Aim: To investigate the effect of interleukin-10 on neurocyte apoptosis in cerebral ischemia in rats.
Methods: 36 adult male Sprague-Dawley rats were randomly assigned into 3 groups: sham operation group, middle cerebral artery occlusion(MCAO) group and MCAO+interleukin-10 treatment group. Terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) staining was used to detect in situ cell apoptosis, immunohistochemical staining and RT-PCR were used to detect the expression of proapoptotic gene Fas, Fas ligand (FasL) and caspase-3 in peri-infarct, respectively.
Results: Cerebral ischemia significantly induced neurocyte apoptosis and upregulated the expression of Fas, FasL and caspase-3, repcetively (P<0.05). IL-10 treatment significantly inhibited neurocyte apoptosis, and suppressed the expression of proapoptotic gene FasL and caspase-3, repcetively (P<0.05), but had no obvious effect on Fas expression (P>0.05).
Conclusion: IL-10 can suppress neurocyte apoptosis in cerebral ischemia, whose mechanisms seemed related to inhibiting the expression of proapoptotic gene FasL and caspase-3.
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Fluids Barriers CNS
January 2025
Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital of Southern Medical University, Guangzhou, 510515, China.
Oxidative stress and neuronal apoptosis could be an important factor leading to post-hemorrhagic consequences after germinal matrix hemorrhage (GMH). Previously study have indicated that relaxin 2 receptor activation initiates anti-oxidative stress and anti-apoptosis in ischemia-reperfusion injury. However, whether relaxin 2 activation can attenuate oxidative stress and neuronal apoptosis after GMH remains unknown.
View Article and Find Full Text PDFJ Nanobiotechnology
January 2025
Department of Orthopedics, Zhuhai Medical College (Zhuhai People's Hospital), State Key Laboratory of Bioactive Molecules and Druggability Assessment, College of Chemistry and Materials Science, Jinan University, Zhuhai, 519000, China.
Spinal cord injury (SCI) is a critical condition affecting the central nervous system that often has permanent and debilitating consequences, including secondary injuries. Oxidative damage and inflammation are critical factors in secondary pathological processes. Selenium nanoparticles have demonstrated significant antioxidative and anti-inflammatory properties via a non-immunosuppressive pathway; however, their clinical application has been limited by their inadequate stability and functionality to cross the blood-spinal cord barrier (BSCB).
View Article and Find Full Text PDFPurpose: We aimed to investigate the role of gallic acid treatment on spinal cord tissues after spinal cord injury (SCI) and its relationship with endoplasmic reticulum (ER) stress by histochemical, immunohistochemical, and in-silico techniques.
Methods: Thirty female Wistar albino rats were divided into three groups: sham, SCI, and SCI+gallic acid. SCI was induced by dropping a 15-g weight onto the exposed T10-T11 spinal cord segment.
Adv Sci (Weinh)
January 2025
Frontiers Science Center for Deep Ocean Multispheres and Earth Systems, Key Laboratory of Marine Chemistry Theory and Technology, Ministry of Education/Sanya Oceanographic Institution, Ocean University of China, Qingdao/Sanya, 266003/572024, China.
The scarcity of effective neuroprotective agents and the presence of blood-brain barrier (BBB)-mediated extremely inefficient intracerebral drug delivery are predominant obstacles to the treatment of cerebral ischemic stroke (CIS). Herein, ROS-responsive borneol-based amphiphilic polymeric NPs are constructed by using traditional Chinese medicine borneol as functional blocks that served as surface brain-targeting ligand, inner hydrophobic core for efficient drug loading of membrane-permeable calcium chelator BAPTA-AM, and neuroprotective structural component. In MCAO mice, the nanoformulation (polymer: 3.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Neuroscience, Laboratory of Prion Neurobiology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.
There is no cure for Marinesco-Sjögren syndrome (MSS), a genetic multisystem disease linked to loss-of-function mutations in the SIL1 gene, encoding a BiP co-chaperone. Previously, we showed that the PERK kinase inhibitor GSK2606414 delays cerebellar Purkinje cell (PC) degeneration and the onset of ataxia in the woozy mouse model of MSS. However, GSK2606414 is toxic to the pancreas and does not completely rescue the woozy phenotype.
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