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马基诺通过抑制 MAPK 调控的细胞凋亡抑制氧化应激诱导的人神经母细胞瘤 SH-SY5Y 细胞损伤。

Makino Inhibits Oxidative Stress-Induced Neuronal Damage in Human Neuroblastoma SH-SY5Y Cells by Suppressing MAPK-Regulated Apoptosis.

机构信息

Department of Convergence Medicine, Pusan National University School of Medicine, Yangsan 50612, Korea.

Department of Life Science and Environmental Biochemistry, Life and Industry Convergence Research Institute, Pusan National University, Miryang 50463, Korea.

出版信息

Molecules. 2022 Aug 26;27(17):5498. doi: 10.3390/molecules27175498.

Abstract

Oxidative stress has been demonstrated to play a pivotal role in the pathological processes of many neurodegenerative diseases. In the present study, we demonstrated that Makino extract (CBME) suppresses oxidative stress-induced neurotoxicity in human neuroblastoma SH-SY5Y cells and elucidated the underlying molecular mechanism. Our observations revealed that CBME effectively protected neuronal cells against HO-induced cell death by preventing caspase-3 activation, Bax upregulation, Bcl-2 downregulation, activation of three mitogen-activated protein kinases (MAPKs), cAMP response element-binding protein (CREB) and NF-κB phosphorylation, and iNOS induction. These results provide evidence that CBME has remarkable neuroprotective properties in SH-SY5Y cells against oxidative damage, suggesting that the complementary or even alternative role of CBME in preventing and treating neurodegenerative diseases is worth further studies.

摘要

氧化应激在许多神经退行性疾病的病理过程中起着关键作用。在本研究中,我们证明了 Makino 提取物(CBME)可抑制人神经母细胞瘤 SH-SY5Y 细胞中氧化应激诱导的神经毒性,并阐明了其潜在的分子机制。我们的观察结果表明,CBME 通过防止 caspase-3 激活、Bax 上调、Bcl-2 下调、三种丝裂原活化蛋白激酶(MAPK)、cAMP 反应元件结合蛋白(CREB)和 NF-κB 磷酸化以及诱导诱导型一氧化氮合酶(iNOS)的激活,有效地保护神经元细胞免受 HO 诱导的细胞死亡。这些结果表明 CBME 对 SH-SY5Y 细胞的氧化损伤具有显著的神经保护作用,提示 CBME 在预防和治疗神经退行性疾病中的互补甚至替代作用值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf79/9457777/f05de9fb4953/molecules-27-05498-g001.jpg

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