of berberine on I/R or OGD/R-induced injuries, and the role of miR-26b-5p in the function of berberine were explored.

Results:OGD/R treatment suppressed viability (0.41 ± 0.05 vs. 0.87 ± 0.13, p< 0.05), while induced apoptosis (6.6 ± 1.0% vs. 26.3 ± 4.8%, p< 0.05) in cardiomyocytes, which was restored by berberine (viability: 0.64 ± 0.01 for 5 μM and 0.72 ± 0.01 for 10 μM, p< 0.05; apoptosis: 10.9 ± 2.2 for 5 μM and 7.9 ± 1.3 for 10 μM). Berberine induced miR-26b-5p and inhibited PTGS2/MAPK pathway. MiR-26b-5p inhibition counteracted the protective function of berberine. In rats, berberine (50 mg/kg) improved heart histological structure and suppressed inflammatory response, which was impaired by miR-26b-5p inhibition.

Discussion and conclusions:Berberine exerted anti-I/R function in heart by inducing miR-26b-5p and suppressing the PTGS2/MAPK pathway. These data promote the application of berberine as an anti-I/R agent.

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