Protective Effect of Manganese on Apoptosis and Mitochondrial Function of Heat-Stressed Primary Chick Embryonic Myocardial Cells

Protective Effect of Manganese on Apoptosis and Mitochondrial Function of Heat-Stressed Primary Chick Embryonic Myocardial Cells
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DOI:
10.1007/s12011-021-03016-2
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发表时间:
2021-11
影响因子:
3.9
通讯作者:
Rui Wang;Zhaoguo Shi;Jinlu Li;D. Tang;Shizhen Qin;Yan-li Guo
Rui Wang;Zhaoguo Shi;Jinlu Li;D. Tang;Shizhen Qin;Yan-li Guo
中科院分区:
生物学3区
文献类型:
--
作者:
Rui Wang;Zhaoguo Shi;Jinlu Li;D. Tang;Shizhen Qin;Yan-li Guo

文献摘要

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热应激作为氧化应激的一种,可诱导细胞凋亡。细胞凋亡是细胞程序性死亡的一种形式,线粒体在细胞凋亡中起重要作用。锰(Mn)通过增强锰超氧化物歧化酶(MnSOD)的活性而具有抗氧化能力。为了研究锰对热应激诱导的细胞凋亡和线粒体功能的潜在影响,我们使用经锰预处理24 h的原代鸡胚心肌细胞来检测热应激背景下的关键相关因素。结果表明,锰可恢复热应激引起的细胞活力下降,并降低caspase-3活性(P< 0.05)。Mn预处理组可显著逆转热应激对细胞内ATP含量和Δ Km的抑制作用(P< 0.05)。此外,锰还抑制了热应激诱导的原代鸡胚心肌细胞线粒体分裂,表现为线粒体分裂相关蛋白动力蛋白相关蛋白1(Drp 1)表达降低,线粒体融合相关蛋白视神经萎缩蛋白1(Opa 1)和线粒体融合蛋白1(Mfn 1)表达增加(P<0. 05)。结果表明,锰可减弱热应激条件下鸡胚心肌细胞线粒体介导的凋亡途径,维持线粒体的结构和功能。
Heat stress, as a kind of oxidative stress, induces cell apoptosis. Apoptosis is a form of programmed cell death, and mitochondria play an important role in apoptosis. Manganese (Mn) has an antioxidant capacity by enhancing the activity of manganese superoxide dismutase (MnSOD). To investigate the potential effect of Mn on heat stress-induced apoptosis and mitochondrial function, we examined crucial related factors in the context of heat stress using primary chick embryonic myocardial cells pretreated with Mn for 24 h. The results showed that Mn restored the heat stress-induced decrease in cell viability and reduced the activities of caspase-3 (P< 0.05). The repression of the Δψm and intracellular ATP content caused by heat stress was reversed dramatically in the Mn pretreatment group (P< 0.05). Additionally, Mn inhibited heat stress-induced mitochondrial fission, as shown by decreased mitochondrial fission-related protein dynamin-related protein 1 (Drp1) expression and increased mitochondrial fusion-related protein optic atrophy 1 (Opa1) and mitofusin 1 (Mfn1) (P< 0.05) in primary chick embryonic myocardial cells. It was concluded that Mn attenuates the mitochondrial-mediated apoptosis pathway and sustains mitochondrial structure and function under heat stress in primary chick embryonic myocardial cells.