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1
New progress of isoflurane, sevoflurane and propofol in hypoxic-ischemic brain injury and related molecular mechanisms based on 75 neurotrophic factor receptor.基于75种神经营养因子受体的异氟烷、七氟烷和丙泊酚在缺氧缺血性脑损伤中的新进展及相关分子机制
Ibrain. 2021 Jun 28;7(2):132-140. doi: 10.1002/j.2769-2795.2021.tb00075.x. eCollection 2021 Jun.
2
Sevoflurane Post-Conditioning Ameliorates Neuronal Deficits and Axon Demyelination After Neonatal Hypoxic Ischemic Brain Injury: Role of Microglia/Macrophage.七氟醚后处理减轻新生鼠缺氧缺血性脑损伤后神经元损伤和轴突脱髓鞘:小胶质细胞/巨噬细胞的作用。
Cell Mol Neurobiol. 2021 Nov;41(8):1801-1816. doi: 10.1007/s10571-020-00949-5. Epub 2020 Sep 2.
3
Isoflurane but not sevoflurane or desflurane aggravates injury to neurons in vitro and in vivo via p75NTR-NF-ĸB activation.异氟烷而非七氟烷或地氟烷通过激活p75神经营养因子受体-核因子-κB在体外和体内加重神经元损伤。
Anesth Analg. 2014 Dec;119(6):1429-41. doi: 10.1213/ANE.0000000000000488.
4
Sevoflurane Postconditioning Inhibits Autophagy Through Activation of the Extracellular Signal-Regulated Kinase Cascade, Alleviating Hypoxic-Ischemic Brain Injury in Neonatal Rats.七氟醚后处理通过激活细胞外信号调节激酶级联反应抑制自噬,减轻新生大鼠缺氧缺血性脑损伤。
Neurochem Res. 2019 Feb;44(2):347-356. doi: 10.1007/s11064-018-2682-9. Epub 2018 Nov 20.
5
Sevoflurane post-conditioning alleviated hypoxic-ischemic brain injury in neonatal rats by inhibiting endoplasmic reticulum stress-mediated autophagy via IRE1 signalings.七氟醚后处理通过抑制内质网应激介导的自噬来减轻新生大鼠缺氧缺血性脑损伤通过 IRE1 信号通路。
Neurochem Int. 2021 Nov;150:105198. doi: 10.1016/j.neuint.2021.105198. Epub 2021 Sep 30.
6
Post-Treatment Sevoflurane Protects Against Hypoxic-Ischemic Brain Injury in Neonatal Rats by Downregulating Histone Methyltransferase G9a and Upregulating Nuclear Factor Erythroid 2-Related Factor 2 (NRF2).术后七氟醚通过下调组蛋白甲基转移酶 G9a 和上调核因子红细胞 2 相关因子 2(NRF2)对新生大鼠缺氧缺血性脑损伤起保护作用。
Med Sci Monit. 2021 Jun 1;27:e930042. doi: 10.12659/MSM.930042.
7
Posttraumatic Propofol Neurotoxicity Is Mediated via the Pro-Brain-Derived Neurotrophic Factor-p75 Neurotrophin Receptor Pathway in Adult Mice.创伤后异丙酚神经毒性是通过成年小鼠中的脑源性神经营养因子-p75 神经营养因子受体通路介导的。
Crit Care Med. 2016 Feb;44(2):e70-82. doi: 10.1097/CCM.0000000000001284.
8
Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a "two-hit" model.心脏骤停后缺氧缺血性脑损伤的临床病理生理学:一种“两次打击”模型。
Crit Care. 2017 Apr 13;21(1):90. doi: 10.1186/s13054-017-1670-9.
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Volatile anesthetics, not intravenous anesthetic propofol bind to and attenuate the activation of platelet receptor integrin αIIbβ3.挥发性麻醉剂,而非静脉麻醉药异丙酚,与血小板受体整合素 αIIbβ3 结合并减弱其激活。
PLoS One. 2013;8(4):e60415. doi: 10.1371/journal.pone.0060415. Epub 2013 Apr 3.
10
Sevoflurane post-conditioning alleviates neonatal rat hypoxic-ischemic cerebral injury via Ezh2-regulated autophagy.七氟醚后处理通过Ezh2调节的自噬减轻新生大鼠缺氧缺血性脑损伤。
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1
Acute effects of single and repeated mild traumatic brain injury on levels of neurometabolites, lipids, and mitochondrial function in male rats.单次和反复轻度创伤性脑损伤对雄性大鼠神经代谢物、脂质水平及线粒体功能的急性影响。
Front Mol Neurosci. 2023 Jun 29;16:1208697. doi: 10.3389/fnmol.2023.1208697. eCollection 2023.

