scholarly journals Ginkgo biloba extract (EGb 761) attenuates lung injury induced by intestinal ischemia/reperfusion in rats: Roles of oxidative stress and nitric oxide

2007 ◽  
Vol 13 (2) ◽  
pp. 299 ◽  
Author(s):  
Ke-Xuan Liu
Shock ◽  
2005 ◽  
Vol 23 (2) ◽  
pp. 150-155 ◽  
Author(s):  
Dan Waisman ◽  
Vera Brod ◽  
Ronit Dickstein ◽  
Amir Abramovich ◽  
Avi Rotschild ◽  
...  

2006 ◽  
Vol 26 (7-8) ◽  
pp. 1341-1351 ◽  
Author(s):  
A. Uríková ◽  
E. Babušíková ◽  
D. Dobrota ◽  
A. Drgová ◽  
P. Kaplán ◽  
...  

2016 ◽  
Vol 39 (6) ◽  
pp. 100 ◽  
Author(s):  
Duygu Aydin ◽  
Emine G G Peker ◽  
Meryem D Karakurt ◽  
Ayşe Gurel ◽  
Mustafa Ayyildiz ◽  
...  

Purpose: The purpose of this study was to evaluate the efficacy of Ginkgo biloba extract (EGb 761) on oxidative events of brain in cisplatin-administrated rats. Methods: Rats were divided into four experimental groups: 1) control (n=6); 2) cisplatin (8 mg/kg, intraperitoneally one dose, n=6); 3) EGb 761 (100 mg/kg intraperitoneally for 15 days, n=6); and 4) cisplatin + EGb 761 (n=6). After drug administration, rats were sacrificed and brain tissues were removed. Nitric oxide (NO), malondialdehyde (MDA) and glutathione (GSH) levels were evaluated in brain tissues. Results: Single dose cisplatin administration significantly increased NO and GSH levels, but decreased MDA levels in brain tissue samples. EGb 761 treatment reversed the effects of cisplatin on NO and GSH levels, but did not affect the decreased MDA levels. Conclusion: Results of the study indicate that oxidative stress can be an important pathogenetic mechanism of cisplatin-induced neurotoxicity. EGb 761, an standardized extract of G. biloba leaves that has antioxidant properties, may improve the oxidative stress-related neurological side effects of cisplatin.


2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Ying Jiang ◽  
Zhen Zhou ◽  
Qing-tao Meng ◽  
Qian Sun ◽  
Wating Su ◽  
...  

Objective. Intestinal ischemia reperfusion (II/R) injury plays a critical role in remote organ dysfunction, such as lung injury, which is associated with nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In the present study, we tested whether ginsenoside Rb1 attenuated II/R induced lung injury by Nrf2/HO-1 pathway.Methods. II/R injury was induced in male C57BL/6J mice by 45 min of superior mesenteric artery (SMA) occlusion followed by 2 hours of reperfusion. Ginsenoside Rb1 was administrated prior to reperfusion with or without ATRA (all-transretinoic acid, the inhibitor of Nrf2/ARE signaling pathway) administration before II/R.Results. II/R induced lung histological injury, which is accompanied with increased levels of malondialdehyde (MDA), interleukin- (IL-) 6, and tumor necrosis factor- (TNF-)αbut decreased levels of superoxide dismutase (SOD) and IL-10 in the lung tissues. Ginsenoside Rb1 reduced lung histological injury and the levels of TNF-αand MDA, as well as wet/dry weight ratio. Interestingly, the increased Nrf2 and HO-1 expression induced by II/R in the lung tissues was promoted by ginsenoside Rb1 treatment. All these changes could be inhibited or prevented by ATRA.Conclusion. Ginsenoside Rb1 is capable of ameliorating II/R induced lung injuries by activating Nrf2/HO-1 pathway.


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