Department of Neurology, The Affiliated Hospital of Hubei University of Chinese Medicine, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, 430061, China.
Department of Cardiovascular Medicine, The Affiliated Hospital of Hubei University of Chinese Medicine, Hubei Provincial Hospital of Traditional Chinese Medicine, No. 856 Luoyu Road, Hongshan District, Wuhan, 430061, China.
J Cardiothorac Surg. 2024 Jul 12;19(1):435. doi: 10.1186/s13019-024-02938-x.
Cerebral ischemia-reperfusion injury (I/R) can affect patient outcomes and can even be life-threatening. This study aimed to explore the role of Shionone in cerebral I/R and reveal its mechanism of action through the cerebral I/R in vitro model.
SH-SY5Y cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to induce cerebral I/R in vitro model. SH-SY5Y cells were treated with different concentrations of Shionone. Cell counting kit-8 and flow cytometry assays were used to detect cell viability and apoptosis levels. The levels of superoxide dismutase, catalase, and malondialdehyde were determined using their corresponding kits to examine the level of oxidative stress. The inflammation response was detected by IL-6, IL-1β, and TNF-α levels, using enzyme-linked-immunosorbent-assay. RT-qPCR was performed to measure the mRNA levels of p38 and NF-κB. Western blotting was used to quantify the apoptosis-related proteins and p38MAPK/NF-κB signaling pathway proteins.
Shionone exhibited no toxic effects on SH-SY5Y cells. Shionone inhibited OGD/R-induced cell apoptosis, improved the inflammatory response caused by OGD/R, and reduced the level of oxidative stress in cells. Western blot assay results showed that Shionone alleviated OGD/R-induced injury by inhibiting the activity of the p38 MAPK/NF-κB signaling pathway. The p38/MAPK agonist P79350 reversed the beneficial effects of Shionone.
Shionone alleviates cerebral I/R and may thus be a novel therapeutic strategy for treating cerebral I/R.
脑缺血再灌注损伤（I/R）可影响患者预后，甚至危及生命。本研究旨在通过体外脑 I/R 模型探讨莪术酮在脑 I/R 中的作用及其作用机制。
采用氧葡萄糖剥夺/复氧（OGD/R）法在体外诱导 SH-SY5Y 细胞脑 I/R 模型。用不同浓度的莪术酮处理 SH-SY5Y 细胞。用细胞计数试剂盒-8 和流式细胞术检测细胞活力和凋亡水平。用相应试剂盒检测超氧化物歧化酶、过氧化氢酶和丙二醛的水平，以评估氧化应激水平。用酶联免疫吸附试验检测白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）水平来检测炎症反应。用 RT-qPCR 检测 p38 和 NF-κB 的 mRNA 水平。用 Western blot 定量检测凋亡相关蛋白和 p38MAPK/NF-κB 信号通路蛋白。
莪术酮对 SH-SY5Y 细胞无毒性作用。莪术酮抑制 OGD/R 诱导的细胞凋亡，改善 OGD/R 引起的炎症反应，降低细胞内氧化应激水平。Western blot 检测结果表明，莪术酮通过抑制 p38MAPK/NF-κB 信号通路的活性减轻 OGD/R 诱导的损伤。p38/MAPK 激动剂 P79350 逆转了莪术酮的有益作用。
莪术酮减轻脑 I/R，可能是治疗脑 I/R 的一种新的治疗策略。
