scholarly journals Adjunction of the Lipase Inhibitor Orlistat Improves Grape Seed Extract Neuroprotection against Brain Ischemia/Reperfusion Injury in Rats

2021 ◽  
Vol 55 (2) ◽  
pp. 527-543
Author(s):  
Slim Ghrir ◽  
Wassim Ben Abbes ◽  
Kamel Charradi ◽  
Salem Elkahoui ◽  
Ferid Limam ◽  
...  
2007 ◽  
Vol 22 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Özer Şehirli ◽  
Yahya Ozel ◽  
Ender Dulundu ◽  
Umit Topaloglu ◽  
Feriha Ercan ◽  
...  

2016 ◽  
Vol 94 (7) ◽  
pp. 719-727 ◽  
Author(s):  
Hussein F. Sakr ◽  
Amr M. Abbas ◽  
Ismaeel Bin-Jaliah

In this study, we investigated the effects of grape seed extract (GSE) on the expression of osteopontin (OPN) and cyclooxygenase-2 (COX-2) in a rat model of spinal cord ischemia–reperfusion injury (SC-IRI). Fifty male rats were divided into 5 groups: control (CON); control + GSE (CON + GSE) (received GSE for 28 days); sham operated (Sham); IRI; and IRI + GSE. SC-IRI was induced by clamping the aorta just above the bifurcation for 45 min, and then the clamp was released for 48 h for reperfusion. IRI + GSE group received GSE for 28 days before SC-IRI. Sensory, motor, and placing/stepping reflex assessment was performed. Prostaglandin E2 (PGE2), thiobarbituric acid reactive substances (TBARs), and total antioxidant capacity (TAC) were measured in spinal cord homogenate. Immunohistochemical examination of the spinal cord for OPN and COX-2 were carried out. SC-IRI resulted in significant increase in plasma nitrite/nitrate level and spinal cord homogenate levels of TBARs and PGE2, and OPN and COX-2 expression with significant decrease in TAC. GSE improves the sensory and motor functions through decreasing OPN and COX-2 expression with reduction of oxidative stress parameters. We conclude a neuroprotective effect of GSE in SC-IRI through downregulating COX-2 and OPN expression plus its antioxidants effects.


2016 ◽  
Vol 31 (3) ◽  
pp. 183-189
Author(s):  
Tuğrul Çakır ◽  
Arif Aslaner ◽  
Seçkin Özgür Tekeli ◽  
Kasım Güneş ◽  
Erdem Kinaci ◽  
...  

Molecules ◽  
2015 ◽  
Vol 20 (8) ◽  
pp. 14487-14503 ◽  
Author(s):  
Denis Silachev ◽  
Egor Plotnikov ◽  
Ljubava Zorova ◽  
Irina Pevzner ◽  
Natalia Sumbatyan ◽  
...  

2020 ◽  
Vol 121 (12) ◽  
pp. 858-863
Author(s):  
E. Arslan ◽  
M. O. Biyik ◽  
M. Kosucu ◽  
A. R. Guvercin ◽  
A. Bodur ◽  
...  

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Shuai Yang ◽  
Bin Hu ◽  
Zongming Wang ◽  
Changming Zhang ◽  
Haosen Jiao ◽  
...  

Abstract Activation of the cannabinoid CB1 receptor induces neuroprotection against brain ischemia/reperfusion injury (IRI); however, the mechanism is still unknown. In this study, we used oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in neuronal cells and middle cerebral artery occlusion (MCAO)-induced brain IRI in rats to mimic ischemic brain injury, and hypothesized that the CB1 receptor agonist arachidonyl-2-chloroethylamide (ACEA) would protect ischemic neurons by inhibiting mitochondrial fission via dynamin-related protein 1 (Drp1). We found that OGD/R injury reduced cell viability and mitochondrial function, increased lactate dehydrogenase (LDH) release, and increased cell apoptosis, and mitochondrial fission. Notably, ACEA significantly abolished the OGD/R-induced neuronal injuries described above. Similarly, ACEA significantly reversed MCAO-induced increases in brain infarct volume, neuronal apoptosis and mitochondrial fission, leading to the recovery of neurological functions. The neuroprotective effects of ACEA were obviously blocked by coadministration of the CB1 receptor antagonist AM251 or by the upregulation of Drp1 expression, indicating that ACEA alleviates brain IRI via the CB1–Drp1 pathway. Our findings suggest that the CB1 receptor links aberrant mitochondrial fission to brain IRI, providing a new therapeutic target for brain IRI treatment.


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