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首页> 外文期刊>Journal of Cellular Physiology >Hydrogen Sulfide Epigenetically Attenuates H omocy stein e-Induced Mitochondria! Toxicity Mediated Through NMDA Receptor in Mouse Brain Endothelial (bEnd3) Cells
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Hydrogen Sulfide Epigenetically Attenuates H omocy stein e-Induced Mitochondria! Toxicity Mediated Through NMDA Receptor in Mouse Brain Endothelial (bEnd3) Cells

机译：硫化氢Epigenetically变弱H omocy斯坦e-Induced线粒体!通过NMDA受体在小鼠大脑内皮(bEnd3)细胞

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Previously we have shown that hoiriocysteine (Hey) caused oxidative stress and altered mitochondria! function. Hydrogen sulfide (H2S) has potent anti-inflammatory, anti-oxidative, and anti-apoptotic effects, Therefore, in the present study we examined whether HjS ameliorates Hcy-induced mitochondrial toxicity which led to endothelial dysfunction in part, by epigenetic alterations in mouse brain endothelial cells (bEnd3). The bEnd3 cells were exposed to 100 jaH Hey treatment in the presence or absence of 30 jxM NaHS (donor of H2S) for 24 h. Hcy-activate NMDA receptor and induced mitochondrial toxicity by increased levels of Ca2' NADPH-oxidase-4 (NOX-4) expression, mitochondrial dehydrogena.se activity and decreased the level of nitrate, superoxide dismutase (SOD-2) expression, mitochondria membrane potentials, ATP production. To confirm the role of epigenetic, S'-azacitidine (an epigenetic modulator) treatment was given to the celfs. Pretreatment with NaHS (30 |xM) attenuated the Hcy-induced increased expression of DNMTI, DNHT3a, Ca2"'"'. and decreased expression of DNHT3b in bEND3 ceils. Furthermore, NaHS treatment also mitigated mitochondrial oxidative stress (NOX4S ROS, and NO) and restored ATP that indicates its protective effects against mitochondrial toxicity. Additional, NaHS significantly alleviated Hcy-induced LC3-I/H, CSE, Atg3/7, and Iowp62 expression which confirm its effect on mitophagy. Likewise, NaHS also restored level ofeNOS, CD31, YE-cadherin and ET-1 and maintains endothelial function in Hey treated cells. Molecular inhibition of NMDA receptor by using small interfering RNA showed protective effect whereas inhibition of H2S production by propargylglycine (PG) (inhibitor of enzyme CSE) showed mitotoxic effect. Taken together, results demonstrate that, administration of HjS protected the ceils from HHcy-induced mitochondrial toxicity and endothelial dysfunction.
机译：之前我们已经证明hoiriocysteine(嘿)引起氧化应激和线粒体改变!函数。抗炎、氧化和抗凋亡作用,因此,在当下我们检查了hj是否改善了学习Hcy-induced线粒体毒性导致内皮功能障碍在某种程度上,通过表观遗传在老鼠大脑内皮细胞变化(bEnd3)。嘿,治疗30的存在与否jxM硫氢化钠(硫化氢供体)24 h。Hcy-activateNMDA受体和诱导线粒体毒性通过增加NADPH-oxidase-4游离钙水平”(NOX-4)表达式,线粒体dehydrogena.se活动和降低硝酸盐的水平,超氧化物歧化酶(SOD-2)表达式,线粒体膜电位、ATP生产。确认表观遗传的作用,“阿扎胞苷(一个后生调制器)都在这里接受治疗celfs。减毒Hcy-induced增加表达式表达式的DNHT3b bEND3装天花板。硫氢化钠治疗也减轻线粒体氧化应激(NOX4S ROS,没有)和恢复ATP,表明其保护作用线粒体毒性。显著减轻Hcy-induced LC3-I / H,CSE Atg3/7, Iowp62表达,证实它对mitophagy的影响。恢复水平ofeNOS、CD31 YE-cadherin ET-1和维护在嘿治疗内皮功能细胞。使用小型干扰RNA显示保护效应而抑制硫化氢生产propargylglycine (PG) (CSE)的酶的抑制剂显示mitotoxic效果。证明,hj管理保护装天花板HHcy-induced线粒体毒性和内皮功能障碍。

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