Erythropoietin protects propofol induced neuronal injury in developing rats by regulating TLR4/NF-κB signaling pathway abstract

Wang, Yuxia; Jin, Jin; Li, Kezhong

doi:10.1016/j.neulet.2019.134517

Cited by 15 publications

(14 citation statements)

References 34 publications

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“…The mechanisms of anesthetic neurotoxicity include excessive and abnormal activation of the N-methyl-D-aspartate (NMDA) and GABA-A receptors, 26 generation of free radicals, 27 activation of P75 growth factor, 28 inflammation, and excessive increase of Ca 2, 29 We considered using edaravone as a free radical scavenger to reduce anesthetic neurotoxicity. In cell proliferation, nestin is an intermediate neurofilament protein that can be used as a marker of neural stem cells for immunolocalization, indicating that neural stem cells are actively proliferating based on the incorporation of ki67.…”

Section: Discussionmentioning

confidence: 99%

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway

Yang¹,

Yi²,

Pan³

et al. 2021

DDDT

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Background: To investigate the neuroprotective effect of edaravone on excessive-dose propofol-induced neurotoxicity in the hippocampus of newborn rats and HT22 cells.Methods: Cell proliferation was investigated by assessing ki67 expression in the neural stem of the hippocampus of newborn rats and by cell counting kit-8 (CCK8) assay in HT22 cells. Cell apoptosis was assessed in vivo by caspase 3 detection in Western blots and measurement of apoptosis in neurons and glial cells by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Apoptosis was analyzed by flow cytometry in HT22 cells. The Morris water maze was used to evaluate the long-term learning and memory ability of rats. Inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA). The expression of mBDNF/TrkB/PI3K pathway-related proteins was detected by Western blot and quantitative reverse transcription-polymerase chain reaction (q-RT PCR). Results: In neonatal rat hippocampus and HT22 cells, edaravone increased cell proliferation and decreased cell apoptosis after excessive propofol-induced neurotoxicity. In addition, the levels of proinflammatory factors interleukin (IL)-6 and tumor necrosis factor (TNF)-α were reduced by edaravone pretreatment. The use of the tropomyosin receptor kinase B (TrkB) antagonist ANA-12 and TrkB agonist 7,8DHF with propofol groups showed that edaravone mitigated excessive propofol-induced neurotoxicity through the mature brain-derived neurotrophic factor (mBDNF)/TrkB/phosphoinositide 3-kinase (PI3K) pathway. However, the current dose of propofol did not significantly affect long-term learning and memory in rats. Conclusion: Edaravone pretreatment ameliorated propofol-induced proliferation inhibition, neuroapoptosis, and neural inflammation by activating the mBDNF/TrkB/PI3K pathway.

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Section: Discussionmentioning

confidence: 99%

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway

Yang¹,

Yi²,

Pan³

et al. 2021

DDDT

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“…There are emerging evidences for the neuroprotection effect of EPO both in vivo and in vitro [21,38,39]. The positive roles that EPO may play in APAC under higher dose, such as anti-apoptotic [12,13], anti-oxidant [14], and antiin ammatory [15,16] make it an ideal treatment in APAC. However, its role in angiogenesis, causing neovascularization is a dreaded occurrence in the eye [40].…”

Section: Discussionmentioning

confidence: 99%

“…However, there has been no research describing the changes of EPO and PDGF levels in APAC eyes. Recent studies have shown that both EPO and PDGF have neuroprotective functions such as anti-apoptotic [12,13], anti-oxidant [14] and anti-in ammatory properties [15,16]. Thus, the uctuations of their levels in aqueous humor may correlate with prognosis of trabeculectomy in APAC eyes.…”

Section: Introductionmentioning

confidence: 99%

Potential Effects of Angiogenesis-related Factors on the Severity of APAC and Surgical Outcomes of Trabeculectomy

