Neuroprotective effects of berberine on stroke models in vitro and in vivo

被引：168
作者：
Zhou, Xi-Qiao [1 ]
Zeng, Xiao-Ning [1 ]
Kong, Hui [1 ]
Sun, Xiu-Lan [1 ]
机构：
[1] Nanjing Med Univ, Dept Pharmacol, Jiangsu Key Lab Neurodegenerat, Nanjing 210029, Jiangsu, Peoples R China
来源：
NEUROSCIENCE LETTERS | 2008年 / 447卷 / 01期
关键词：
Ischemia-reperfusion; Neuroprotection; Berberine; Apoptosis; Mitochondria;
D O I：
10.1016/j.neulet.2008.09.064
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Berberine is an alkaloid derived from herb medicine Coptidis Rhizom. Although there are increasing evidences that berberine exhibits neuroprotective effects against ischemic brain damage, little is known about the mechanism. In this study, we investigated the effect of berberine on ischemic injury in a middle cerebral artery occlusion (MCAO) model. We found that berberine improved neurological outcome and reduced ischemial/reperfusion (I/R)-induced cerebral infarction 48 h after MCAO. The protective effect of berberine was confirmed in in vitro study. Berberine protected PC12 cells against oxygen-glucose deprivation (OGD)-induced injury. The results showed that berberine inhibited reactive oxygen species (ROS) generation, and subsequent release of pro-apoptotic factor cytochrome c and apoptosis-inducing factors (AlFs) evoked by OGD. Findings of this study suggest that berberine protects against ischemic brain injury by decreasing the intracellular ROS level and subsequently inhibiting mitochondrial apoptotic pathway. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：31 / 36
页数：6
相关论文
共 34 条
[1]   APPARENT HYDROXYL RADICAL PRODUCTION BY PEROXYNITRITE - IMPLICATIONS FOR ENDOTHELIAL INJURY FROM NITRIC-OXIDE AND SUPEROXIDE [J].
BECKMAN, JS ;
BECKMAN, TW ;
CHEN, J ;
MARSHALL, PA ;
FREEMAN, BA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (04) :1620-1624
[2]   RAT MIDDLE CEREBRAL-ARTERY OCCLUSION - EVALUATION OF THE MODEL AND DEVELOPMENT OF A NEUROLOGIC EXAMINATION [J].
BEDERSON, JB ;
PITTS, LH ;
TSUJI, M ;
NISHIMURA, MC ;
DAVIS, RL ;
BARTKOWSKI, H .
STROKE, 1986, 17 (03) :472-476
[3]  
BERBERINE, 2000, ALTERN MED REV, V5, P175
[4]   Reactive oxygen radicals in signaling and damage in the ischemic brain [J].
Chan, PH .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2001, 21 (01) :2-14
[5]   Mitochondria: A target for neuroprotective interventions in cerebral ischemia-reperfusion [J].
Chtistophe, M ;
Nicolas, S .
CURRENT PHARMACEUTICAL DESIGN, 2006, 12 (06) :739-757
[6]   Cerebral ischemia: Gene activation, neuronal injury, and the protective role of antioxidants [J].
Clemens, JA .
FREE RADICAL BIOLOGY AND MEDICINE, 2000, 28 (10) :1526-1531
[7]   Procedural and strain-related variables significantly affect outcome in a murine model of focal cerebral ischemia [J].
Connolly, ES ;
Winfree, CJ ;
Stern, DM ;
Solomon, RA ;
Pinsky, DJ .
NEUROSURGERY, 1996, 38 (03) :523-531
[8]   Cerebral protection in homozygous null ICAM-1 mice after middle cerebral artery occlusion - Role of neutrophil adhesion in the pathogenesis of stroke [J].
Connolly, ES ;
Winfree, CJ ;
Springer, TA ;
Naka, Y ;
Liao, H ;
Yan, SD ;
Stern, DM ;
Solomon, RA ;
GutierrezRamos, JC ;
Pinsky, DJ .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (01) :209-216
[9]   Increased infarct size and exacerbated apoptosis in the glutathione peroxidase-1 (Gpx-1) knockout mouse brain in response to ischemia/reperfusion injury [J].
Crack, PJ ;
Taylor, JM ;
Flentjar, NJ ;
de Haan, J ;
Hertzog, P ;
Iannello, RC ;
Kola, I .
JOURNAL OF NEUROCHEMISTRY, 2001, 78 (06) :1389-1399
[10]   Cell death: Critical control points [J].
Danial, NN ;
Korsmeyer, SJ .
CELL, 2004, 116 (02) :205-219
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