2013
DOI: 10.1016/j.freeradbiomed.2013.07.007
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SIRT1 activation by curcumin pretreatment attenuates mitochondrial oxidative damage induced by myocardial ischemia reperfusion injury

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Cited by 204 publications
(193 citation statements)
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“…These chemicals include a number of agents including resveratrol, 19) cilostazol, 41) paeonol, 43) statins, 21) hydrogen sulfide 23,44) and persimmon. 45) Yang et al 15) demonstrated that pretreatment with curcumin attenuated mitochondrial oxidative damage induced by myocardial ischemia reperfusion injury through activation of SIRT1. In addition, a recent study showed that curcumin blocked the neurotoxicity of amyloid-beta [25][26][27][28][29][30][31][32][33][34][35] in rat cortical neurons and activation of SIRT1.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…These chemicals include a number of agents including resveratrol, 19) cilostazol, 41) paeonol, 43) statins, 21) hydrogen sulfide 23,44) and persimmon. 45) Yang et al 15) demonstrated that pretreatment with curcumin attenuated mitochondrial oxidative damage induced by myocardial ischemia reperfusion injury through activation of SIRT1. In addition, a recent study showed that curcumin blocked the neurotoxicity of amyloid-beta [25][26][27][28][29][30][31][32][33][34][35] in rat cortical neurons and activation of SIRT1.…”
Section: Discussionmentioning
confidence: 99%
“…13,14) Recently, several studies found that pretreatment with curcumin significantly improves SIRT1 activation and attenuates oxidative stress. 15,16) Besides, many polyphenols have been shown to activate SIRT1 directly or indirectly, decrease SIPS and therefore have therapeutic potential for age-related vascular diseases. [17][18][19][20] However, whether or not pretreatment with curcumin affects the activation of SIRT1 in H 2 O 2 -treated endothelial cells and attenuate cellular senescence is unclear.…”
mentioning
confidence: 99%
“…Reperfusion injury occurs due to ischaemia followed by reintroduction of blood flow to a previously ischaemic tissue, causing additional myocardial damage and cardiac contractile dysfunction (Silambarasan et al, 2015). As oxidative stress is an important contributor to ischaemia/reperfusion (I/R) injury, antioxidants have been considered as a potential therapeutic option (Yang et al, 2013). Oral pre-treatment with SA significantly improved the percent rate-pressure product and percent coronary flow when compared to untreated I/R hearts.…”
Section: Protective Role In Cardiovascular Diseasementioning
confidence: 99%
“…Determination of myocardial apoptosis Myocardial apoptosis was analyzed by a TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) assay using an in situ cell death detection kit, as described previously [33] . The apoptosis index was expressed as the number of apoptotic myocytes/the total number of myocytes counted ×100%.…”
Section: Acta Pharmacologica Sinicamentioning
confidence: 99%