Emergency and Critical Care Center, Intensive Care Unit, Zhejiang Provincial People’s Hospital (Affiliated People’s Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Center for General Practice Medicine, Department of Nursing, Zhejiang Provincial People’s Hospital (Affiliated People’s Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Aging (Albany NY). 2023 Sep 11;15(17):9041-9058. doi: 10.18632/aging.205014.
Intracerebral hemorrhage (ICH) is a stroke subtype with high mortality and disability rate, and neuroinflammation is involved in secondary brain injury. Galectin-3 (Gal-3) is one of the scaffold proteins of Galectins. Studies have indicated that Gal-3 plays an important role in the physiological and pathological state of the nervous system. Here we focus on the role of Gal-3 in ICH, especially in neuroinflammation.
Injection of autologous blood into the right basal ganglia was used to simulate ICH injury, and the level of Gal-3 in brain was regulated by related means. The changes of Gal-3 were detected by western blot and immunofluorescence, the level of neuroinflammation by immunofluorescence staining and ELISA. Apoptosis and neuron loss were detected by TUNEL staining FJB staining and Nissl staining, and neurological deficits were judged by neurobehavioral tests.
The protein level of Gal-3 increased at 24 h after ICH. Downregulation of Gal-3 level can reduce the infiltration of M1-type microglia and peripheral inflammatory cells, thus alleviating post-ICH neuroinflammation, and reducing cell apoptosis and neuron loss in brain tissue. ICH-induced neurological damage was rescued. Meanwhile, the promotion in the expression level of Gal-3 increased neuroinflammatory activation and nerve cell death, aggravating ICH-induced brain injury.
This study proves that Gal-3 is involved in neuroinflammation and nerve damage after ICH. Gal-3 expression should not be encouraged early on to prevent neuroinflammation. which provides a new possibility for clinical treatment for ICH patients.
脑出血（ICH）是一种死亡率和致残率较高的中风类型，神经炎症参与了继发性脑损伤。半乳糖凝集素-3（Gal-3）是半乳糖凝集素的支架蛋白之一。研究表明，Gal-3 在神经系统的生理和病理状态中发挥着重要作用。在这里，我们重点关注 Gal-3 在 ICH 中的作用，特别是在神经炎症中的作用。
通过向右侧基底节注射自体血来模拟 ICH 损伤，并通过相关手段调节脑内 Gal-3 水平。通过 Western blot 和免疫荧光检测 Gal-3 的变化，通过免疫荧光染色和 ELISA 检测神经炎症水平。通过 TUNEL 染色、FJB 染色和尼氏染色检测细胞凋亡和神经元丢失，通过神经行为学测试判断神经功能缺损。
ICH 后 24 小时，Gal-3 蛋白水平升高。下调 Gal-3 水平可减少 M1 型小胶质细胞和外周炎性细胞的浸润，从而减轻 ICH 后的神经炎症，减少脑组织中的细胞凋亡和神经元丢失，减轻 ICH 引起的神经损伤。同时，Gal-3 表达水平的升高促进了神经炎症激活和神经细胞死亡，加重了 ICH 引起的脑损伤。
本研究证明 Gal-3 参与了 ICH 后的神经炎症和神经损伤。Gal-3 表达不应早期被鼓励，以防止神经炎症，这为 ICH 患者的临床治疗提供了新的可能性。
