The protective role of oxymatrine on neuronal cell apoptosis in the hemorrhagic rat brain

2012 ◽  
Vol 143 (1) ◽  
pp. 228-235 ◽  
Author(s):  
Man Huang ◽  
Yue-Yu Hu ◽  
Xiao-Qiao Dong ◽  
Qiu-Ping Xu ◽  
Wen-Hua Yu ◽  
...  
Keyword(s):  
Rat Brain ◽  
Cell Apoptosis ◽  
Neuronal Cell ◽  
Protective Role

scholarly journals The protective role of (−)-epigallocatechin-3-gallate in thrombin-induced neuronal cell apoptosis and JNK-MAPK activation

Neuroreport ◽  
2015 ◽  
Vol 26 (7) ◽  
pp. 416-423 ◽  
Author(s):  
Qianqian He ◽  
Lei Bao ◽  
Jeffrey Zimering ◽  
Kun Zan ◽  
Zuohui Zhang ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Neuronal Cell ◽  
Protective Role ◽  
Mapk Activation

Overexpression of miR-431 attenuates hypoxia/reoxygenation-induced myocardial damage via autophagy-related 3

2020 ◽  
Author(s):  
Kang Zhou ◽  
Yan Xu ◽  
Qiong Wang ◽  
Lini Dong
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Myocardial Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Protective Role ◽  
Human Cardiomyocytes ◽  
Hypoxia Reoxygenation

Abstract Myocardial injury is still a serious condition damaging the public health. Clinically, myocardial injury often leads to cardiac dysfunction and, in severe cases, death. Reperfusion of the ischemic myocardial tissues can minimize acute myocardial infarction (AMI)-induced damage. MicroRNAs are commonly recognized in diverse diseases and are often involved in the development of myocardial ischemia/reperfusion injury. However, the role of miR-431 remains unclear in myocardial injury. In this study, we investigated the underlying mechanisms of miR-431 in the cell apoptosis and autophagy of human cardiomyocytes in hypoxia/reoxygenation (H/R). H/R treatment reduced cell viability, promoted cell apoptotic rate, and down-regulated the expression of miR-431 in human cardiomyocytes. The down-regulation of miR-431 by its inhibitor reduced cell viability and induced cell apoptosis in the human cardiomyocytes. Moreover, miR-431 down-regulated the expression of autophagy-related 3 (ATG3) via targeting the 3ʹ-untranslated region of ATG3. Up-regulated expression of ATG3 by pcDNA3.1-ATG3 reversed the protective role of the overexpression of miR-431 on cell viability and cell apoptosis in H/R-treated human cardiomyocytes. More importantly, H/R treatments promoted autophagy in the human cardiomyocytes, and this effect was greatly alleviated via miR-431-mimic transfection. Our results suggested that miR-431 overexpression attenuated the H/R-induced myocardial damage at least partly through regulating the expression of ATG3.

Protective Role of Gallic Acid on Sodium Fluoride Induced Oxidative Stress in Rat Brain

2012 ◽  
Vol 89 (1) ◽  
pp. 73-77 ◽  
Author(s):  
Seyed Fazel Nabavi ◽  
Solomon Habtemariam ◽  
Mahtab Jafari ◽  
Antoni Sureda ◽  
Seyed Mohammad Nabavi
Keyword(s):  
Oxidative Stress ◽  
Rat Brain ◽  
Gallic Acid ◽  
Sodium Fluoride ◽  
Protective Role

scholarly journals Regulation of the p75 Neurotrophin Receptor Attenuates Neuroinflammation and Stimulates Hippocampal Neurogenesis in Experimental Streptococcus Pneumoniae Meningitis

2021 ◽  
Author(s):  
Dandan Zhang ◽  
Shengnan Zhao ◽  
Zhijie Zhang ◽  
Danfeng Xu ◽  
Di Lian ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Streptococcus Pneumoniae ◽  
Cell Apoptosis ◽  
Neuronal Cell ◽  
Hippocampal Neurogenesis ◽  
Clinical Severity ◽  
Neurotrophin Receptor ◽  
Double Labeling

