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Source: Experimental Neurology
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Total 393 results found since Jan 2013.
TSPO exacerbates acute cerebral ischemia/reperfusion injury by inducing autophagy dysfunction
Exp Neurol. 2023 Sep 15:114542. doi: 10.1016/j.expneurol.2023.114542. Online ahead of print.ABSTRACTAutophagy is considered a double-edged sword, with a role in the regulation of the pathophysiological processes of the central nervous system (CNS) after cerebral ischemia-reperfusion injury (CIRI). The 18-kDa translocator protein (TSPO) is a highly conserved protein, with its expression level in the nervous system closely associated with the regulation of pathophysiological processes. In addition, the ligand of TSPO reduces neuroinflammation in brain diseases, but the potential role of TSPO in CIRI is largely undiscovered. ...
Source: Experimental Neurology - September 17, 2023 Category: Neurology Authors: Yusufu Mahemuti Kaheerman Kadeer Riqing Su Abudureheman Abula Yirizhati Aili Aierpati Maimaiti Subinuer Abulaiti Maimaitiyasheng Maimaitituerxun Tong Miao Shihao Jiang Aximujiang Axier Maimaitili Aisha Yongxin Wang Xiaojiang Cheng Source Type: research
Rhein attenuates cerebral ischemia-reperfusion injury via inhibition of ferroptosis through NRF2/SLC7A11/GPX4 pathway
CONCLUSION: Rhein attenuates cerebral I/R injury by inhibiting ferroptosis via the NRF2/SLC7A11/GPX4 axis, highlighting its potential as a therapeutic agent for ischemic stroke.PMID:37714424 | DOI:10.1016/j.expneurol.2023.114541
Source: Experimental Neurology - September 15, 2023 Category: Neurology Authors: Hua Liu Tian-Ai Zhang Wen-Yue Zhang Si-Rui Huang Yue Hu Jia Sun Source Type: research
MCPIP-1 knockdown enhances endothelial colony-forming cell angiogenesis via the TFRC/AKT/mTOR signaling pathway in the ischemic penumbra of MCAO mice
In this study, we performed Proteome Profiler™ Human Angiogenesis Antibody arrays and tandem mass tag protein profiling to investigate the effect of MCPIP-1 on ECFCs. We demonstrated that MCPIP-1 knockdown enhanced the proliferation, migration, and in vivo and in vitro angiogenic capacity of ECFCs by upregulating the transferrin receptor-activated AKT/m-TOR signaling pathway to promote cellular trophic factor secretion. Furthermore, we found that the lateral ventricular transplantation of ECFCs with lentiviral MCPIP-1 knockdown into mice with middle cerebral artery occlusion increased serum vacular endothelial growth fac...
Source: Experimental Neurology - September 9, 2023 Category: Neurology Authors: Xiaoxiong Zou Yu Xie Zhongfei Zhang Zhiming Feng Jianbang Han Qian Ouyang Shiting Hua Sixian Huang Cong Li Zhizheng Liu Yingqian Cai Yuxi Zou Yanping Tang Haijia Chen Xiaodan Jiang Source Type: research
Phenothiazines reduced autophagy in ischemic stroke through endoplasmic reticulum (ER) stress-associated PERK-eIF2 α pathway
CONCLUSION: The combined treatment of C + P plays a crucial role in stroke therapy by inhibiting ER stress-mediated autophagy, thereby leading to reduced apoptosis and increased neuroprotection. Our findings highlight the PERK-eIF2α pathway as a central mechanism through which C + P exerts its beneficial effects. The results from this study may pave the way for the development of more targeted and effective treatments for stroke patients.PMID:37673390 | DOI:10.1016/j.expneurol.2023.114524
Source: Experimental Neurology - September 6, 2023 Category: Neurology Authors: Shuyu Lv Xiaokun Geng Ho Jun Yun Yuchuan Ding Source Type: research
Caveolin-1 aggravates neurological deficits by activating neuroinflammation following experimental intracerebral hemorrhage in rats
CONCLUSIONS: Our research revealed CAV1 aggravated neurological dysfunction in a rat ICH model. CAV1 knockdown exerted neuroprotective effect by suppressing microglia activation and neuroinflammation after ICH might via the C-Src/CAV1/IKK-β/NF-κB signaling pathway.PMID:37598879 | DOI:10.1016/j.expneurol.2023.114508
Source: Experimental Neurology - August 20, 2023 Category: Neurology Authors: Demao Cao Bing Li Cheng Cao Juyi Zhang Xiang Li Haiying Li Zhengquan Yu Haitao Shen Ming Ye Source Type: research
