臺大醫(yī)院醫(yī)生湯頌君日前研究發(fā)現(xiàn),，“免疫球蛋白”治療急性栓塞性腦中風(fēng)老鼠有顯著效果,。
據(jù)臺灣《中國時報》報道,，湯頌君前年至美國國家衛(wèi)生研究院老年研究中心神經(jīng)科學(xué)實驗室進(jìn)修,。上述研究形成的論文發(fā)表于八月的美國國家科學(xué)期刊(PNAS)上,。
湯頌君說,，該研究室證實缺血性(即栓塞性)腦中風(fēng)發(fā)生后,，腦部發(fā)炎反應(yīng)是引起神經(jīng)細(xì)胞死亡主因之一，若能控制腦部發(fā)炎就能控制病情惡化,。
據(jù)悉,，免疫球蛋白是具有抗體活性的蛋白，可有效抑制體內(nèi)免疫反應(yīng),，SARS,、嚴(yán)重腸病毒七十一型治療就是以此為主，但從未應(yīng)用于腦中風(fēng)治療,。
此研究結(jié)果是新發(fā)現(xiàn),，因急性缺血性腦中風(fēng)，目前仍無有效治療方法,，雖中風(fēng)三小時以內(nèi),，病患可于靜脈注射血栓溶解劑，但在臺灣只有1%的病患符合治療條件,。湯頌君有關(guān)腦中風(fēng)的兩篇論文引起美國國家衛(wèi)生研究院高度重視,，正申請人體臨床實驗及用藥劑量與時機(jī)。（中新網(wǎng)）
原始出處:
Published online before print August 21, 2007, 10.1073/pnas.0700506104
PNAS | August 28, 2007 | vol. 104 | no. 35 | 14104-14109
BIOLOGICAL SCIENCES / NEUROSCIENCE
Intravenous immunoglobulin (IVIG) protects the brain against experimental stroke by preventing complement-mediated neuronal cell death
Thiruma V. Arumugam*,, Sung-Chun Tang*,, Justin D. Lathia*, Aiwu Cheng*, Mohamed R. Mughal*, Srinivasulu Chigurupati*, Tim Magnus*, Sic L. Chan*,, Dong-Gyu Jo*, Xin Ouyang*, David P. Fairlie¶, Daniel N. Granger||, Alexander Vortmeyer**, Milan Basta,, and Mark P. Mattson*,
*Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224; Department of Pharmaceutical Sciences, Texas Tech University Health Sciences Center 1400 Wallace Boulevard, Amarillo, TX 79106; Biomolecular Science Center, University of Central Florida, Orlando, FL 32816; ||Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130; Department of Neurology, National Taiwan University Hospital, Yun-Lin Branch, Yun-Lin 640, Taiwan; ¶Centre for Drug Design and Development, Institute for Molecular Bioscience, University of Queensland, Brisbane, Qld 4072, Australia; Neuronal Excitability Section and **Neurosurgical Division, National Institute for Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892; and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205
Edited by Michael V. L. Bennett, Albert Einstein College of Medicine, Bronx, NY, and approved July 24, 2007 (received for review January 18, 2007)
Stroke is among the three leading causes of death worldwide and the most frequent cause of permanent disability. Brain ischemia induces an inflammatory response involving activated complement fragments. Here we show that i.v. Ig (IVIG) treatment, which scavenges complement fragments, protects brain cells against the deleterious effects of experimental ischemia and reperfusion (I/R) and prevents I/R-induced mortality in mice. Animals administered IVIG either 30 min before ischemia or after 3 h of reperfusion exhibited a 50–60% reduction of brain infarct size and a 2- to 3-fold improvement of the functional outcome. Even a single low dose of IVIG given after stroke was effective. IVIG was protective in the nonreperfusion model of murine stroke as well and did not exert any peripheral effects. Human IgG as well as intrinsic murine C3 levels were significantly higher in the infarcted brain region compared with the noninjured side, and their physical association was demonstrated by immuno-coprecipitation. C5-deficient mice were significantly protected from I/R injury compared with their wild-type littermates. Exposure of cultured neurons to oxygen/glucose deprivation resulted in increased levels of C3 associated with activation of caspase 3, a marker of apoptosis; both signals were attenuated with IVIG treatment. Our data suggest a major role for complement-mediated cell death in ischemic brain injury and the prospect of using IVIG in relatively low doses as an interventional therapy for stroke.
C5a | cerebral cortex apoptosis | ischemic stroke | lymphocyte | microglia
Author contributions: T.V.A. and S.-C.T. and M.B. and M.P.M. contributed equally to this work; M.B. and M.P.M. designed research; T.V.A., S.-C.T., J.D.L., A.C., M.R.M., S.C., T.M., S.L.C., D.-G.J., X.O., D.N.G., and A.V. performed research; D.-G.J., X.O., D.P.F., and D.N.G. contributed new reagents/analytic tools; T.V.A., S.-C.T., and M.B. analyzed data; and M.B. and M.P.M. wrote the paper
