Human neutrophils ROS inhibition and protective effects of Myrtus communis leaves essential oils against intestinal ischemia/reperfusion injury

The aim of the present work was to investigate the mechanism implicated in the protective effects ofMyrtus communisleaves essential oils (MCEO) on human neutrophils reactive oxygen species (ROS) production.

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Protective effects of ascorbic acid pretreatment in a rat model of intestinal ischemia-reperfusion injury: a histomorphometric study

Clinics ◽

10.1590/s1807-59322007000300017 ◽

2007 ◽

Vol 62 (3) ◽

pp. 315-320 ◽

Cited By ~ 20

Author(s):

Oscar Haruo Higa ◽

Edwin Roger Parra ◽

Alexandre Muxfeldt Ab'Saber ◽

Cecilia Farhat ◽

Rita Higa ◽

...

Keyword(s):

Ascorbic Acid ◽

Reperfusion Injury ◽

Rat Model ◽

Intestinal Ischemia ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Protective Effects ◽

Acid Pretreatment ◽

Histomorphometric Study ◽

Intestinal Ischemia Reperfusion

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Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3β/Nrf2 Pathway in Mice

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/6954764 ◽

2020 ◽

Vol 2020 ◽

pp. 1-14 ◽

Cited By ~ 3

Author(s):

Rong Chen ◽

Yun-yan Zhang ◽

Jia-nan Lan ◽

Hui-min Liu ◽

Wei Li ◽

...

Keyword(s):

Oxidative Stress ◽

Intestinal Ischemia ◽

Nuclear Translocation ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Ischemic Postconditioning ◽

Intestinal Barrier Function ◽

Protective Effects ◽

Nrf2 Pathway ◽

Intestinal Ischemia Reperfusion

Aims. Ischemic postconditioning (IPO) has a strong protective effect against intestinal ischemia-reperfusion (IIR) injury that is partly related to autophagy. However, the precise mechanisms involved are unknown. Methods. C57BL/6J mice were subjected to unilateral IIR with or without IPO. After 45 min ischemia and 120 min reperfusion, intestinal tissues and blood were collected for examination. HE staining and Chiu’s score were used to evaluate pathologic injury. We test markers of intestinal barrier function and oxidative stress. Finally, we used WB to detect the expression of key proteins of autophagy and the Akt/GSK-3β/Nrf2 pathway. Results. IPO significantly attenuated IIR injury. Expression levels of LC3 II/I, Beclin-1, and p62 were altered during IIR, indicating that IPO enhanced autophagy. IPO also activated Akt, inhibited GSK-3β, induced Nrf2 nuclear translocation, and upregulated HO-1 and NQO1 expression, thus providing protective effects against IIR injury by suppressing oxidative stress. Consistently, the beneficial effects of IPO were abolished by pretreatment with 3-methyladenine, SC66, and brusatol, potent inhibitors of autophagy, Akt, and Nrf2, respectively. Conclusion. Our study indicates that IPO can ameliorate IIR injury by evoking autophagy, activating Akt, inactivating GSK-3β, and activating Nrf2. These findings may provide novel insights for the alleviation of IIR injury.

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