本文引用的文献

1
p75NTR Promotes Astrocyte Proliferation in Response to Cortical Stab Wound.p75NTR 促进皮质刺伤后的星形胶质细胞增殖。
Cell Mol Neurobiol. 2022 May;42(4):1153-1166. doi: 10.1007/s10571-020-01006-x. Epub 2020 Nov 17.
2
Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer.神经营养因子脑源性神经营养因子(BDNF)在抑郁症、神经退行性变和脑癌中的生理功能和治疗潜力。
Int J Mol Sci. 2020 Oct 21;21(20):7777. doi: 10.3390/ijms21207777.
3
Neural stem cell therapies and hypoxic-ischemic brain injury.神经干细胞治疗与缺氧缺血性脑损伤。
Prog Neurobiol. 2019 Feb;173:1-17. doi: 10.1016/j.pneurobio.2018.05.004. Epub 2018 May 21.
4
Rapamycin Promotes the Survival and Adipogenesis of Ischemia-Challenged Adipose Derived Stem Cells by Improving Autophagy.雷帕霉素通过改善自噬促进缺血应激下脂肪来源干细胞的存活和脂肪生成。
Cell Physiol Biochem. 2017;44(5):1762-1774. doi: 10.1159/000485783. Epub 2017 Dec 6.
5
Neonatal hypoxic ischemic encephalopathy: an update on disease pathogenesis and treatment.新生儿缺氧缺血性脑病:疾病发病机制与治疗的最新进展
Expert Rev Neurother. 2017 May;17(5):449-459. doi: 10.1080/14737175.2017.1259567. Epub 2016 Nov 23.
6
Increased extrasynaptic GluN2B expression is involved in cognitive impairment after isoflurane anesthesia.突触外GluN2B表达增加与异氟烷麻醉后的认知障碍有关。
Exp Ther Med. 2016 Jul;12(1):161-168. doi: 10.3892/etm.2016.3306. Epub 2016 Apr 28.
7
Posttraumatic Propofol Neurotoxicity Is Mediated via the Pro-Brain-Derived Neurotrophic Factor-p75 Neurotrophin Receptor Pathway in Adult Mice.创伤后异丙酚神经毒性是通过成年小鼠中的脑源性神经营养因子-p75 神经营养因子受体通路介导的。
Crit Care Med. 2016 Feb;44(2):e70-82. doi: 10.1097/CCM.0000000000001284.
8
Novel Stroke Therapeutics: Unraveling Stroke Pathophysiology and Its Impact on Clinical Treatments.新型中风治疗方法:解析中风病理生理学及其对临床治疗的影响。
Neuron. 2015 Jul 15;87(2):297-309. doi: 10.1016/j.neuron.2015.05.041.
9
Intra-arterial therapy for acute ischemic stroke: a golden age.急性缺血性卒中的动脉内治疗:黄金时代。
Curr Treat Options Neurol. 2015 Jul;17(7):360. doi: 10.1007/s11940-015-0360-7.
10
Isoflurane but not sevoflurane or desflurane aggravates injury to neurons in vitro and in vivo via p75NTR-NF-ĸB activation.异氟烷而非七氟烷或地氟烷通过激活p75神经营养因子受体-核因子-κB在体外和体内加重神经元损伤。
Anesth Analg. 2014 Dec;119(6):1429-41. doi: 10.1213/ANE.0000000000000488.

基于75种神经营养因子受体的异氟烷、七氟烷和丙泊酚在缺氧缺血性脑损伤中的新进展及相关分子机制

New progress of isoflurane, sevoflurane and propofol in hypoxic-ischemic brain injury and related molecular mechanisms based on 75 neurotrophic factor receptor.

作者信息

Zhu Yi, Zhou Hong-Su, Chen Dong-Qin, Zhou Di, Zhao Nan, Xiong Liu-Lin, Deng Issac, Zhou Xin-Fu, Zhu Zhao-Qiong

机构信息

School of Anesthesiology Zunyi Medical University Zunyi Guizhou China.

Department of Anesthesia Hospital of Stomatology, Zunyi Medical University Zunyi Guizhou China.

出版信息

Ibrain. 2021 Jun 28;7(2):132-140. doi: 10.1002/j.2769-2795.2021.tb00075.x. eCollection 2021 Jun.

DOI:10.1002/j.2769-2795.2021.tb00075.x
PMID:37786902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10528789/
Abstract

Hypoxic ischemic brain injury (HIBI) is one of the most common clinical disorders, especially in neonates. The complex pathophysiology of HIBI is an important cause of disability and even death of patients, however, being without effective clinical treatments. Common anesthetics (such as isoflurane, propofol and sevoflurane) have an adverse impact on neuronal cells for HIBI via the regulation of 75 neurotrophic factor receptor (P75NTR). In order to protect the injured brains and study the effect of underlying treatments, it is particularly significant to understand and master the developmental mechanism of anesthetics for the occurrence of HIBI related molecular mechanisms. Therefore, this paper will mainly review the corresponding pathogenic and protective mechanisms about HIBI binding to the research progress of the role of P75NTR. In conclusion, the effects of neuroprotection and injured nerves are involved in the expression and activation of P75NTR, mainly increased P75NTR mRNA, protein levels and calpain-dependent for propofol, and inducing neuronal apoptosis for isoflurane and sevoflurane, and we look forward to that connection with P75NTR, common anaesthetic and HIBI may be a new direction of research and gain perfect outcomes in the future.

摘要

缺氧缺血性脑损伤(HIBI)是最常见的临床病症之一,尤其是在新生儿中。HIBI复杂的病理生理学是导致患者残疾甚至死亡的重要原因,然而目前尚无有效的临床治疗方法。常见的麻醉剂(如异氟烷、丙泊酚和七氟烷)通过调节75神经营养因子受体(P75NTR)对HIBI患者的神经元细胞产生不利影响。为了保护受损大脑并研究潜在治疗方法的效果,了解和掌握麻醉剂对HIBI发生相关分子机制的发展机制尤为重要。因此,本文将主要结合P75NTR作用的研究进展,综述HIBI相应的致病和保护机制。总之,神经保护和神经损伤的作用涉及P75NTR的表达和激活,主要表现为丙泊酚使P75NTR mRNA、蛋白水平升高且依赖钙蛋白酶,而异氟烷和七氟烷则诱导神经元凋亡,我们期待与P75NTR相关的研究、常见麻醉剂和HIBI可能成为未来一个新的研究方向并取得理想成果。