陈忠教课题组《J Cerebr Blood F Met》最新研究成果
近日，卫生部医学神经生物学重点实验室和浙江省神经生物学重点实验室陈忠教授课题组在国际著名学术期刊J Cerebr Blood F Met上发表题为‘A novel neuroprotective strategy for ischemic stroke: transient mild acidosis treatment by CO2inhalation at reperfusion’的研究论文，该文首次报道了酸后处理对脑缺血再灌注损伤有明显的保护作用。
缺血后处理是近期发现的一种基于内源性神经保护策略的新干预措施，但由于缺血后处理在临床应用上存在困难，因此寻找其它后处理手段显得尤为必要。组织酸化是脑缺血后处理的重要因素之一，本研究旨在探讨酸后处理，即在再灌早期给予一段短时间的酸化处理，是否对脑缺血再灌注损伤具有保护作用。结果发现再灌5 min和50 min后给予酸后处理均能明显减少再灌24 h后的脑梗死体积并改善神经症状。相似地，在神经元OGD模型中，再灌后立即或15min后给予酸后处理可显著提高再灌24 h的细胞存活率。体外和在体实验进一步发现，酸后处理可显著抑制缺血再灌引起的神经元凋亡。本研究表明，酸后处理作为一种新的内源性保护策略，同时具有较宽的时间窗，对于治疗缺血性脑损伤具有潜在的临床应用价值。该论文已被J Cerebr Blood F Met杂志录用，J Cerebr Blood F Met2012年影响因子为5.398。本文共同第一作者为范彦英博士和沈哲博士，本研究受到了国家自然科学基金 (81030061,81273506)、973子课题 (2011CB504403)、国家自然科学基金创新研究群体 (81221003)的资助。
Recently, a research group headed by Professor CHENZhong at Department of Pharmacology, Key Laboratory of Medical Neurobiology of the Ministry of Health of China and Zhejiang Province Key Laboratory of Neurobiology, College of Pharmaceutical Sciences, Zhejiang University has published a research paper titled‘A novel neuroprotective strategy for ischemic stroke: transient mild acidosis treatment by CO2inhalation at reperfusion’in J Cerebr Blood F Met(IF=5.398). In this paper, Prof. Chen’s group reported for the first time thatacidosis treatment at reperfusion protectsagainst cerebral ischemia/reperfusion injury.
Cerebral ischemic postconditioning is anew intervention that has emerged recently as an endogenous strategy for neuroprotection. However,the clinical application of ischemic postconditionding is difficult. Therefore to seek other postproceeding treatments is particularly important. Tissue acidification is one of the most importantcomponentsof ischemic postconditioning. We set out to test whether acidosis treatment at reperfusion can protect against cerebral ischemia/reperfusion injury. Our results showed that 5 min of acidosistreatment at 5min and 50 min afterthe onset ofreperfusioninduced optimal neuroprotection, as revealed by reduced infarct volumeand improve neurological deficit scores at 24h of reperfusion.We further demonstrated that the acidosis treatment inhibits neuronal apoptosis both in vivo and in vitro.Taken together, these findings indicate that transient mild acidosis treatment at reperfusion protectsagainst cerebral ischemia/reperfusion injury.As anewendogenous strategywith a wider therapeutic time window, acidosis treatmenthas a potential clinical application valuefor neuroprotection.
Co-first authors of thisarticle arePh.Dstudents Fan Yanying andShen Zhe.Thiswork was funded bythe National Natural Science Foundation of China (81030061, 81273506) ,the National Basic Research of China 973 Program (2011CB504403) , the China Science Fund for Creative Research Groups (81221003).
