Berberine Protests the Heart from Ischemic Reperfusion Injury via Interference with Oxidative and Inflammatory Pathways

小檗碱通过干扰氧化和炎症通路来保护心脏免受缺血再灌注损伤

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Abstract

BACKGROUND: Ischemia and reperfusion (I/R) is a pathological condition characterized by an initial restriction of blood supply to an organ followed by the subsequent restoration of perfusion and concomitant reoxygenation. OBJECTIVE: The aim of the study is to assess the possible cardioprotective potential effect of berberine in myocardial ischemia reperfusion injury induced by ligation of coronary artery in a male rat model. METHODS: Total amount of 28 adult male albino rats were randomized into 4 equal groups: 1) Sham group, rats underwent the same anesthetic and surgical procedure as the control group except for LAD ligation; 2), Active control group, rats subjected to regional ischemia for 30 min by ligation of LAD coronary artery and reperfusion for 2 hours, 3), Control vehicle group, rats received dimethyl sulphoxide (DMSO) (vehicle of berberine) via IP route and subjected to ischemia for 30 minutes before ligation of LAD coronary artery & reperfusion for 2 hr; 4), Berberine treated group, rats pretreated with berberine10 mg/kg via IP injection 30minutes before ligation of LAD coronary artery & then subjected to reperfusion for 2 hr. RESULTS: In the control group, as compared with sham, tissue TNF-α, IL-6, IL-10, caspase-3 and BAX, plasma cTn-T and serum MDA significantly increased (P<0.05), while serum GSH significantly decreased (P<0.05). The histopathological control group showed a significant cardiac injury (P<0.05) compared with the sham group. Berberine significantly counteracted (P<0.05) the increase of TNF-α, IL-6, caspase-3 and BAX and counteracted the increase in plasma cTn-T and serum MDA. Berberine produces a significant elevation (P<0.05) in cardiac IL-10 and serum GSH with a significant reduction in (P<0.05) cardiac injury. CONCLUSION: Berberine attenuates myocardial I/R injury in male rats via interfering with inflammatory reactions and apoptosis which were induced by I/R injury.

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