Molecular mechanism of long-term neuroprotective effects of gradual flow restoration on cerebral ischemia reperfusion injury in MCAO rats

Zhang, Aiping; Zhang, Yingying; Liu, Ao-Fei; Wang, Kai; Li, Chen; Liu, Yun-e; Zhou, Jingbo; Lv, Jin; Jiang, Weijian

doi:10.1016/j.jstrokecerebrovasdis.2020.105041

Cited by 6 publications

(5 citation statements)

References 34 publications

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“…Therefore, it is extremely urgent to develop effective therapeutic drugs. As mentioned in previous reports, BA liposomes can improve nerve function defect, reduce infarct volume, and effectively improve CI reperfusion conditions (Zhang et al., 2020 ). Whilst the researchers are studying the mechanism evaluation, they are also devoting themselves to the development of new drug formulations for better neurotherapeutic effect.…”

Section: Discussionmentioning

confidence: 54%

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Preparation of baicalin-loaded ligand-modified nanoparticles for nose-to-brain delivery for neuroprotection in cerebral ischemia

et al. 2022

Drug Delivery

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Neuroprotection in cerebral ischemia (CI) has received increasing attention. However, efficient delivery of therapeutic agents to the brain remains a major challenge due to the complex environment of the brain. Nose-to-brain-based delivery is a promising approach. Here, we optimized a nanocarrier formulation of neuroprotective agents that can be used for nose-to-brain delivery by obtaining RVG29 peptide-modified polyethylene glycol–polylactic acid-co-glycolic acid nanoparticles (PEG–PLGA RNPs) that have physicochemical properties that lead to stable and sustained drug release and thereby improve the bioavailability of neuroprotective agents. The brain-targeting ability of PEG–PLGA RNPs administered through nasal inhalation was verified in a rat model of CI. It was found that delivery to the whole brain can be achieved with little delivery to the peripheral circulation. Baicalin (BA) was selected as the neuroprotective agent for delivery. After intranasal administration of BA–PEG–PLGA RNPs, the neurological dysfunction of rats with ischemic brain injury was significantly alleviated, the cerebral infarction area was reduced, and nerve trauma and swelling were relieved. Furthermore, it was demonstrated that the neuroprotective effects of BA in a rat model of CI may be mediated by inhibition of inflammation and alleviation of oxidative stress. The immunohistochemical results obtained after treatment with nanoparticles loaded with BA showed that Nrf2/HO-1 was activated in the area in which ischemic brain damage had occurred and that its expression was significantly higher in the group treated with BA–PEG–PLGA RNPs than in the other groups. The ELISA results showed that the levels of IL-1β, IL-6, and TNF-α were abnormally increased in the serum of rats with cerebral ischemia. After treatment with BA-loaded nanoparticles, IL-1β, IL-6, and TNF-α levels decreased significantly. Oxidative stress was alleviated; the levels of glutathione and superoxide dismutase increased; and the levels of reactive oxygen species and malondialdehyde decreased, in animals to which BA–PEG–PLGA RNPs were delivered by intranasal inhalation. In conclusion, BA–PEG–PLGA RNPs can effectively deliver BA to rats and thereby exert neuroprotective effects against CI.

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Section: Discussionmentioning

confidence: 54%

“…Neuroprotection has always been one of the key points in the treatment of ischemic stroke. However, the molecular mechanism involved in CI is complex, and the therapeutic effect may not be ideal (Zhang et al., 2020 ). Therefore, it is extremely urgent to develop effective therapeutic drugs.…”

