Estrogen and propofol combination therapy inhibits endoplasmic reticulum stress and remarkably attenuates cerebral ischemia-reperfusion injury and OGD injury in hippocampus

Xu, Feng; Ma, Rongji; Zhang, Guixing; Wang, Sheng; Yin, Jiangwen; Wang, Erqiang; Xiong, Erfeng; Zhang, Qingtong; Li, Yan

doi:10.1016/j.biopha.2018.09.167

Cited by 49 publications

(23 citation statements)

References 54 publications

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“…2 Currently, the main clinical regimen for ischemic stroke depends on re-perfusing the ischemic area via drugs or early thrombolysis, thereby restoring oxygen and glucose supply, 3 which therefore gives rise to ischemic-reperfusion (I/R) injury. 4 Cerebral I/R injury is known as brain tissue deterioration as a result of ischemia, which simultaneously reverses the cerebral blood flow in patients with acute ischemic stroke following mechanical or chemical therapies. 5 Natural compounds with the functions of anti-inflammation, anti-oxidation, anti-apoptosis and calcium antagonization, as well as neurofunctional modulation, present either preventive or therapeutic roles on cerebral I/R injury.…”

Section: Introductionmentioning

confidence: 99%

Protective Role of Astrocyte-Derived Exosomal microRNA-361 in Cerebral Ischemic-Reperfusion Injury by Regulating the AMPK/mTOR Signaling Pathway and Targeting CTSB

Dong

Wang

et al. 2020

NDT

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Background: Evidence has shown that microRNAs (miRNAs) are implicated in ischemic diseases. Therefore, the aim of the present study was to identify the functions of astrocyte (ATC)-derived exosomal miR-361 on cerebral ischemic-reperfusion (I/R) injury. Methods: A rat model of cerebral I/R injury was initially established, followed by injection of ATC-derived exosomes. Next, the protective function of ATC-derived exosomes in rats with cerebral I/R injury was evaluated, and then the effect of miR-361 on rats with cerebral I/R injury was evaluated by changing miR-361 expression in exosomes. PC12 cells that underwent oxygenglucose deprivation/reoxygenation were used to simulate I/R in vitro. The effect of ATC-derived exosomal miR-361 on the viability and apoptosis of OGD/R-treated PC12 cells was also assessed. The bioinformatic analysis predicted the targeted gene of miR-361. Results: It was found that I/R was damaging to the brain nerves of rats, while ATC-derived exosomal miR-361 relieved nerve damage caused by I/R. Furthermore, the in vitro experiments demonstrated that ATC-derived exosomal miR-361 increased OGD/R-inhibited PC12 cell activity and suppressed cell apoptosis. Bioinformatics predicted that miR-361 targeted cathepsin B (CTSB). CTSB upregulation blocked the protective roles of miR-361. In addition, miR-361 was found to downregulate the AMPK/mTOR signaling pathway by targeting CTSB. Conclusion: The present study demonstrated that ATC-derived exosomal miR-361 alleviates nerve damage in rats with cerebral I/R injury by targeting CTSB and downregulating the AMPK/mTOR pathway. This may offer novel insights into treatment for I/R injury.

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Section: Introductionmentioning

confidence: 99%

Protective Role of Astrocyte-Derived Exosomal microRNA-361 in Cerebral Ischemic-Reperfusion Injury by Regulating the AMPK/mTOR Signaling Pathway and Targeting CTSB

Dong

Wang

et al. 2020

NDT

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“…Free radical NO plays a key role in the pathophysiology of cerebral ischemia. It was found in the primarily cultured nerve cells that NO could reduce the content of calcium ions in the ER and promote CHOP gene transcription (27). Our study indicates the possibility of future clinic treatment in IRI, but its safety, side effect now attracts little concern.…”

Section: Discussionmentioning

confidence: 61%

Protective effect of hydrogen against ischemia-reperfusion induced spinal nerve cell apoptosis

Sun¹,

Shi²,

Yuan³

et al. 2021

Preprint

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Background: This study aims to explore the protective effect of hydrogen against oxygen-glucose-serum deprivation/restoration (OGSD/R)-induced PC12 cell apoptosis in vitro and the possible underlying mechanism. Methods: A normal control (NC) group was set where PC12 cells were cultured normal, while a positive control (PC) group, where PC12 cells were exposed to OGSD 12h/R1h without intervention, and a hydrogen intervention (HI) group, where PC12 cells were exposed to OGSD 12h/R1h plus HI, were conducted at the same time. At OGSD 12h/R 1h, cells were DAPI stained to detect viability and changes in the expression of apoptosis-associated proteins caspase-3, caspase-12 and CHOP/GADD153, and the endoplasmic reticulum-related signaling pathway protein PERK-eIF2α-ATF4. At the same time, the effect of HI was observed. Results: The result revealed that compared with NC group, cell apoptosis was more severe and cell viability was reduced significantly in PC group, while cell apoptosis was ameliorated and cell viability was increased significantly in HI as compared with PC group. In addition, the content of caspase-3 and caspase-12 in HI group was decreased significantly as compared with that in PC group. During this process, the endoplasmic reticulum-related signaling pathway protein PERK-eIF2α-ATF4 was activated. In HI group, the expression of this protein was decreased and cell viability was increased significantly as compared with those in PC group. Conclusions: Hydrogen was able to inhibit OGSD/R-induced PC12 cell apoptosis and exert a protective effect against ischemia-repurfusion injury (IRI) to nerve cells, probably through inhibiting the endoplasmic reticulum-related signaling pathway protein.

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“…When blood recanalization occurs after cerebral ischaemia, the reperfusion brain injury caused by intracellular Ca2 + overload, 39 damage of free radicals and inflammatory cytokines, 40 neurotoxic effects of excitatory amino acids, 41 disorder of water electrolyte and other factors 42 . These factors interact and eventually lead to severe oedema, necrosis and apoptosis of vertebral neuronal cells.…”

Section: Discussionmentioning

confidence: 99%

Isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway

Zhang

Yin

et al. 2021

J Cellular Molecular Medi

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The mechanisms of brain protection during ischaemic reperfusion injury induced by isoflurane (ISO) post‐conditioning are unclear. Myocyte enhancement factor 2 (MEF2D) has been shown to promote neural survival in a variety of models, in which multiple survival and death signals converge on MEF2D and modulate its activity. Here, we investigated the effect of MEF2D on the neuroprotective effects of ISO post‐conditioning on rats after cerebral ischaemia/reperfusion (I/R) injury. Rats underwent middle cerebral artery occlusion (MCAO) surgery with ischaemia for 90 minutes and reperfusion for 24‐48 hours. After MCAO, neurological status was assessed at 12, 24 and 48 hours by the Modified Neurological Severity Score (mNSS) test. The passive avoidance test (PAT) was used to assess cognition function. Histological and neuropathological evaluations were performed with HE staining and Nissl's staining, respectively. We measured the expression of MEF2D, ERK5, GFAP and caspase‐3 by immunofluorescent staining and Western blotting, and TUNEL staining to assess the severity of apoptosis in hippocampal CA1 area. We found that MEF2D was involved in nerve protection after I/R injury, and post‐treatment of ISO significantly promoted the phosphorylation of ERK5, increased MEF2D transcriptional activity, inhibited the expression of caspase‐3 and played a role of brain protection.

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Estrogen and propofol combination therapy inhibits endoplasmic reticulum stress and remarkably attenuates cerebral ischemia-reperfusion injury and OGD injury in hippocampus

Cited by 49 publications

References 54 publications

<p>Protective Role of Astrocyte-Derived Exosomal <em>microRNA-361</em> in Cerebral Ischemic-Reperfusion Injury by Regulating the <em>AMPK/mTOR</em> Signaling Pathway and Targeting <em>CTSB</em></p>

<p>Protective Role of Astrocyte-Derived Exosomal <em>microRNA-361</em> in Cerebral Ischemic-Reperfusion Injury by Regulating the <em>AMPK/mTOR</em> Signaling Pathway and Targeting <em>CTSB</em></p>

Protective effect of hydrogen against ischemia-reperfusion induced spinal nerve cell apoptosis

Isoflurane post‐conditioning contributes to anti‐apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway

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