scholarly journals Gingko bilobaextract (EGb 761) attenuates ischemic brain injury-induced reduction in Ca2+sensor protein hippocalcin

2012 ◽  
Vol 28 (3) ◽  
pp. 199 ◽  
Author(s):  
Phil-Ok Koh
2009 ◽  
Vol 37 (03) ◽  
pp. 547-555 ◽  
Author(s):  
Jae-Hyeon Cho ◽  
Jin-Hee Sung ◽  
Eun-Hae Cho ◽  
Chung-Kil Won ◽  
Hyo-Jong Lee ◽  
...  

EGb 761 is a standardized extract of Gingko biloba that exerts protective effects against ischemic brain injury. This study investigated whether EGb 761 modulates the neuroprotective effects through Akt and its downstream targets, Bad and FKHR. Adult male rats were treated with EGb 761 (100 mg/kg) or vehicle prior to middle cerebral artery occlusion (MCAO). Brains were collected 24 hours after MCAO and infarct volumes were analyzed. EGb 761 significantly reduced infarct volume. Potential activation was mearsured by phosphorylation of Akt at Ser473, Bad at Ser136, and FKHR at Ser256 using Western blot analysis. EGb 761 prevented the injury-induced decrease of pAkt and its down stream targets, pBad and pFKHR. Furthermore, EGb 761 prevented the injury-induced increase of cleaved caspase-3 levels. In conclusion, this study suggests that EGb 761 prevents cell death due to brain injury and that EGb 761 protection is affected by preventing the injury-induce decrease of Akt phosphorylation.


2009 ◽  
Vol 37 (05) ◽  
pp. 867-876 ◽  
Author(s):  
Phil-Ok Koh

A standardized extract of Gingko biloba, EGb 761, has been shown to exert a neuroprotective effect against permanent and transient focal cerebral ischemia. This study investigated whether EGb 761 modulates Bcl-2 family proteins in ischemic brain injury. Male adult rats were treated with EGb 761 (100 mg/kg) or vehicle prior to middle cerebral artery occlusion (MCAO), brain tissues were collected 24 hours after MCAO. EGb761 administration significantly decreased the number of TUNEL-positive cells in the cerebral cortex. Ischemic brain injury induced decrease of Bcl-2 and Bcl- X L levels. EGb 761 prevented not only the injury-induced decrease of Bcl-2 and Bcl- X L levels, but also the injury-induced increase of Bax. Moreover, in the presence of EGb 761, the interaction of Bad and Bcl- X L decreased compared to that of vehicle-treated animals. In addition, EGb 761 prevented the injury-induced increase of cleaved PARP. The finding suggests that EGb 761 prevents cell death against ischemic brain injury and EGb 761 neuroprotection is affected by preventing the injury-induced increase of Bad and Bcl- X L interaction.


2010 ◽  
Vol 38 (04) ◽  
pp. 727-734 ◽  
Author(s):  
Phil-Ok Koh

EGb 761 is an extract of Gingko biloba that exhibits neuroprotective effects against cerebral ischemia. The mammalian target of rapamycin (mTOR) is a critical downstream effector of Akt and a central regulator of ribosomal biogenesis and protein synthesis. We investigated whether EGb 761 regulates Akt downstream targets, including mTOR, p70S6 kinase, and S6 phosphorylation. Adult male rats were treated with vehicle or EGb 761 (100 mg/kg) prior to middle cerebral artery occlusion (MCAO). Brains were collected at 24 hours after MCAO and the cerebral cortex regions were examined. We previously showed that EGb 761 significantly reduces infarct volume and decreases the number of TUNEL-positive cells in the cerebral cortex. Ischemic brain injury induces a decrease in Akt up-stream target, PDK1 phosphorylation. The levels of phospho-mTOR, phospho-p70S6 kinase, and phospho-S6 are subsequently decreased in regions affected by ischemic injury. However, EGb 761 prevented injury-induced decreases in these protein levels. We confirmed that EGb 761 inhibits injury-induced decreases in the number of positive cells for phospho-p70S6 kinase and phospho-S6. The results of this study provide evidence that EGb 761 protects neuronal cells against ischemic brain injury by preventing injury-induced decreases in p70S6 kinase and S6 phosphorylation.


2012 ◽  
Vol 28 (2) ◽  
pp. 77 ◽  
Author(s):  
Jin-Hee Sung ◽  
Fawad-Ali Shah ◽  
Eun-Hae Cho ◽  
Sang-Ah Gim ◽  
Seong-Jun Jeon ◽  
...  

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