Nitric Oxide Alleviated High Salt-Induced Cardiomyocyte Apoptosis and Autophagy Independent of Blood Pressure in Rats.
Nitric Oxide Alleviated High Salt-Induced Cardiomyocyte Apoptosis and Autophagy Independent of Blood Pressure in Rats.
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DOI：
10.3389/fcell.2021.646575
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发表时间：
2021
影响因子：
5.5
通讯作者：
Li P
中科院分区：
文献类型：
--
作者：
Li Y;Wu X;Mao Y;Liu C;Wu Y;Tang J;Zhao K;Li P
本研究旨在探讨高盐饮食（HSD）是否会导致与血压无关的心脏损伤，以及一氧化氮（NO）是否可以减轻高盐诱导的大鼠心肌细胞凋亡和自噬。大鼠体内接受8% HSD。 H9C2 细胞或原代新生大鼠心肌细胞 (NRCM) 在体外用氯化钠 (NaCl) 处理。高血压 HSD 大鼠 (HTN) 以及高血压倾向 (HP) 和高血压抵抗 (HR) 大鼠心脏中 cleaved-caspase 3/caspase 3、cleaved-caspase 8/caspase 8、Bax/Bcl2、LC3 II/LC3 I、Beclin-1 和自噬相关 7 (ATG7) 水平升高。中剂量和高剂量（50 和 100 mM）的 NaCl 增加了 H9C2 细胞和 NRCM 中 cleaved-caspase 3/caspase 3、cleaved-caspase 8/caspase 8、Bax/Bcl2、LC3 II/LC3 I、Beclin-1 和 ATG7 的水平。在用 100 mM NaCl 处理的 HSD 大鼠和 H9C2 细胞的心脏中，内皮一氧化氮合酶 (eNOS) 水平升高，但 p-eNOS 水平降低。 HSD大鼠血清和心脏中NO水平降低。 NO 供体硝普钠 (SNP) 逆转了 H9C2 细胞和 NRCM 中 NaCl (100 mM) 诱导的 cleaved-caspase 3/caspase 3、cleaved-caspase 8/caspase 8、Bax/Bcl2 的增加。 SNP 治疗减弱了心脏中 cleaved-caspase 3/caspase 3、Bax/Bcl2、LC3 II/LC3 I、Beclin-1 和 ATG7 的增加，但对 HR 的 HSD 大鼠的血压没有影响。这些结果表明，HSD 会增强心脏损伤，而与血压无关。补充外源NO可以减轻高盐诱导的心肌细胞凋亡和自噬。
The present study aimed to explore whether high-salt diet (HSD) could cause cardiac damage independent of blood pressure, and whether nitric oxide (NO) could alleviate high-salt–induced cardiomyocyte apoptosis and autophagy in rats. The rats received 8% HSD in vivo. H9C2 cells or primary neonatal rat cardiomyocytes (NRCM) were treated with sodium chloride (NaCl) in vitro. The levels of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1 and autophagy related 7 (ATG7) were increased in the heart of HSD rats with hypertension (HTN), and in hypertension-prone (HP) and hypertension-resistant (HR) rats. Middle and high doses (50 and 100 mM) of NaCl increased the level of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and ATG7 in H9C2 cells and NRCM. The endothelial NO synthase (eNOS) level was increased, but p-eNOS level was reduced in the heart of HSD rats and H9C2 cells treated with 100 mM NaCl. The level of NO was reduced in the serum and heart of HSD rats. NO donor sodium nitroprusside (SNP) reversed the increases of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2 induced by NaCl (100 mM) in H9C2 cells and NRCM. SNP treatment attenuated the increases of cleaved-caspase 3/caspase 3, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and ATG7 in the heart, but had no effect on the blood pressure of HSD rats with HR. These results demonstrated that HSD enhanced cardiac damage independently of blood pressure. Exogenous NO supplementarity could alleviate the high salt–induced apoptosis and autophagy in cardiomyocytes.
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