Title : Protective effects of metformin against myocardial ischemia‑reperfusion injury via AMPK‑dependent suppression of NOX4.

Pub. Date : 2021 Oct

PMID : 34396450






6 Functional Relationships(s)
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1 Furthermore, NADPH oxidase 4 (NOX4) was downregulated by metformin at both the mRNA and protein levels, and adenosine 5"-monophosphate-activated protein kinase (AMPK) phosphorylation was increased by metformin. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
2 Furthermore, NADPH oxidase 4 (NOX4) was downregulated by metformin at both the mRNA and protein levels, and adenosine 5"-monophosphate-activated protein kinase (AMPK) phosphorylation was increased by metformin. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
3 It was also found that metformin upregulated the phosphorylation of AMPK and decreased the expression of NOX4. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
4 Furthermore, pre-treatment with AMPK inhibitor compound-C could block the effect of metformin, indicated by increased NOX4 compared with metformin treatment alone. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
5 Furthermore, pre-treatment with AMPK inhibitor compound-C could block the effect of metformin, indicated by increased NOX4 compared with metformin treatment alone. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
6 In conclusion, the present study indicated that metformin activated AMPK to inhibit the expression of NOX4, leading to a decrease in myocardial oxidative damage and apoptosis, thus alleviating reperfusion injury. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus