Limb remote ischemic post-conditioning mitigates brain recovery in a mouse model of ischemic stroke by regulating reactive astrocytic plasticity

Cheng, Xue; Zhao, Haiping; Yan, Feng; Tao, Zhen; Wang, Rongliang; Han, Ziping; Li, Guangwen; Luo, Yumin; Ji, Xunming

doi:10.1016/j.brainres.2018.02.019

Cited by 19 publications

(40 citation statements)

References 27 publications

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“…Ischemic postconditioning (IPO) is defined as repetitive brief periods of ischemia followed by short intervals of reperfusion before the final restoration of blood flow [5]. IPO has been shown to have a strong protective effect against IR injury in the heart, brain, liver, kidney, and spi-nal cord [6][7][8]. Nevertheless, the identification of the mechanism related to the multiple and interacting components of this process requires further study.…”

Section: Introductionmentioning

confidence: 99%

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

Chen

Zhang

Lan

et al. 2020

Oxidative Medicine and Cellular Longevity

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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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Section: Introductionmentioning

confidence: 99%

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

Chen

Zhang

Lan

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…In contrast, as a non-invasive method, LIPOC shows obvious superiority by simply applying transient I/R on limb, not influencing operation procedures, and without extending the operation time. Although LIPOC has been demonstrated effective on protecting heart and brain from ischemic injury 34-36, there is limited information about its effects on liver protection. Prior to our study, there was no previous clinical data to demonstrate the efficacy of LIPOC or other remote lower limb ischemia-reperfusion on liver protection using both rat model and human pilot trial.…”

Section: Discussionmentioning

confidence: 99%

Hepatoprotective effects of limb ischemic post-conditioning in hepatic ischemic rat model and liver cancer patients via PI3K/ERK pathways

Gao¹,

Zhou²,

Wang³

et al. 2018

Int. J. Biol. Sci.

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The most effective way of treating liver cancer is surgical resection, which usually requires blocking the hepatic portal circulation, and may result in hepatic ischemia-reperfusion injury (HIRI). It is of paramount importance to control HIRI for liver cancer surgical resection. In this study, a 70% ischemia-reperfusion (I/R) model of rat liver was established, and the protective effect and mechanism of limb ischemic post-conditioning (LIPOC) on HIRI was investigated. We show that LIPOC has a protective effect on hepatic ischemia-reperfusion injury in rats, which reduces the elimination of superoxide dismutase, thereby increasing oxygen free radical scavenging, decreasing lipid peroxidation, inhibiting neutrophil aggregation, as well as reducing TNFα, IL1β, and other inflammatory cytokines. In addition, LIPOC inhibited the apoptosis of hepatocytes induced by I/R injury, and decreased the Bax/Bcl-2 ratio. Furthermore, LIPOC promoted the phosphorylation of Akt and ERK1/2. The use of PI3K inhibitor LY294002 and ERK1/2 blocker PD98059 inhibited the phosphorylation of Akt and ERK1/2 caused by LIPOC and abolished the injury protection of liver I/R. Moreover, through 16 cases of hepatocellular carcinoma resections, we found that short-term LIPOC treatment significantly suppressed the elevated alanine aminotransferase, aspartic transaminase, and total bilirubin in the early post-operation of liver resection, and reduced reperfusion injury to the ischemic liver. In summary, our study demonstrates that LIPOC could be an effective method for HIRI in the clinical implementation of liver resection and uncovers the potential mechanism of LIPOC in the protective effects of HIRI.

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“…Cheng et al reported that RIC could protect NVU by adjusting the proportion of astrocyte subtypes and weakening the activation of astrocytes in the brains of ischemic mice, thereby improving neurological function as well as reducing mortality, infarct area, and hemispheric swelling after ischemic stroke. 5 The evidences above give us reason to think that RIC can be effective in improving CBF by protecting NVU during ischemic stroke. The understanding of NVU highlights that attention should be shifted from neurons or blood vessels, respectively, to the whole NVU.…”

Section: Ric Can Protect the Neurovascular Unitmentioning

confidence: 99%

<p>Effects of Remote Ischemic Conditioning on Cerebral Hemodynamics in Ischemic Stroke</p>

Chen¹,

Yan²,

Jin³

et al. 2020

NDT

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Ischemic stroke is one of the most common cerebrovascular diseases and is the leading cause of disability all over the world. It is well known that cerebral blood flow (CBF) is disturbed or even disrupted when ischemic stroke happens. The imbalance between demand and shortage of blood supply makes ischemic stroke take place or worsen. The search for treatments that can preserve CBF, especially during the acute phase of ischemic stroke, has become a research hotspot. Animal and clinical experiments have proven that remote ischemic conditioning (RIC) is a beneficial therapeutic strategy for the treatment of ischemic stroke. However, the mechanism by which RIC affects CBF has not been fully understood. This review aims to discuss several possible mechanisms of RIC on the cerebral hemodynamics in ischemic stroke, such as the improvement of cardiac function and collateral circulation of cerebral vessels, the protection of neurovascular units, the formation of gas molecules, the effect on the function of vascular endothelial cells and the nervous system. RIC has the potential to become a therapeutic treatment to improve CBF in ischemic stroke. Future studies are needed to highlight our understanding of RIC as well as accelerate its clinical translation.

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Limb remote ischemic post-conditioning mitigates brain recovery in a mouse model of ischemic stroke by regulating reactive astrocytic plasticity

Cited by 19 publications

References 27 publications

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

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

Hepatoprotective effects of limb ischemic post-conditioning in hepatic ischemic rat model and liver cancer patients via PI3K/ERK pathways

<p>Effects of Remote Ischemic Conditioning on Cerebral Hemodynamics in Ischemic Stroke</p>

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