Abstract Background: Streptococcus pneumoniae meningitis is a destructive central nervous system (CNS) infection with acute and long-term neurological disorders. Compelling evidence provided by previous studies suggests that p75NTR signaling influences cell survival, apoptosis, and proliferation in brain-injured conditions. However, the role of p75NTR signaling in regulating pneumococcal meningitis (PM)-induced neuroinflammation and altered neurogenesis remains largely to be elucidated.Methods: p75NTR signaling activation in the pathological process of PM was assessed. During acute PM, a small-molecule p75NTR modulator LM11A-31 or vehicle was intranasally administered for 3 days prior to S.pneumoniae exposure. At 24h post-infection, clinical severity, histopathology, astrocytes/microglia activation, neuronal cell apoptosis and death, inflammation-related transcription factors and inflammatory factors were evaluated. Additionally, p75NTR was knocked down by the adenovirus-mediated short-hairpin RNA (shRNA) to ascertain the role of p75NTR in PM. During long-term PM, the intranasal administration of LM11A-31 or vehicle was continued for 7 days after successfully establishing the PM model. Hippocampal neurogenesis was evaluated by double-labeling immunofluorescence with EdU, DCX and NeuN. Results: Our results revealed that both 24h (acute) and 7,14,28day (long-term) groups of infected rats demonstrated increased p75NTR expression in the brain. During acute PM, modulation of p75NTR through pretreatment of PM model with LM11A-31 significantly alleviated S.pneumoniae-induced clinical severity, histopathological injury and the activation of astrocytes and microglia. LM11A-31 pretreatment also significantly ameliorated neuronal cell apoptosis and death. Moreover, we found that blocking p75NTR with LM11A-31 decreased the expression of inflammation-related transcription factors (NF-κBp65, C/EBPβ) and proinflammatory cytokine (IL-1β, TNF-α, IL-6 and iNOS) in the cortex and hippocampus. Furthermore, p75NTR knockdown induced significant changes in histopathology and inflammation-related transcription factors expression. Importantly, combined LM11A-31 adjuvant therapy significantly improved hippocampal neurogenesis.Conclusion: Our findings suggest that the p75NTR signaling plays an essential role in the pathogenesis of PM. Targeting p75NTR has benefit effects on PM rats by alleviating neuroinflammation and promoting hippocampal neurogenesis. Thus, the p75NTR signaling may be a potential therapeutic target to improve the outcome of PM.

scholarly journals Congestive heart failure induces endothelial cell apoptosis: protective role of carvedilol

2000 ◽  
Vol 36 (7) ◽  
pp. 2081-2089 ◽  
Author(s):  
Lothar Rössig ◽  
Judith Haendeler ◽  
Ziad Mallat ◽  
Benedicte Hugel ◽  
Jean-Marie Freyssinet ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Protective Role ◽  
Endothelial Cell Apoptosis

Protective Role of Cynodon dactylon in Ameliorating the Aluminium-Induced Neurotoxicity in Rat Brain Regions

2011 ◽  
Vol 144 (1-3) ◽  
pp. 843-853 ◽  
Author(s):  
Thangarajan Sumathi ◽  
Chandrasekar Shobana ◽  
Balasubramanian Rathina Kumari ◽  
Devarajulu Nisha Nandhini
Keyword(s):  
Rat Brain ◽  
Cynodon Dactylon ◽  
Brain Regions ◽  
Protective Role ◽  
Rat Brain Regions

Protective role of MnSOD and redox regulation of neuronal cell survival

2005 ◽  
Vol 59 (4) ◽  
pp. 197-203 ◽  
Author(s):  
T. Galeotti ◽  
G. Pani ◽  
C. Capone ◽  
B. Bedogni ◽  
S. Borrello ◽  
...  
Keyword(s):  
Cell Survival ◽  
Redox Regulation ◽  
Neuronal Cell ◽  
Protective Role
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