Preconditioning of H 2 S inhalation protects against cerebral ischemia/reperfusion injury by induction of HSP70 through PI3K/Akt/Nrf2 pathway

Ji, Kangxiang; Xue, Long; Cheng, Jiwei; Bai, Yu

doi:10.1016/j.brainresbull.2015.12.007

Cited by 67 publications

(45 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the current study, this notion is supported by the observed substantial reduction in edema formation and VILI score compared to non-pretreated mice. These findings are in line with results from animal models of myocardial infarct injury [29] and hepatic [24], cardiac [30], cerebral [25], or retinal ischemia-reperfusion injury [20]. Here, H 2 S preconditioning clearly prevented organ injury.…”

Section: Discussionsupporting

confidence: 87%

“…These findings are in contrast to previously reported data. In a cerebral ischemia-reperfusion injury model, pretreatment with 40 ppm H 2 S for 8 h each day for 7 days reduced IL-6 and TNF-α cytokine release [25]. Similar results were found in a rat model of small intestine ischemia-reperfusion injury [21].…”

Section: Discussionsupporting

confidence: 53%

“…For instance, Ji et al . observed in a rat model of cerebral ischemia-reperfusion injury that malondialdehyd and 8-hydroxy-2'-deoxyguanosine readings, as markers for oxidative stress, were reduced due to H 2 S inhalation for 8 h per day on 7 days prior to ischemia-reperfusion [25]. Incubation of neuronal cells [32–34], H9c2 cardiomyoblasts [35,36], or kidney epithelial cells [37] with H 2 S prior to injurious treatment resulted in a marked decrease of ROS production, which was accompanied by cell protection.…”

Section: Discussionmentioning

confidence: 99%

“…Up to now, only in ischemia-reperfusion models, pre- or postconditioning with H 2 S have been described, resulting in protection from cardiac (reviewed in [19]), retinal [20], intestinal [21–23], hepatic [24], or neuronal insults [25]. However, virtually nothing is known about time-dependent effects of H 2 S treatment in lung injury.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Pre- and posttreatment with hydrogen sulfide prevents ventilator-induced lung injury by limiting inflammation and oxidation

et al. 2017

View full text Add to dashboard Cite

Although essential in critical care medicine, mechanical ventilation often results in ventilator-induced lung injury. Low concentrations of hydrogen sulfide have been proven to have anti-inflammatory and anti-oxidative effects in the lung. The aim of this study was to analyze the kinetic effects of pre- and posttreatment with hydrogen sulfide in order to prevent lung injury as well as inflammatory and oxidative stress upon mechanical ventilation. Mice were either non-ventilated or mechanically ventilated with a tidal volume of 12 ml/kg for 6 h. Pretreated mice inhaled hydrogen sulfide in low dose for 1, 3, or 5 h prior to mechanical ventilation. Posttreated mice were ventilated with air followed by ventilation with hydrogen sulfide in various combinations. In addition, mice were ventilated with air for 10 h, or with air for 5 h and subsequently with hydrogen sulfide for 5 h. Histology, interleukin-1β, neutrophil counts, and reactive oxygen species formation were examined in the lungs. Both pre-and posttreatment with hydrogen sulfide time-dependently reduced or even prevented edema formation, gross histological damage, neutrophil influx and reactive oxygen species production in the lung. These results were also observed in posttreatment, when the experimental time was extended and hydrogen sulfide administration started as late as after 5 h air ventilation. In conclusion, hydrogen sulfide exerts lung protection even when its application is limited to a short or delayed period. The observed lung protection is mediated by inhibition of inflammatory and oxidative signaling.

show abstract

Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Pre- and posttreatment with hydrogen sulfide prevents ventilator-induced lung injury by limiting inflammation and oxidation

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Aside from autophagy, other mechanisms may also be involved in the protective effect of H 2 S against cerebral ischemia/reperfusion injury. Preconditioning with H 2 S inhalation protects against cerebral ischemia/reperfusion injury by inducing HSP70 through the PI3K/Akt/Nrf2 pathway . In an in vitro study, it was found that the protective effects of H 2 S are mediated by thiosulfate, which exerts antiapoptotic effects via persulfidation of caspase‐3 .…”

