间奥酸对D-半乳糖诱导的衰老具有心脏保护作用的潜在机制之一是线粒体生物生成和凋亡。
Mitochondrial biogenesis and apoptosis as underlying mechanisms involved in the cardioprotective effects of Gallic acid against D-galactose-induced aging.
发表日期:2023 Aug 04
作者:
Mohammad Zarei, Abdolrahman Sarihi, Alireza Zamani, Safoura Raoufi, Seyed Asaad Karimi, Fatemeh Ramezani-Aliakbari
来源:
ANTIOXIDANTS & REDOX SIGNALING
摘要:
衰老是心血管疾病(CVDs)发展的主要风险因素。没食子酸(GA)是一种来源于各种水果的酚类化合物。GA具有广泛的药理学特性,包括抗氧化、抗炎和心脏保护作用。本研究旨在确定GA对老年大鼠心肌肥大的心脏保护作用。通过组织学评估和观察心脏,我们发现GA改善了D-半乳糖(D-GAL)诱导的心肌肥大。为了阐明这种抗衰老作用的原因,我们评估了大鼠心脏组织中的丙二醛水平和抗氧化酶活性。测量了血清中乳酸脱氢酶(LDH)和肌酸激酶(CK-MB)的水平。调查了与心脏组织的线粒体生物发生、线粒体嗜食作用和凋亡相关的基因水平。结果表明,GA改善了抗氧化酶活性,同时显著降低了丙二醛水平。实时PCR分析提出,GA通过调控Sirtuin 1(SIRT1)、PPARγ辅激活因子1α(PGC1-α)、核因子2相关因子2(Nrf2)和线粒体转录因子A(TFAM)的表达水平,有效改善了心脏中的线粒体生物发生。GA还通过调节B细胞淋巴瘤蛋白2(Bcl-2)和Bcl-2相关X蛋白(Bax)的表达水平来减轻心脏中的凋亡。此外,GA改善了血清LDH和CK-MB的水平。GA可能通过抗氧化、线粒体保护和抗凋亡机制减轻老化引起的心肌肥大。© 2023. 作者(根据Springer Nature B.V.的独家许可)
Aging is a main risk factor for the development of cardiovascular diseases (CVDs). Gallic acid (GA) is a phenolic compound derived from a wide range of fruits. GA has a wide spectrum of pharmacological properties, including anti-oxidative, anti-inflammatory, and cardioprotective effects. This research was conducted to determine the cardioprotective effect of GA on cardiac hypertrophy in aged rats.Following histological evaluation and through observing the heart, we found that GA improved the cardiac hypertrophy induced by D-galactose (D-GAL) in cardiac cells. To clarify the causes for this anti-aging effect, we evaluated the malonic dialdehyde levels and antioxidant enzyme activity in rat cardiac tissue. The levels of lactate dehydrogenase (LDH) and creatine kinase (CK-MB) in serum were measured. The levels of genes related to mitochondrial biogenesis, mitophagy, and apoptosis in cardiac tissue were surveyed. The findings represented that GA ameliorated antioxidant enzyme activity while significantly decreasing the malonic dialdehyde levels. Real-time PCR analysis proposed that GA effectively improved mitochondrial biogenesis in the heart via regulating the expression levels of Sirtuin 1 (SIRT1), PPARγ coactivator 1α (PGC1-α), nuclear factor erythroid 2-related factor 2 (Nrf2), and mitochondrial transcription factor A (TFAM). GA also mitigated apoptosis in the heart by modulating the expression levels of B-cell lymphoma protein 2 (Bcl-2) and Bcl-2-associated X (Bax). In addition, GA improved serum LDH and CK-MB levels.GA may alleviate aging-induced cardiac hypertrophy via anti-oxidative, mitoprotective, and anti-apoptotic mechanisms.© 2023. The Author(s), under exclusive licence to Springer Nature B.V.