scholarly journals A Novel NGF Receptor Agonist B355252 Ameliorates Neuronal Loss and Inflammatory Responses in a Rat Model of Cerebral Ischemia

2021 ◽  
Vol Volume 14 ◽  
pp. 2363-2376
Author(s):  
Hao-Kuang Wang ◽  
Jui-Sheng Chen ◽  
Chien-Yu Hsu ◽  
Yu-Ting Su ◽  
Tzu-Ching Sung ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Rat Model ◽  
Receptor Agonist ◽  
Inflammatory Responses ◽  
Neuronal Loss ◽  
Ngf Receptor

L-theanine Administration Results in Neuroprotection and Prevents Glutamate Receptor Agonist-Mediated Injury in the Rat Model of Cerebral Ischemia-Reperfusion

2012 ◽  
Vol 27 (9) ◽  
pp. 1282-1287 ◽  
Author(s):  
Mavdzhuda Zukhurova ◽  
Maria Prosvirnina ◽  
Anastasia Daineko ◽  
Anna Simanenkova ◽  
Nikolay Petrishchev ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Glutamate Receptor ◽  
Rat Model ◽  
Receptor Agonist ◽  
Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion ◽  
Glutamate Receptor Agonist

Ephedrine attenuates cerebral ischemia/reperfusion injury in rats through NF-κB signaling pathway

2020 ◽  
pp. 096032712097545
Author(s):  
Chanhong Shi ◽  
Jianhong Li ◽  
Jianwei Li
Keyword(s):  
Cerebral Ischemia ◽  
Protein Expression ◽  
Reperfusion Injury ◽  
Rat Model ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Infarct Volume ◽  
Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

The inflammation and immune responses are critical in ischemic stroke and contribute to aggravated brain damage. Ephedrine was reported to play an important role in the control of inflammatory responses. This study was to investigate the repairing effects and potential mechanisms of ephedrine on cerebral ischemic injury in a rat model of focal cerebral ischemia. The rat model of cerebral ischemia/reperfusion injury was established using the middle cerebral artery occlusion (MCAO) method and then rats were treated with ephedrine (5 and 10 mg/kg) for 7 days. The neurobehavioral progression was assessed using the neurological scoring method. The pathology of brain tissue was evaluated by hematoxylin and eosin (H&E) staining. The infarct volume was examined by triphenyltetrazolium chloride (TTC) staining. The apoptosis in ischemic brain tissues was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA). Gene quantification and protein expression were detected by real-time PCR and western blot, respectively. Ephedrine treatment significantly alleviated the cerebral ischemia/reperfusion injury, evidenced by decreased neurological deficit score, infarct volume and water content. Ephedrine also decreased autophagy and apoptosis in brain tissues. Moreover, ephedrine treatment significantly reduced inflammatory responses, associating with decreasing the protein expression of p-NF-κB. These results demonstrated neuroprotective properties of ephedrine and highlighted it as a new potential anti-inflammatory agent against injury of cerebral ischemia/reperfusion.

Low doses of the selective adenosine A2A receptor agonist CGS21680 are protective in a rat model of transient cerebral ischemia

2014 ◽  
Vol 1551 ◽  
pp. 59-72 ◽  
Author(s):  
Alessia Melani ◽  
Francesca Corti ◽  
Lucrezia Cellai ◽  
Maria Giuliana Vannucchi ◽  
Felicita Pedata
Keyword(s):  
Cerebral Ischemia ◽  
Rat Model ◽  
Receptor Agonist ◽  
Adenosine A2a Receptor ◽  
Transient Cerebral Ischemia ◽  
Low Doses ◽  
A2a Receptor ◽  
Adenosine A2a

scholarly journals Effects of β-Adrenergic Blockade on Metabolic and Inflammatory Responses in a Rat Model of Ischemic Stroke