Section: Discussionmentioning

confidence: 99%

Sodium hydrosulfide attenuates cerebral ischemia/reperfusion injury by suppressing overactivated autophagy in rats

et al. 2017

View full text Add to dashboard Cite

Ischemic stroke is a leading cause of death and disability worldwide, and autophagy may be involved in the pathological process of cerebral ischemia/reperfusion injury. Hydrogen sulfide (H2S) is an endogenous gasotransmitter with protective effects against multiple diseases. Here, we tested the effect of H2S on cerebral ischemia/reperfusion injury in rats. Sodium hydrosulfide (NaHS), an H2S donor, improved neurological function and reduced the size of the infarcts induced by transient middle cerebral artery occlusion (MCAO) followed by reperfusion in rats. NaHS treatment reduced the lactate dehydrogenase (LDH) activity in the serum (a marker of cellular membrane integrity) and the expression of cleaved caspase‐3 (a marker for apoptosis) in the brains of MCAO rats. We also found that autophagy was overactivated in the brains of MCAO rats, as indicated by an increased ratio of LC3 II to I, decreased expression of p62, and transmission electron microscope detection. NaHS treatment significantly inhibited the autophagic activity in the brains of MCAO rats. Furthermore, PC12 cells were subjected to oxygen–glucose deprivation/reoxygenation (OGD/R) to mimic MCAO in vitro. We found that NaHS treatment reduced cellular injury and suppressed overactivated autophagy induced by OGD/R in PC12 cells. An autophagy stimulator (rapamycin) eliminated the protective effect of NaHS against LDH release and caspase‐3 activity induced by OGD/R in PC12 cells. An autophagy inhibitor (3‐methyladenine, 3‐MA) also reduced the cellular injury induced by OGD/R in PC12 cells. In conclusion, the results indicate that overactivated autophagy accelerates cellular injury after MCAO in rats and that exogenous H2S attenuates cerebral ischemia/reperfusion injury via suppressing overactivated autophagy in rats.

show abstract

Heat shock protein 70: A promising therapeutic target for myocardial ischemia–reperfusion injury

Song

Zhong

Wang

2018

Journal Cellular Physiology

View full text Add to dashboard Cite

Acute myocardial infarction is a major cause of death worldwide. The most important therapy for limiting ischemic injury and infarct size is timely and efficient myocardial reperfusion treatment, which may instead induce cardiomyocyte necrosis due to myocardial ischemia-reperfusion (I/R) injury. Heat shock protein 70 (HSP70), a stress-inducible protein, is overexpressed during myocardial I/R. The induced HSP70 is shown to regulate several intracellular proteins (e.g., transcription factors, enzymes, and apoptosis-related proteins) and signaling pathways (e.g., c-Jun N-terminal kinase pathway and extracellular-signal-regulated kinase 1/2 pathway), forming a complicated network that contributes to reducing reactive oxygen species accumulation, improving calcium homeostasis, inhibiting cellular apoptosis, thereby enhancing the stress adaption of myocardium to I/R injury. In addition, the extracellular HSP70, which is released from injured cardiomyocytes during I/R, acts as a proinflammatory mediator that results in cell death, while the intracellular HSP70 exerts antiinflammatory effects by suppressing proinflammatory signaling pathways. Notably, HSP70 is induced and contributes to the cardioprotection in several types of preconditioning and postconditioning. Meanwhile, it is shown that the cardioprotective effectiveness of preconditioning-induced HSP70 (e.g., hyperthermia preconditioning-induced HSP70) can be impaired by certain pathological conditions, such as hyperlipidemia and hyperglycemia. Thus, we highlight the widespread cardioprotective involvement of HSP70 in preconditioning and postconditioning and elucidate how HSP70-mediated cardioprotection is impaired in these pathological conditions. Furthermore, several therapeutic potentials of HSP70 against myocardial I/R injury and potential directions for future studies are also provided in this review.

show abstract

Preconditioning of H 2 S inhalation protects against cerebral ischemia/reperfusion injury by induction of HSP70 through PI3K/Akt/Nrf2 pathway

Cited by 67 publications

References 26 publications

Pre- and posttreatment with hydrogen sulfide prevents ventilator-induced lung injury by limiting inflammation and oxidation

Pre- and posttreatment with hydrogen sulfide prevents ventilator-induced lung injury by limiting inflammation and oxidation

Sodium hydrosulfide attenuates cerebral ischemia/reperfusion injury by suppressing overactivated autophagy in rats

Heat shock protein 70: A promising therapeutic target for myocardial ischemia–reperfusion injury

Contact Info

Product

Resources

About