College of Animal Science and Technology, Gansu Agricultural University, Lanzhou, 730070, People's Republic of China.
Biol Trace Elem Res. 2022 Oct;200(10):4419-4429. doi: 10.1007/s12011-021-03016-2. Epub 2021 Nov 15.
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.
热应激作为一种氧化应激，会诱导细胞凋亡。细胞凋亡是一种程序性细胞死亡形式，而线粒体在凋亡中起着重要作用。锰 (Mn) 通过增强锰超氧化物歧化酶 (MnSOD) 的活性具有抗氧化能力。为了研究 Mn 对热应激诱导的细胞凋亡和线粒体功能的潜在影响，我们使用经过 24 小时 Mn 预处理的原代鸡胚心肌细胞研究了热应激背景下的关键相关因素。结果表明，Mn 恢复了热应激诱导的细胞活力下降，并降低了 caspase-3 的活性（P<0.05）。Mn 预处理组中，热应激引起的 Δψm 和细胞内 ATP 含量下降得到显著逆转（P<0.05）。此外，Mn 抑制了热应激诱导的线粒体裂变，表现为线粒体裂变相关蛋白动力相关蛋白 1 (Drp1) 表达减少和线粒体融合相关蛋白视神经萎缩 1 (Opa1) 和线粒体融合蛋白 1 (Mfn1) 增加（P<0.05）。综上所述，Mn 减轻了线粒体介导的细胞凋亡途径，并在原代鸡胚心肌细胞中维持了线粒体的结构和功能。