Section: Discussionmentioning

confidence: 99%

Preparation of baicalin-loaded ligand-modified nanoparticles for nose-to-brain delivery for neuroprotection in cerebral ischemia

et al. 2022

Drug Delivery

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“…These rats were divided into two groups (sham and ischemia reperfusion group, six rats per group). The rats model of ischemia reperfusion was established according the referenced method [ 23 ]. The hearts of rats were collected and used for the subsequent experiments after the rats were killed.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of PLK1 relieved the myocardial ischemia-reperfusion injury of rats through inducing the mitophagy and regulating the p-AMPK/FUNDC1 axis

et al. 2021

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Myocardial cell injury caused by myocardial ischemia and reperfusion is one of the main causes of the occurrence and development of heart disease. Recent study has shown that inducing mitophagy of cardiomyocytes is a crucial method to alleviate ischemia-reperfusion injury. While, Polo-like kinase 1 (PLK1) can induce the mitophagy of breast cancer cells. Moreover, PLK1 was able to promote the expression of p-AMPK and FUNDC1, which are the protective factors for myocardium. Therefore, the mouse model of ischemia/reperfusion was established and the effect of PLK1 on ischemia reperfusion induced myocardial damage was investigated. The PLK1 was overexpressed in H9c2 cells and rat model of ischemia/reperfusion. Ischemia reperfusion inhibited the expression of PLK1. While overexpression of PLK1 relieved the myocardial infarction and myocardium apoptosis through inducing mitophagy in rats model of ischemia reperfusion. In vitro, the H9c2 cells overexpressing the PLK1 were treated with the hypoxia and reoxygenation and the apoptosis, survival rate and expression of mitophagy-related proteins of H9c2 cells were detected using the flow cytometry, CCK-8 assay and western blotting. The results reveled that overexpression of PLK1 alleviated the hypoxia and reoxygenation induced apoptosis of H9c2 cells and promoted the expression of mitophagy-related proteins. In addition, enhanced PLK1 expression promoted the expression of p-AMPK and FUNDC1 in H9c2 cells. However, the inhibition of FUNDC1 abolished the positive effect of PLK1 on H9c2 cells mentioned above. In conclusion, PLK1 alleviated the ischemia reperfusion induced myocardial damage by inducing the mitophagy in a p-AMPK/FUNDC1 signaling dependent pathway.

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“…18 The severity of stroke injury was assessed by behavioral examination of each rat 60 min after the onset of MCAo. Rats that did not demonstrate high-grade contralateral deficit (score of [10][11][12] were excluded from further study. All tests were conducted by an investigator who was blinded to the treatment groups at 60 min (during MCAo) and then on days 1, 2, 3, and 7 after MCAo.…”

Section: Behavioral Testsmentioning

confidence: 99%

“… 9 Activating inflammatory factors is a significant obstacle in the reperfusion process due to the disturbance of metabolic processes. 10 We questioned whether joint inhibition and inflammation resolution of both processes would be more neuroprotective than either on its own. The following small molecules were investigated: a) LAU-0901, a plate-let-activating factor receptor (PAFR) antagonist that blocks pro-inflammatory signaling, and b) aspirin-trig-gered Neuroprotectin D1 (AT-NPD1), which activates cell-survival pathways and exerts potent anti-inflammatory activity in the brain.…”

Section: Introductionmentioning

confidence: 99%

Synergistic Neuroprotection by a PAF Antagonist Plus a Docosanoid in Experimental Ischemic Stroke: Dose-Response and Therapeutic Window

Reid

Obenaus

Mukherjee

et al. 2022

Journal of Stroke and Cerebrovascular Diseases

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Molecular mechanism of long-term neuroprotective effects of gradual flow restoration on cerebral ischemia reperfusion injury in MCAO rats

Cited by 6 publications

References 34 publications

Preparation of baicalin-loaded ligand-modified nanoparticles for nose-to-brain delivery for neuroprotection in cerebral ischemia

Preparation of baicalin-loaded ligand-modified nanoparticles for nose-to-brain delivery for neuroprotection in cerebral ischemia

Overexpression of PLK1 relieved the myocardial ischemia-reperfusion injury of rats through inducing the mitophagy and regulating the p-AMPK/FUNDC1 axis

Synergistic Neuroprotection by a PAF Antagonist Plus a Docosanoid in Experimental Ischemic Stroke: Dose-Response and Therapeutic Window

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