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Source: Free Radical Biology and Medicine
Procedure: Perfusion

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Total 2 results found since Jan 2013.

Endothelial deletion of mTORC1 protects against hindlimb ischemia in diabetic mice via activation of autophagy, attenuation of oxidative stress and alleviation of inflammation.
In conclusion, our present study demonstrates that endothelial mTORC1 deletion protects against hindlimb ischemic injury in diabetic mice possibly via activation of autophagy, attenuation of oxidative stress and alleviation of inflammation. Therapeutics targeting mTORC1 may therefore represents a promising strategy to rescue limb ischemia in diabetes mellitus. PMID: 28473248 [PubMed - as supplied by publisher]
Source: Free Radical Biology and Medicine - May 1, 2017 Category: Biology Authors: Fan W, Han D, Sun Z, Ma S, Gao L, Chen J, Li X, Li X, Fan M, Li C, Hu D, Wang Y, Cao F Tags: Free Radic Biol Med Source Type: research

Liraglutide protects cardiac microvascular endothelial cells against hypoxia/reoxygenation injury through the suppression of the SR-Ca(2+)-XO-ROS axis via activation of the GLP-1R/PI3K/Akt/Survivin pathways.
Abstract Microvascular endothelial cells (CMECs) oxidative damage resulting from hypoxia/reoxygenation (H/R) injury is responsible for microcirculation perfusion disturbances and the progression of cardiac dysfunction. However, few strategies are available to reverse such pathologies. Here, we studied the effects and mechanisms of liraglutide on CEMCs oxidative damage, focusing in particular on calcium overload-triggered free radical injury signals and the GLP-1R/PI3K/Akt/Survivin survival pathways. The results indicate that H/R increased IP3R expression but reduced SERCA2a expression, which rapidly raised intrace...
Source: Free Radical Biology and Medicine - March 29, 2016 Category: Biology Authors: Zhang Y, Zhou H, Wu W, Shi C, Hu S, Yin T, Ma Q, Han T, Zhang Y, Tian F, Chen Y Tags: Free Radic Biol Med Source Type: research