Protective effects of atractylenolide III on oxygen-glucose-deprivation/reperfusion-induced injury in HT22 cells.

Human & experimental toxicology Pub Date : 2024-01-01 DOI:10.1177/09603271241288508

Roujia Guo, Siqi Quan, Yuan Liu, Jiahui Wang, Ziyang Huang, Xiuhui Guo, Ming Bai, Erping Xu, Xiangli Yan, Yucheng Li

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Abstract

Background: Atractylenolide III (ATL III) is a natural bioactive compound, that possesses anti-inflammatory, antioxidant, and neuroprotective properties. However, whether ATL III can protect against neuronal injury induced by cerebral ischemia/reperfusion (I/R) have not yet been studied. This study aimed to investigate the protective effects of ATL III on neuronal injury using an oxygen-glucose deprivation/reperfusion (OGD/R) model in HT22 cells.

Methods: Establishment of OGD/R model to induce HT22 cell injury in vitro. Cell viability, live-dead cell staining, oxidative stress levels, and pro-inflammatory cytokine levels were detected using kits. Cell apoptosis was observed by flow cytometry, and the expression of Bax, Bcl-2, and Caspase-3 proteins was detected by western blot.

Results: ATL III significantly alleviates OGD/R-induced cell injury, as evidenced by the increased cell viability and reduced apoptosis rate. ATL III increased the levels of superoxide dismutase (SOD) and glutathione (GSH), while reducing malondialdehyde (MDA), reactive oxygen species (ROS), and the levels of TNF-α, IL-1β, and IL-6. The protein expression of Bax and Caspase-3 was downregulated, while Bcl-2 expression was upregulated by ATL III.

Conclusion: ATL III as a potential therapeutic agent for reducing neuronal injury by mitigating oxidative stress, apoptosis, and inflammation.

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白术内酯 III 对缺氧-葡萄糖/再灌注诱导的 HT22 细胞损伤的保护作用

背景：白术内酯 III（ATL III）是一种天然生物活性化合物，具有抗炎、抗氧化和神经保护特性。然而，ATL III 是否能保护脑缺血/再灌注（I/R）引起的神经元损伤尚无研究。本研究旨在利用氧-葡萄糖剥夺/再灌注（OGD/R）模型研究 ATL III 对 HT22 细胞神经元损伤的保护作用：方法：建立OGD/R模型，在体外诱导HT22细胞损伤。用试剂盒检测细胞活力、活死亡细胞染色、氧化应激水平和促炎细胞因子水平。流式细胞术观察细胞凋亡，Western 印迹检测 Bax、Bcl-2 和 Caspase-3 蛋白的表达：结果：ATL III 能明显减轻 OGD/R 诱导的细胞损伤，表现为细胞存活率提高，细胞凋亡率降低。ATL III 提高了超氧化物歧化酶（SOD）和谷胱甘肽（GSH）的水平，同时降低了丙二醛（MDA）、活性氧（ROS）以及 TNF-α、IL-1β 和 IL-6 的水平。ATL III可下调Bax和Caspase-3的蛋白表达，上调Bcl-2的表达：结论：ATL III 是一种潜在的治疗药物，可通过减轻氧化应激、细胞凋亡和炎症减轻神经元损伤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Human & experimental toxicology

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