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通过p38MAPK-PGC-1α-PPARγ通路调节微质极化,缓解创伤性脑损伤

Hanjian Du¹, Jun Lai¹, Bo Lin¹

¹Department of Neurosurgery, Chongqing General Hospital, Chongqing University, Chongqing, 401147, China.

Cell biochemistry and biophysics

|December 17, 2024

概括

在创伤性脑损伤 (TBI) 后释放的Lipocalin 2 (LCN2) 促进神经元的存活,并通过激活关键途径来减少脑损伤. 沉默LCN2会使TBI的结果变得更糟,这表明它的保护作用.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

创伤性脑损伤 (TBI) 是一个重要的全球健康问题,具有重大的社会和家庭影响.
利波卡林2 (LCN2) 是一种具有多种生物功能的分泌蛋白质.
在TBI病理生理学的背景下,LCN2的特定作用仍然不完全理解.

研究的目的:

调查LCN2在TBI中的作用.
阐明LCN2影响TBI结果的潜在分子机制.

主要方法:

建立TBI的老鼠模型.
使用腺关联病毒介导的shRNA对LCN2进行基因沉默.
评估神经严重程度 (mNSS),认知功能,脑组织病理,神经细胞存活率,神经营养因子,炎症性细胞因子,微质极化 (M1/M2) 和p38MAPK-PGC-1α-PPARγ信号通路.

主要成果:

在TBI大鼠大脑中,LCN2表达升高,与认知缺陷和脑损伤相关.
沉默LCN2加剧了神经系统缺陷,学习和记忆障碍,增加了大脑,恶化了组织病理,降低了神经元的存活率,并降低了神经营养因子表达.
LCN2沉默促进了M1微质极化和抑制了M2极化,同时也抑制了p38MAPK-PGC-1α-PPARγ通路.

结论:

创伤后神经元释放的LCN2通过激活p38MAPK-PGC-1α-PPARγ通路来发挥保护作用.
这种激活促进M2微质极化,增强神经营养因子的分泌,最终减轻二次脑损伤.
LCN2代表了治疗TBI的潜在治疗目标.

关键词:

在 LCN2 中, LCN2 是微质细胞的两极分化通过p38MAPK-PGC-1α-PPARγ通路进行检测.创伤性脑损伤是一种创伤性脑损伤.

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