Targeting ischemic brain injury with intravenous immunoglobulin

被引：30

作者：

Arumugam, Thiruma V. ^{[1
]}

Selvaraj, Pradeep K. ^{[1
]}

Woodruff, Trent M. ^{[2
]}

Mattson, Mark P. ^{[3
,4
]}

机构：

[1] Texas Tech Univ, Hlth Sci Ctr, Dept Pharmaceut Sci, Sch Pharm, Amarillo, TX 79106 USA

[2] Univ Queensland, Sch Biomed Sci, Brisbane, Qld, Australia

[3] NIA, Intramural Res Program, Neurosci Lab, Baltimore, MD 21224 USA

[4] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA

来源：

EXPERT OPINION ON THERAPEUTIC TARGETS | 2008年 / 12卷 / 01期

关键词：

apoptosis; cerebral ischemia; complement; intravenous immunoglobulin; ischemic stroke; T lymphocytes;

D O I：

10.1517/14728222.12.1.19

中图分类号：

R9 [药学];

学科分类号：

1007 [药学];

摘要：

Background: Intravenous immunoglobulin (IVIG) is a therapeutic modality approved for the treatment of autoimmune disorders. Objective: This review discusses how IVIG can prevent brain damage following ischemic stroke and discuss the potential mechanisms of action. Methods: Medline and the world wide web were searched and the relevant literature was classified under the following categories: IVIG, IVIG mechanism of action, and ischemic stroke injury mechanisms. Results/conclusion: Brain ischemia induces an inflammatory response that contributes to neuronal cell death. Because of its ability to block multiple molecular events, IVIG may have particularly strong neuroprotective action against ischemic brain injury. In light of the extensive clinical experience with IVIG for other indications, development of clinical trials to evaluate the use of IVIG in human stroke patients are warranted.

引用

页码：19 / 29

页数：11

共 115 条

[1]

ANTI-CYTOKINE NATURE OF NATURAL HUMAN-IMMUNOGLOBULIN - ONE POSSIBLE MECHANISM OF THE CLINICAL EFFECT OF INTRAVENOUS IMMUNOGLOBULIN THERAPY [J].

ABE, Y ;

HORIUCHI, A ;

MIYAKE, M ;

KIMURA, S .

IMMUNOLOGICAL REVIEWS, 1994, 139 :5-19

[2]

Abe Yasuhito, 1996, Frontiers in Bioscience (online), V1, pE26

[3]

Stroke: a vascular pathology with inadequate management [J].

Adams, HR .

JOURNAL OF HYPERTENSION, 2003, 21 :S3-S7

[4]

3-DIMENSIONAL STRUCTURE OF IMMUNOGLOBULINS [J].

AMZEL, LM ;

POLJAK, RJ .

ANNUAL REVIEW OF BIOCHEMISTRY, 1979, 48 :961-997

[5]

Intravenous immune globulin affects cytokine production in T lymphocytes and monocytes macrophages [J].

Andersson, J ;

SkansenSaphir, U ;

Sparrelid, E ;

Andersson, U .

CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 1996, 104 :10-20

[6]

ANDERSSON UG, 1993, IMMUNOLOGY, V79, P211

[7]

IGG INDUCTION OF IL-1 RECEPTOR ANTAGONIST PRODUCTION BY HUMAN MONOCYTES [J].

AREND, WP ;

LEUNG, DYM .

IMMUNOLOGICAL REVIEWS, 1994, 139 :71-78

[8]

Intravenous immunoglobulin (IVIG) protects the brain against experimental stroke by preventing complement-mediated neuronal cell death [J].

Arumugam, Thiruma V. ;

Tang, Sung-Chun ;

Lathia, Justin D. ;

Cheng, Aiwu ;

Mughal, Mohamed R. ;

Chigurupati, Srinivasulu ;

Magnus, Tim ;

Chan, Sic L. ;

Jo, Dong-Gyu ;

Ouyang, Xin ;

Fairlie, David P. ;

Granger, Daniel N. ;

Vortmeyer, Alexander ;

Basta, Milan ;

Mattson, Mark P. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (35) :14104-14109

[9]

Complement mediators in ischemia-reperfusion injury [J].

Arumugam, Thiruma V. ;

Magnus, Tim ;

Woodruff, Trent M. ;

Proctor, Lavinia M. ;

Shiels, Ian A. ;

Taylor, Stephen M. .

CLINICA CHIMICA ACTA, 2006, 374 (1-2) :33-45

[10]

Stroke and T-cells [J].

Arumugam, TV ;

Granger, DN ;

Mattson, MP .

NEUROMOLECULAR MEDICINE, 2005, 7 (03) :229-242

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