Department of Neurology, Yixing Traditional Chinese Medicine Hospital, Yixing, Jiangsu, 214200, China.
Division of Nephrology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China.
Adv Biol (Weinh). 2024 Nov;8(11):e2400180. doi: 10.1002/adbi.202400180. Epub 2024 Sep 27.
Xinglou Chengqi decoction (XLCQD) is a Chinese formula that offers benefits in ischemic stroke. However, the underlying mechanism of the effects of XLCQD-mediated anti-ischemic stroke effects remains obscure. This study investigates the ferroptosis mechanism of XLCQD against cerebral ischemia/reperfusion (I/R) injury using rat models of middle cerebral artery occlusion/reperfusion (MCAO/R). Ferroptosis differs from traditional cell death pathways and is linked to oxidative stress-induced lipid peroxidation and glutathione (GSH) depletion, which is essential to the development of ischemic stroke. In this study, it is shown that XLCQD improves brain infarction, neurological dysfunction, and histopathological changes caused by MCAO/R exposure, and improving I/R-induced oxidative damage through inhibition of ferroptosis via (Solute Carrier Family 7 Member 11) SLC7A11/ (glutathione peroxidase 4) GPX4 pathway. Interestingly, it is found that XLCQD-mediated protection in I/R is reversed by the silence of SLC7A11. XLCQD intervention significantly promotes GSH content and suppresses Reactive Oxygen Species(ROS), iron accumulation, as well as Malondialdehyde (MDA) generation, are markedly abrogated when SLC7A11 is knockdown by SLC7A11-shRNA transfection, indicating that SLC7A11 is the main target of XLCQD to further trigger intracellular events. In conclusion, XLCQD attenuates in vivo cerebral I/R injury by reducing ferroptosis via the SLC7A11/GPX4 pathway.
星蒌承气汤(XLCQD)是一种对缺血性脑卒中有益的中药方剂。然而,XLCQD 介导的抗缺血性脑卒中作用的潜在机制尚不清楚。本研究使用大脑中动脉闭塞/再灌注(MCAO/R)大鼠模型,探讨 XLCQD 对脑缺血/再灌注(I/R)损伤的铁死亡机制。铁死亡不同于传统的细胞死亡途径,与氧化应激诱导的脂质过氧化和谷胱甘肽(GSH)耗竭有关,这对缺血性脑卒中的发展至关重要。本研究表明,XLCQD 改善了 MCAO/R 暴露引起的脑梗死、神经功能障碍和组织病理学变化,并通过抑制铁死亡(通过溶质载体家族 7 成员 11 [SLC7A11]/(谷胱甘肽过氧化物酶 4 [GPX4] 途径)减轻 I/R 诱导的氧化损伤。有趣的是,发现 XLCQD 在 I/R 中的保护作用可通过 SLC7A11 的沉默而逆转。XLCQD 干预可显著增加 GSH 含量,并抑制活性氧(ROS)、铁积累以及丙二醛(MDA)的生成,而当用 SLC7A11-shRNA 转染沉默 SLC7A11 时,这些作用明显被阻断,表明 SLC7A11 是 XLCQD 进一步触发细胞内事件的主要靶点。综上所述,XLCQD 通过 SLC7A11/GPX4 通路减少铁死亡从而减轻体内脑 I/R 损伤。