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Sinapic acid protects heart against ischemia/reperfusion injury and H9c2 cardiomyoblast cells against oxidative stress.
Silambarasan, Thangarasu; Manivannan, Jeganathan; Priya, Mani Krishna; Suganya, Natarajan; Chatterjee, Suvro; Raja, Boobalan.
Afiliação
  • Silambarasan T; Cardiovascular Biology Lab, Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Tamil Nadu, India.
  • Manivannan J; Cardiovascular Biology Lab, Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Tamil Nadu, India; Vascular Biology Lab, AU-KBC Research Centre, Anna University, Chennai, Tamil Nadu, India.
  • Priya MK; Vascular Biology Lab, AU-KBC Research Centre, Anna University, Chennai, Tamil Nadu, India.
  • Suganya N; Vascular Biology Lab, AU-KBC Research Centre, Anna University, Chennai, Tamil Nadu, India.
  • Chatterjee S; Vascular Biology Lab, AU-KBC Research Centre, Anna University, Chennai, Tamil Nadu, India; Department of Biotechnology, Anna University, Chennai, Tamil Nadu, India.
  • Raja B; Cardiovascular Biology Lab, Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Tamil Nadu, India. Electronic address: drrajaau@gmail.com.
Biochem Biophys Res Commun ; 456(4): 853-9, 2015 Jan 24.
Article em En | MEDLINE | ID: mdl-25511706
ABSTRACT
The present study was designed to evaluate antioxidant and cardioprotective potential of sinapic acid (SA) against ischemia/reperfusion (I/R) injury. Cardiac functional recovery after I/R was evaluated by percentage rate pressure product (%RPP) and percentage coronary flow (%CF). Myocardial injury was evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) staining and LDH enzyme leakage. Oxidative stress was estimated by lipid peroxidation level. eNOS protein expression in reperfused heart was assessed using Western blot method. Finally, in order to support the antioxidant effect of SA, in vitro protective potential of SA was assessed on H2O2-induced oxidative stress in H9c2 cardiomyoblast cells. The overall results demonstrated that I/R induced cardiac dysfunction, injury and oxidative stress was attenuated by SA treatment. Moreover, in vitro results also shown that, SA protects H9c2 cells from oxidative stress and modulates mitochondrial membrane permeability transition (MPT). In conclusion, coupled results from both in vivo and in vitro experiments have confirmed that SA with antioxidant role protects cardiac cells and its functions from I/R induced oxidative stress.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Cardiotônicos / Traumatismo por Reperfusão Miocárdica / Estresse Oxidativo / Ácidos Cumáricos / Miócitos Cardíacos / Mioblastos Idioma: En Ano de publicação: 2015 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Cardiotônicos / Traumatismo por Reperfusão Miocárdica / Estresse Oxidativo / Ácidos Cumáricos / Miócitos Cardíacos / Mioblastos Idioma: En Ano de publicação: 2015 Tipo de documento: Article