Wang

Zhou

et al. 2020

Preprint

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Background. Acute primary angle closure (APAC) caused by an abrupt closure of trabecular meshwork can develop into angle closure glaucoma due to uncontrolled IOP. Under reduced oxygen tension, hypoxia inducible transcription factors will be accumulated. EPO (erythropoietin) and PDGF (platelet derived growth factor) families are thought to be associated with angiogenesis under hypoxic condition.Methods. Concentrations of EPO, PDGF-AA, -BB, -CC and -DD collected in aqueous humor samples were measured. Before operations, correlations between target proteins and IOP were detected between APAC (acute primary angle closure) and cataract patients. Based on the post-operative follow-up, the effects of EPO and PDGF family members on the successful rate of trabeculectomy were tested. Results. The levels of EPO, PDGF-CC and -DD were significantly elevated in the APAC group compared to the cataract group. During the post-operative follow-up, EPO, PDGF-CC and -DD showed significant differences between the success and failure groups. In multivariable linear regression analyses, failed filtration surgery was more likely in APAC eyes with higher EPO level. The Kaplan-Meier survival plot suggested that the success rate in eyes with low EPO level was significantly higher than that in eyes with high EPO level.Conclusion. The levels of EPO, PDGF-CC and -DD were significantly elevated in failure group. EPO level correlated with preoperative IOP and numbers of eyedrops, and higher EPO level in aqueous humor is a risk factor for trabeculectomy failure. It can be a biomarker to estimate the severity of APAC and the success rate of surgery. The investigation of mechanism of EPO in APAC a may have potential clinical applications for the surgical treatment of APAC.

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“…The IL-6 and TNFα ELISA kits were detected at 450nm from instructions. 6…”

Section: Enzyme-linked Immunosorbent Assay (Elisa) Of Pro-inflammatory Factors (Il-6 Tnfα)mentioning

confidence: 99%

Edaravone alleviated propofol‐induced neural injury in developing rats by BDNF/TrkB pathway

Yang

Pan

et al. 2021

J Cellular Molecular Medi

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As a variety of free radical scavenger, edaravone has shown its potential in producing antioxidant, anti‐inflammatory and neuroprotective effects in various disease models. However, the underlying mechanism behind the neuroprotective effects of edaravone remained unclear. This study is aimed at determining the effects of edaravone on neuroprotection and anti‐inflammatory through a propofol‐induced neural injury rat model. Firstly, an observation was made of apoptosis and neuroinflammation in the hippocampus of developing under the influence of propofol. It was found out that propofol could produce inflammatory effects in the hippocampus by enhancing the astrogliosis (GFAP) activation and elevating the level of neuronal nitric oxide synthase (nNOS), pro‐inflammatory cytokines interleukin‐6 (IL‐6) and tumour necrosis factor‐α (TNF‐α). Meanwhile, the increase of apoptosis cells and the decrease of neurons (NeuN) were speculated to aggravate neural injury. Furthermore, it was demonstrated that edaravone intervention can reverse the neural apoptosis and inflammation. Additionally, the intraperitoneal injection of edaravone, the intraperitoneal injection of the brain‐derived neurotrophic factor (BDNF)‐mimicking small compound (7,8 dihydroxyflavone) and the intracranial injection of the exogenous BDNF were all respectively effective in alleviating the propofol‐induced neural apoptosis and inflammation in the hippocampus. It was also found out that edaravone‐activated downstream signalling through tyrosine kinase receptor B (TrkB) receptors in astrocyte, microglia and neuron. However, the neural injury of propofol had no impact on long‐term learning and memory, except causing a short‐term neurotoxicity. In conclusion, edaravone could alleviate the propofol‐induced neural injury in developing rats through BDNF/TrkB pathway.

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Erythropoietin protects propofol induced neuronal injury in developing rats by regulating TLR4/NF-κB signaling pathway abstract

Cited by 15 publications

References 34 publications

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway

Potential Effects of Angiogenesis-related Factors on the Severity of APAC and Surgical Outcomes of Trabeculectomy

Edaravone alleviated propofol‐induced neural injury in developing rats by BDNF/TrkB pathway

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