Apigenin inhibits the production of NO and PGE2 in microglia and inhibits neuronal cell death in a middle cerebral artery occlusion-induced focal ischemia mice model

2008 ◽  
Vol 52 (4-5) ◽  
pp. 878-886 ◽  
Author(s):  
Sang Keun Ha ◽  
Pyeongjae Lee ◽  
Jeong A Park ◽  
Hye Rim Oh ◽  
Sang Yeon Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Focal Ischemia ◽  
Artery Occlusion ◽  
Mice Model ◽  
Cerebral Artery Occlusion

Acupuncture attenuates neuronal cell death in middle cerebral artery occlusion model of focal ischemia

2010 ◽  
Vol 32 (sup1) ◽  
pp. 84-87 ◽  
Author(s):  
Kyoung Ah Kang ◽  
Eun Sim Shin ◽  
Jinyoung Hur ◽  
Mohmmad Rakibul Hasan ◽  
Hyejung Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Focal Ischemia ◽  
Artery Occlusion ◽  
Occlusion Model ◽  
Cerebral Artery Occlusion

scholarly journals Quercetin attenuates the reduction of parvalbumin in middle cerebral artery occlusion animal model

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Dong-Ju Park ◽  
Ju-Bin Kang ◽  
Fawad-Ali Shah ◽  
Phil-Ok Koh
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Male Rats ◽  
Neurological Deficits ◽  
Glutamate Toxicity ◽  
Cerebral Artery Occlusion

Abstract Background Calcium is a critical factor involved in modulation of essential cellular functions. Parvalbumin is a calcium buffering protein that regulates intracellular calcium concentrations. It prevents rises in calcium concentrations and inhibits apoptotic processes during ischemic injury. Quercetin exerts potent antioxidant and anti-apoptotic effects during brain ischemia. We investigated whether quercetin can regulate parvalbumin expression in cerebral ischemia and glutamate toxicity-induced neuronal cell death. Adult male rats were treated with vehicle or quercetin (10 mg/kg) 30 min prior to middle cerebral artery occlusion (MCAO) and cerebral cortical tissues were collected 24 h after MCAO. We used various techniques including Western blot, reverse transcription-PCR, and immunohistochemical staining to elucidate the changes of parvalbumin expression. Results Quercetin ameliorated MCAO-induced neurological deficits and behavioral changes. Moreover, quercetin prevented MCAO-induced a decrease in parvalbumin expression. Conclusions These findings suggest that quercetin exerts a neuroprotective effect through regulation of parvalbumin expression.

scholarly journals Transient Focal Ischemia Induces Extensive Temporal Changes in Rat Cerebral MicroRNAome

2009 ◽  
Vol 29 (4) ◽  
pp. 675-687 ◽  
Author(s):  
Ashuthosh Dharap ◽  
Kellie Bowen ◽  
Robert Place ◽  
Long-Cheng Li ◽  
Raghu Vemuganti
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Noncoding Rna ◽  
Critical Role ◽  
In Silico Analysis ◽  
Focal Ischemia ◽  
Artery Occlusion ◽  
Mirna Biogenesis ◽  
Cerebral Artery Occlusion

MicroRNAs (miRNAs) are ∼22 nucleotides long, noncoding RNAs that control cellular function by either degrading mRNAs or arresting their translation. To understand their functional significance in ischemic pathophysiology, we profiled miRNAs in adult rat brain as a function of reperfusion time after transient middle cerebral artery occlusion. Of the 238 miRNAs evaluated, 8 showed increased and 12 showed decreased expression at least at 4 out of 5 reperfusion time points studied between 3 h and 3 days compared with sham. Of those, 17 showed > 5 fold change. Bioinformatics analysis indicated a correlation between miRNAs altered to several mRNAs known to mediate inflammation, transcription, neuroprotection, receptors function, and ionic homeostasis. Antagomir-mediated prevention of mir-145 expression led to an increased protein expression of its downstream target superoxide dismutase-2 in the postischemic brain. In silico analysis showed sequence complementarity of eight miRNAs induced after focal ischemia to 877 promoters indicating the possibility of noncoding RNA-induced activation of gene expression. The mRNA expression of the RNases Drosha and Dicer, cofactor Pasha, and the pre-miRNA transporter exportin-5, which modulate miRNA biogenesis, were not altered after transient middle cerebral artery occlusion. Thus, the present studies indicate a critical role of miRNAs in controlling mRNA transcription and translation in the postischemic brain.

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