Reactive oxygen species (ROS) are continuously produced and eliminated by living organisms normally maintaining ROS at certain steady-state levels Under some circumstances, the balance between ROS generation and elimination is disturbed leading to enhanced ROS level called "oxidative stress" The primary goal of this review is to characterize two principal mechanisms of protection against oxidative stress - regulation of membrane permeability and antioxidant potential The ancillary goals of this work are to describe up to date knowledge on the regulation of the previously mentioned mechanisms and to identify areas of prospective research and emerging directions in investigation of adaptation to oxidative stress The ubiquity for challenges leading to oxidative stress development calls for identification of common mechanisms They are cysteine residues and [Fe,S]-clusters of specific regulatory proteins The latter mechanism is realized via SoxR bacterial protein, whereas the former mechanism is involved in operation of bacterial OxyR regulon, yeast H(2)O(2)-stimulon, plant NPR1/TGA and Rap24a systems, and animal Keap1/Nrf2, NF-κB and AP-1, and others Although hundreds of studies have been carried out in the field with different taxa, the comparative analysis of adaptive response is quite incomplete and therefore, this work aims to cover a plethora of phylogenetic groups to delineate common mechanisms In addition, this article raises some questions to be elucidated and points out future directions of this research The comparative approach is used to shed light on fundamental principles and mechanisms of regulation of antioxidant systems The idea is to provide starting points from which we can develop novel tools and hypothesis to facilitate meaningful investigations in the physiology and biochemistry of organismic response to oxidative stress

Adaptive response to oxidative stress: Bacteria, fungi, plants and animals.

Rosenroot (Rhodiola rosea): traditional use, chemical composition, pharmacology and clinical efficacy.

Neuroprotective effects of salidroside against beta-amyloid-induced oxidative stress in SH-SY5Y human neuroblastoma cells.

Protective activity of salidroside against ethanol-induced gastric ulcer via the MAPK/NF-κB pathway in vivo and in vitro

Salidroside attenuates beta amyloid-induced cognitive deficits via modulating oxidative stress and inflammatory mediators in rat hippocampus

Salidroside protects cardiomyocyte against hypoxia-induced death: A HIF-1α-activated and VEGF-mediated pathway

Cerebral ischemia results in loss of cerebral blood flow, which contributes to neuronal damage, neurocognitive impairment, as well as learning and memory difficulties. Although reperfusion is necessary to restore the blood supply to the brain, it also leads to several detrimental effects on the brain. The purpose of this study was to assess the effects of ulinastatin (UTI) on preventing focal cerebral ischemia/reperfusion‐induced injury (FCIRI). First, a rat model of FCIRI was established and treated with UTI. The effects of UTI on FCIRI in rats were evaluated using Morris water maze assay, triphenyl tetrazolium chloride staining, TUNEL, western blot assay, and enzyme‐linked immunosorbent assay analysis. UTI was found to improve the learning memory ability, reduce infarction area, inhibit apoptosis and decrease inflammation in FCIRI rats. Messenger RNA microarray analysis of hippocampal tissues revealed that suppressor of cytokine signalling‐1 (SOCS1) was the downstream target of UTI in FCIRI. SOCS1 depletion impaired the protective effect of UTI on FCIRI in rats. SOCS1 blocked the activation of the JAK2/STAT3 pathway. JAK2 inhibitor caused the JAK2/STAT3 pathway deficit, hence reversing the effect of sh‐SOCS1 on FCIRI in rats. Taken together, our results demonstrate that UTI alleviated FCIRI in rats, which was, to some extent, related to SOCS1‐mediated JAK2/STAT3 pathway.

Juan Zhang

Papers

Salidroside protects cardiomyocyte against hypoxia-induced death: A HIF-1α-activated and VEGF-mediated pathway

Ulinastatin affects focal cerebral ischemia–reperfusion injury via SOCS1‐mediated JAK2/STAT3 signalling pathway

Broadening horizons: The role of ferroptosis in myocardial ischemia-reperfusion injury.