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1373 ◽  
Author(s):  
Shih-Yi Lin ◽  
Ya-Yu Wang ◽  
Cheng-Yi Chang ◽  
Chih-Cheng Wu ◽  
Wen-Ying Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Rat Model ◽  
Inflammatory Responses ◽  
Brain Infarction ◽  
Brain Inflammation ◽  
Adrenergic Blockade ◽  
Anti Inflammatory

Ischemic stroke provokes an inflammatory response concurrent with both sympathetic nervous system activation and hyperglycemia. Currently, their crosstalk and consequences in stroke outcomes are of clinical attraction. We have provided experimental evidence showing the suppressive effects of the nonselective β-adrenoreceptor antagonist propranolol on hyperglycemia, inflammation, and brain injury in a rat model experiencing cerebral ischemia. Pretreatment with propranolol protected against postischemic brain infarction, edema, and apoptosis. The neuroprotection caused by propranolol was accompanied by a reduction in fasting glucose, fasting insulin, glucose tolerance impairment, plasma C-reactive protein, plasma free fatty acids, plasma corticosterone, brain oxidative stress, and brain inflammation. Pretreatment with insulin alleviated—while glucose augmented—postischemic brain injury and inflammation. Additionally, the impairment of insulin signaling in the gastrocnemius muscles was noted in rats with cerebral ischemia, with propranolol improving the impairment by reducing oxidative stress and tumor necrosis factor-α signaling. The anti-inflammatory effects of propranolol were further demonstrated in isoproterenol-stimulated BV2 and RAW264.7 cells through its ability to decrease cytokine production. Despite their potential benefits, stroke-associated hyperglycemia and inflammation are commonly linked with harmful consequences. Our findings provide new insight into the anti-inflammatory, neuroprotective, and hypoglycemic mechanisms of propranolol in combating neurodegenerative diseases, such as stroke.

scholarly journals Therapeutics potentiating microglial p21-Nrf2 axis can rescue neurodegeneration caused by neuroinflammation

2020 ◽  
Vol 6 (46) ◽  
pp. eabc1428
Author(s):  
A. Nakano-Kobayashi ◽  
A. Fukumoto ◽  
A. Morizane ◽  
D. T. Nguyen ◽  
T. M. Le ◽  
...  
Keyword(s):  
Neurodegenerative Disorders ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Neuronal Survival ◽  
Disease Model ◽  
Neuronal Loss ◽  
Induced Pluripotent Stem Cell ◽  
Related Factor ◽  
Induced Pluripotent ◽  
Novel Therapeutic

Neurodegenerative disorders are caused by progressive neuronal loss, and there is no complete treatment available yet. Neuroinflammation is a common feature across neurodegenerative disorders and implicated in the progression of neurodegeneration. Dysregulated activation of microglia causes neuroinflammation and has been highlighted as a treatment target in therapeutic strategies. Here, we identified novel therapeutic candidate ALGERNON2 (altered generation of neurons 2) and demonstrate that ALGERNON2 suppressed the production of proinflammatory cytokines and rescued neurodegeneration in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)–induced Parkinson’s disease model. ALGERNON2 stabilized cyclinD1/p21 complex, leading to up-regulation of nuclear factor erythroid 2–related factor 2 (Nrf2), which contributes to antioxidative and anti-inflammatory responses. Notably, ALGERNON2 enhanced neuronal survival in other neuroinflammatory conditions such as the transplantation of induced pluripotent stem cell–derived dopaminergic neurons into murine brains. In conclusion, we present that the microglial potentiation of the p21-Nrf2 pathway can contribute to neuronal survival and provide novel therapeutic potential for neuroinflammation-triggered neurodegeneration.

scholarly journals Effects of Triflusal and Aspirin in a Rat Model of Cerebral Ischemia

Stroke ◽  
2007 ◽  
Vol 38 (2) ◽  
pp. 381-387 ◽  
Author(s):  
Shawn N. Whitehead ◽  
Nestor A. Bayona ◽  
Guanliang Cheng ◽  
Gary V. Allen ◽  
Vladimir C. Hachinski ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Rat Model
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