scholarly journals Expression Pattern of Peroxisome Proliferator-Activated Receptors in Rat Hippocampus following Cerebral Ischemia and Reperfusion Injury

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Hong Wang ◽  
Rong Jiang ◽  
Qin He ◽  
Yunmei Zhang ◽  
Yanli Zhang ◽  
...  

The present study was designed to investigate the pattern of time-dependent expression of peroxisome proliferator-activated receptors (PPARα,β, andγ) after global cerebral ischemia and reperfusion (I/R) damage in the rat hippocampus. Male Sprague Dawley (SD) rats were subjected to global cerebral I/R. The rat hippocampi were isolated to detect the expression of PPARs mRNA and protein levels at 30 min–30 d after I/R by RT-PCR and Western blot analysis, respectively. The expression levels of PPARs mRNA and protein in the rat hippocampus significantly increased and peaked at 24 h for PPARαandγ(at 48 h for PPARβ) after I/R, then gradually decreased, and finally approached control levels on d 30. The present results suggest that global cerebral I/R can cause obvious increases of hippocampal PPARs mRNA and protein expression within 15 d after I/R. These findings may help to guide the experimental and clinical therapeutic use of PPARs agonists against brain injury.

2020 ◽  
Author(s):  
Lin Wang ◽  
Lijuan Zhang

Abstract Background: Barbaloin (BAR) is a bioactive anthracycline derived from the leaf exudates of aloe plants with a variety of biological and pharmacological properties. The present study was performed to investigate the neuroprotective effects of BAR against cerebral ischemia and reperfusion (I/R) injury in rats as well as the possible underlying mechanisms. Middle cerebral artery occlusion followed by reperfusion was used to induce cerebral I/R injury in rats, and BAR was administered intraperitoneally after the onset of ischemia. Results: We found that BAR remarkably improved neurological scores, reduced brain infarct volume, and inhibited neuronal apoptosis in cerebral I/R rats. Furthermore, BAR up-regulated Bcl-2 protein levels and down-regulated Bax, active caspase-3, and inducible nitric oxide synthase (iNOS) in ischemic cortex. I/R injury-induced increases in malondialdehyde content and decreases in glutathione peroxidase, glutathione, and superoxide dismutase activities were significantly attenuated by BAR administration. In vitro, BAR pretreatment inhibited the contents of proinflammatory cytokines (tumor necrosis factor-α, iNOS, and interleukin-6) and reduced protein levels of iNOS and nuclear expression of nuclear factor-κB p65 in lipopolysaccharide-stimulated BV-2 microglial cells. Conclusion: Taken together, our data suggest that BAR possesses neuroprotective effects against cerebral I/R injury through anti-oxidative, anti-apoptotic, and anti-inflammatory activities.


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