8-Gingerol 通过 PI3K/Akt/mTOR 信号通路减弱活性氧种类、细胞凋亡和自噬来改善心肌纤维化。,Frontiers in Pharmacology

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8-Gingerol 通过 PI3K/Akt/mTOR 信号通路减弱活性氧种类、细胞凋亡和自噬来改善心肌纤维化。
Frontiers in Pharmacology ( IF 4.4 ) Pub Date : 2021-07-28 , DOI: 10.3389/fphar.2021.711701
Yucong Xue ₁ , Muqing Zhang _{1,

2} , Miaomiao Liu ₃ , Yu Liu ₃ , Li Li ₄ , Xue Han _{3,

5} , Zhenqing Sun ₆ , Li Chu _{3,

7}

Affiliation

8-姜酚（8-Gin）是从生姜中提取的一系列酚类物质。尽管许多研究表明 8-Gin 具有多种药理特性，但 8-Gin 对抗心肌纤维化 (MF) 的可能潜在机制仍不清楚。该研究检查了 8-Gin 对异丙肾上腺素 (ISO) 诱导的 MF 的确切作用和潜在机制。雄性小鼠腹腔注射 8-Gin（10 和 20 毫克/千克/天），同时皮下注射 ISO（10 毫克/千克/天），持续 2 周。测量心电图、病理心脏形态、心肌酶、活性氧 (ROS) 生成、细胞凋亡程度和自噬途径相关蛋白。我们的研究观察到 8-Gin 显着降低 J 点升高和心率。除了，8-Gin 导致心脏重量指数和左心室重量指数、肌酸激酶和乳酸脱氢酶（分别为 CK 和 LDH）的血清水平、ROS 生成和减弱 ISO 诱导的病理性心脏损伤的显着降低。此外，用 8-Gin 治疗导致心脏组织中 I 型和 III 型胶原以及 TGF-β 的水平显着降低。我们的结果表明，8-Gin 暴露显着抑制了 ISO 诱导的自噬体形成。8-Gin还可导致基质金属蛋白酶9（MMP-9）、Caspase-9和Bax蛋白活性下调，Bcl-2蛋白活性上调，缓解心肌细胞凋亡。此外，8-Gin 使 PI3K/Akt/mTOR 信号通路相关蛋白的表达明显增加。

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8-Gingerol Ameliorates Myocardial Fibrosis by Attenuating Reactive Oxygen Species, Apoptosis, and Autophagy via the PI3K/Akt/mTOR Signaling Pathway.

8-gingerol (8-Gin) is the series of phenolic substance that is extracted from ginger. Although many studies have revealed that 8-Gin has multiple pharmacological properties, the possible underlying mechanisms of 8-Gin against myocardial fibrosis (MF) remains unclear. The study examined the exact role and potential mechanisms of 8-Gin against isoproterenol (ISO)-induced MF. Male mice were intraperitoneally injected with 8-Gin (10 and 20 mg/kg/d) and concurrently subcutaneously injected with ISO (10 mg/kg/d) for 2 weeks. Electrocardiography, pathological heart morphology, myocardial enzymes, reactive oxygen species (ROS) generation, degree of apoptosis, and autophagy pathway-related proteins were measured. Our study observed 8-Gin significantly reduced J-point elevation and heart rate. Besides, 8-Gin caused a marked decrease in cardiac weight index and left ventricle weight index, serum levels of creatine kinase and lactate dehydrogenase (CK and LDH, respectively), ROS generation, and attenuated ISO-induced pathological heart damage. Moreover, treatment with 8-Gin resulted in a marked decrease in the levels of collagen types I and III and TGF-β in the heart tissue. Our results showed 8-Gin exposure significantly suppressed ISO-induced autophagosome formation. 8-Gin also could lead to down-regulation of the activities of matrix metalloproteinases-9 (MMP-9), Caspase-9, and Bax protein, up-regulation of the activity of Bcl-2 protein, and alleviation of cardiomyocyte apoptosis. Furthermore, 8-Gin produced an obvious increase in the expressions of the PI3K/Akt/mTOR signaling pathway-related proteins. Our data showed that 8-Gin exerted cardioprotective effects on ISO-induced MF, which possibly occurred in connection with inhibition of ROS generation, apoptosis, and autophagy via modulation of the PI3K/Akt/mTOR signaling pathway.

更新日期：2021-07-28

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