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Apocynin prevents reduced myocardial nerve growth factor, contributing to amelioration of myocardial apoptosis and failure.
Jie, Xi; Yang, Hong; Wang, Ke; Zhu, Zong-Feng; Wang, Jia-Pu; Yang, Li-Guo; Yang, Zi-Jian; Zhang, Xiao-Juan; Wang, Ai-Ling; Li, Lu; Chi, Rui-Fang; Qin, Fu-Zhong; Li, Bao; Fan, Bianai.
Afiliación
  • Jie X; The Second Hospital of Shanxi Medical University, Taiyuan, China.
  • Yang H; Shanxi Medical University, Taiyuan, China.
  • Wang K; The Second Hospital of Shanxi Medical University, Taiyuan, China.
  • Zhu ZF; Shanxi Medical University, Taiyuan, China.
  • Wang JP; The Second Hospital of Shanxi Medical University, Taiyuan, China.
  • Yang LG; Shanxi Medical University, Taiyuan, China.
  • Yang ZJ; The Second Hospital of Shanxi Medical University, Taiyuan, China.
  • Zhang XJ; Shanxi Medical University, Taiyuan, China.
  • Wang AL; Shanxi Province Cardiovascular Hospital, Taiyuan, China.
  • Li L; The Second Hospital of Shanxi Medical University, Taiyuan, China.
  • Chi RF; Shanxi Medical University, Taiyuan, China.
  • Qin FZ; Shanxi Province Cardiovascular Hospital, Taiyuan, China.
  • Li B; Shanxi Medical University, Taiyuan, China.
  • Fan B; Shanxi Province Cardiovascular Hospital, Taiyuan, China.
Clin Exp Pharmacol Physiol ; 48(5): 704-716, 2021 05.
Article en En | MEDLINE | ID: mdl-33650189
Reduced nerve growth factor (NGF) is associated with cardiac sympathetic nerve denervation in heart failure (HF) which is characterized by increased oxidative stress. Apocynin is considered an antioxidant agent which inhibits NADPH oxidase activity and improves reactive oxygen species scavenging. However, it is unclear whether apocynin prevents reduced myocardial NGF, leading to improvement of cardiac function in HF. In this study, we tested the hypothesis that apocynin prevents reduced myocardial NGF, contributing to amelioration of myocardial apoptosis and failure. Rabbits with myocardial infarction (MI) or sham operation were randomly assigned to receive apocynin or placebo for 4 weeks. MI rabbits exhibited left ventricular (LV) dysfunction, and elevation in oxidative stress, as evidenced by a decreased reduced-to-oxidized glutathione ratio and an increased 4-hydroxynonenal expression, and reduction in NGF and NGF receptor tyrosine kinase A (TrKA) expression in the remote non-infarcted myocardium. Apocynin treatment ameliorated LV dysfunction, reduced oxidative stress, prevented decreases in NGF and TrKA expression and reduced cardiomyocyte apoptosis after MI. In cultured H9C2 cardiomyocytes, hypoxia or hydrogen peroxide decreased NGF expression, and apocynin normalized hypoxia-induced reduction of NGF. Recombinant NGF attenuated hypoxia-induced apoptosis. Apocynin prevented hypoxia-induced apoptosis, and the suppressive effect of apocynin on apoptosis was abolished by NGF receptor TrKA inhibitor K252a. We concluded that apocynin prevented reduced myocardial NGF, leading to attenuation of cardiomyocyte apoptosis and LV remodelling and dysfunction in HF after MI. These findings suggest that strategies to prevent NGF reduction by inhibition of oxidative stress may be of value in amelioration of LV dysfunction in HF.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Acetofenonas Límite: Animals Idioma: En Revista: Clin Exp Pharmacol Physiol Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Australia

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Acetofenonas Límite: Animals Idioma: En Revista: Clin Exp Pharmacol Physiol Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Australia