星形胶质细胞
豪华耐晒蓝
电针
医学
胶质纤维酸性蛋白
白质
缺血
药理学
免疫印迹
小胶质细胞
免疫组织化学
胼胝体
麻醉
星形胶质增生
水通道蛋白4
病理
内分泌学
少突胶质细胞
内科学
炎症
髓鞘
神经炎症
治疗效果
髓鞘碱性蛋白
脑缺血
神经胶质
脑损伤
神经保护
谷氨酸受体
缺血性损伤
促炎细胞因子
神经科学
化学
梗塞
氧化应激
活性氧
胶质瘢痕
作者
C Chan,Wei Wang,Xinyu Fan,Feng Wu,Jian Zhao
出处
期刊:Acupuncture & electro-therapeutics research
[Cognizant]
日期:2026-03-02
标识
DOI:10.1177/03601293261427029
摘要
Background White matter injury (WMI) is a major contributor to neurological dysfunction following ischemic stroke. Electroacupuncture (EA) has been shown to alleviate ischemic WMI and improve neurological deficits; however, the underlying mechanisms remain unclear. Objective In this study, we investigated whether EA exerts therapeutic effects on ischemic WMI by regulating the Nrf2/heme oxygenase-1 (HO-1) axis as well as reactive astrocyte (AS) activity. Methods Male Sprague–Dawley rats were subjected to permanent middle cerebral artery occlusion (pMCAO) using the intraluminal filament method. Neurological function was assessed using the modified neurological severity score. Luxol Fast Blue staining was used to evaluate corpus callosum (CC) damage. Western blot and immunohistochemistry were used to detect the expression of Nrf2, HO-1, and glial fibrillary acidic protein (GFAP). Quantitative real-time polymerase chain reaction was used to assess the release of pro-inflammatory cytokines. Results EA significantly increased the expression of Nrf2 and HO-1 in the CC and effectively suppressed GFAP overexpression and the release of pro-inflammatory cytokines TNF-α and IL-1β, thereby improving myelin damage and neurological deficits in pMCAO rats. These beneficial effects of EA were abolished by the Nrf2 inhibitor luteolin. Conclusion Inactivation of the Nrf2/HO-1 axis and excessive activation of reactive AS accompanied by pro-inflammatory cytokine release may be critical contributors to ischemic WMI. EA may exert therapeutic effects by activating the Nrf2/HO-1 axis, inhibiting excessive AS activation, and inducing the release of inflammatory cytokines.
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