首页出版说明中文期刊中文图书环宇英文官网付款页面

缺血性脑卒中的发病机制及治疗药物的最新进展

王宝 忠1, 李秀 华2, 陈 琦1, 崔 博1, 齐贺 彬1
1.华北理工大学;2.唐山市工人医院

摘要


摘要:中风是全球残疾的主要原因和第二大死亡原因。随着全球65岁及以上人口的增长速度快于所有其他年龄组,中风的发病率也在增加。此外,卒中的总体负担正在向较年轻的年龄组转移,特别是在低收入和中等收入国家。在大多数情况下,中风是由于缺血性中风脑卒中引起的,但在某些情况下,中风可能是由于血管破裂时出血到脑组织引起的。尽管卒中的治疗选择仍然有限,但随着使用药物和机械溶栓的再通治疗的进步,在帮助患者从缺血性脑卒中中恢复方面取得了一些进展。然而,仍然需要开发用于急性缺血性卒中神经保护的治疗药物,以保护大脑在再通之前和期间免受损伤,延长干预的治疗时间窗口并进一步改善功能结局。本综述评估了临床试验的最新进展,总结了每种神经保护策略的潜在分子机制,这可能有助于制定未来脑卒中治疗联合治疗策略。

关键词


关键词:缺血性,细胞,中风,脑卒中,治疗

全文:

PDF


参考


[1].Donkor ES, 2018. Stroke in the 21(st) Century: A Snapshot of theBurden, Epidemiology, and Quality of Life. Stroke Res Treat 2018,3238165.[2].Karatepe AG, Gunaydin R, Kaya T, Turkmen G, 2008.Comorbidity in patients after stroke: impact on functional outcome. JRehabil Med 40, 831-835.[3].Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK,He J, 2005. Global burden of hypertension: analysis of worldwide data.Lancet 365, 217-223.[4].Sato M, Tani E, Fujikawa H, Kaibuchi K, 2000. Involvement ofRho-kinase-mediated phosphorylation of myosin light chain inenhancement of cerebral vasospasm. Circ Res 87, 195-200.[5]. Zhang X,Dong H,LiN,et al.Activated brain mast cells contributeto postoperative cognitive dysfunction by evoking microglia activation andneuronal apoptosis[1].Journal of neuroinflammation, 2016,13(1): 1-15.[6].Herpich F, Rincon F. Management of Acute Ischemic Stroke.Crit Care Med. 2020 Nov;48(11):1654-1663. doi: 10.1097/CCM. 0000000000004597. PMID: 32947473; PMCID: PMC7540624.[7].McKay , J.; Mensah, G.A.; Mendis, S.; Greenlund, K.; WorldHealth Organization. The Atlas of Heart Diseaseand Stroke; WHO:Geneva, Switzerland, 2004.[8].孙慧英,李涛.脑卒中及其危险因素分析[J].卒中与神经疾病,2012,19(03):167-170.[9].涂雪松.缺血性脑卒中的流行病学研究[J].中国临床神经科学,2016,24(05):594-599.[10].Mishra, M.; Hedna, V .S. Neuroinflammation after acuteischemic stroke: A volcano hard to contain. Chin.J. Contemp. Neurol.Neurosurg. 2013, 13, 964.[11]. Iadecola, C.; Anrather, J. The immunology of stroke: Frommechanisms to translation. Nat. Med. 2011, 17,796-808.[12].Weiner, H.L.; Selkoe, D.J. Inflammation and therapeuticvaccination in CNS diseases. Nature 2002, 420,879-884.[13].Tuttolomondo, A.; Maida, C.; Pinto, A. Inflammation andInflammatory Cell Recruitment in AcuteCerebrovascular Diseases. Curr.Immunol. Rev. 2015, 11, 24-32.[14].Wei Z, Lyu Y, Yang X, Chen X, Zhong P, Wu D, 2018.Therapeutic Values of Human Urinary Kallidinogenase on Cerebrovascular Diseases. Front Neurol 9, 403.[15].Lee MMY, Sattar N, McMurray JJV, Packard CJ, 2019. Statinsin the Prevention and Treatment of Heart Failure: a Review of theEvidence. Curr Atheroscler Rep 21, 41.[16].Balduini W, De Angelis V, Mazzoni E, Cimino M, 2001.Simvastatin protects against long-lasting behavioral and morphologicalconsequences of neonatal hypoxic/ischemic brain injury. Stroke 32,2185-2191.[17].Jincai W, Tingfang D, Yongheng Z, Zhongmin L, Kaihua Z,Xiaohong L, 2014. Effects of vinpocetine and ozagrel on behavioralrecovery of rats after global brain ischemia. J Clin Neurosci 21, 661²663.[18].Wang H, Zhang K, Zhao L, Tang J, Gao L, Wei Z, 2014.Anti-inflammatory effects of vinpocetine on the functional expression ofnuclear factor-kappa B and tumor necrosis factor-alpha in a rat model ofcerebral ischemia-reperfusion injury. Neurosci Lett 566, 247-251.[19].Yoshida H, Yanai H, Namiki Y, Fukatsu-Sasaki K, Furutani N,Tada N, 2006. Neuroprotective effects of edaravone: a novel free radicalscavenger in cerebrovascular injury. CNS Drug Rev 12, 920.[20].Kitagawa Y, 2006. Edaravone in acute ischemic stroke. InternMed 45, 225-226.[21].Banno M, Mizuno T, Kato H, Zhang G, Kawanokuchi J, Wang J,Kuno R, Jin S, Takeuchi H, Suzumura A, 2005. The radical scavengeredaravone prevents oxidative neurotoxicity induced by peroxynitrite andactivated microglia. Neuropharmacology 48, 283²290.[22]Zhu Z, Fu Y, Tian D, Sun N, Han W, Chang G, Dong Y, Xu X,Liu Q, Huang D, Shi FD, 2015. Combination of the Immune ModulatorFingolimod With Alteplase in Acute Ischemic Stroke: A Pilot Trial.Circulation 132, 1104-1112.[23]Ellery SJ, Goss MG, Brew N, Dickinson H, Hale N, LaRosa DA,Walker DW, Wong FY, 2019. Evaluation of 3K3A-Activated Protein C toTreat Neonatal Hypoxic Ischemic Brain Injury in the Spiny Mouse.Neurotherapeutics 16, 231-243.




DOI: http://dx.doi.org/10.12361/2661-3603-05-18-145511

Refbacks

  • 当前没有refback。