Protective effects of scoparone against ischemia‑reperfusion‑induced myocardial injury

Abstract

The present study aimed to investigate the protective effects and molecular mechanisms of scoparone on ischemia‑reperfusion (I/R) injury in primary cultured cardiac myocytes and rats. An in vivo rat model of I/R injury and an in vitro primary cultured cardiac myocyte model of oxygen‑glucose deprivation/reoxygenation were used to investigate the protective effects of scoparone. Cell viability, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD), creatine kinase (CK) and malondialdehyde (MDA) levels, and reactive oxygen species (ROS) production were subsequently measured. In addition, cell apoptosis was assessed by terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling staining, and myocardial infarct area (IA) was determined by triphenyl tetrazolium chloride staining. Furthermore, the protein expression levels of B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein (Bax), cytochrome c (Cyt C) and caspase‑3 were assessed by western blotting. The results demonstrated that treatment with scoparone markedly increased cell viability, SOD levels and Bcl‑2 protein expression, and decreased LDH release, MDA production, CK levels, ROS concentration, cell apoptotic rate, myocardial IA, and Bax, caspase‑3 and Cyt C protein expression. These findings indicated that scoparone may have a protective effect against I/R injury, thus suggesting that scoparone may be a considered a potential drug for the treatment of I/R injury via the inhibition of oxidative stress and cell apoptosis.

Scoparone protects neuronal cells from oxygen glucose deprivation/reoxygenation injury

“…Besides, scoparone markedly improved cell viability of OGD/R-induced primary cardiac myocytes. 13 Scoparone inhibits lactate dehydrogenase (LDH) release, MDA production and ROS production, and expressions of bax, caspase-3 and cytochrome c, while induces expressions of SOD and bcl-2 in OGD/R-induced primary cardiac myocytes. 13 In the present study, we found that scoparone improved cell viability of OGD/R-induced hippocampal neurons.…”

“…12 Previous study has demonstrated that scoparone exhibits protective effects against I/R-induced myocardial injury via the inhibition of oxidative stress and cell apoptosis. 13 Another study showed that scoparone suppressed the lipopolysaccharidestimulated inammatory responses in BV-2 microglial cells. 14 However, the role of scoparone in cerebral I/R injury remains unclear.…”

Dietary Coumarins

“…Coumarin 8 could attenuate myocardial ischemia/reperfusion-induced injury in rats by inhibiting the receptor-interacting protein 140 (RIP140)/nuclear factor kappa B (NF-κB) inflammatory pathway. Another simple coumarin, scoparone (22), also known as 3,4-dimethoxycoumarin, was found to possess cardioprotective property in an in vivo rat model of ischemia-reperfusion injury and an in vitro primary cultured cardiac myocyte model of oxygen-glucose deprivation/re-oxygenation (Wan et al 2018). The treatment with 22 increased cell viability, superoxide dismutase levels, and B cell lymphoma 2 protein expression and decreased lactate dehydrogenase release, malondialdehyde production, creatine kinase levels, reactive oxygen species concentration, cell apoptotic rate, myocardial infarct area, and Bcl-2-associated X protein, and caspase-3 and cytochrome c protein expression.…”

Scoparone alleviates Ang II‐induced pathological myocardial hypertrophy in mice by inhibiting oxidative stress

“…SCO could inhibit Ang II‐induced extracellular matrix remodelling in cardiac fibroblasts in vitro at least partly by inhibiting TGF‐β1/Smad signalling 16 . SCO also showed a protective effect against ischaemia‑reperfusion‑induced myocardial injury by counteracting oxidative stress 17 . However, the effect of SCO on Ang II‐induced myocardial hypertrophy is still unknown.…”

“…16 SCO also showed a protective effect against ischaemia-reperfusion-induced myocardial injury by counteracting oxidative stress. 17 However, the effect of SCO on Ang II-induced myocardial hypertrophy is still unknown.…”