Protective effect of Nardostachys jatamansi in rat cerebral ischemia

被引:77
作者
Salim, S [1 ]
Ahmad, M [1 ]
Zafar, KS [1 ]
Ahmad, AS [1 ]
Islam, F [1 ]
机构
[1] Jamia Hamdard, Dept Med Elementol & Toxicol, Neurotoxicol Lab, New Delhi 110062, India
关键词
cerebral ischemia; Nardostachys jatamansi; neuro behaviour; oxidative stress; neuroprotection;
D O I
10.1016/S0091-3057(02)01030-4
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
The protective effect of Nardostachys jatamansi (NJ) on neurobehavioral activities, thiobarbituric acid reactive substance (TBARS), reduced glutathione (GSH), thiol group, catalase and sodium-potassium ATPase activities was studied in middle cerebral artery (MCA) occlusion model of acute cerebral ischemia in rats. The right MCA of male Wistar rats was occluded for 2 h using intraluminal 4-0 monofilament and reperfusion was allowed for 22 h. MCA occlusion caused significant depletion in the contents of glutathione and thiol group and a significant elevation in the level of TBARS. The activities of Na+ K+ ATPase and catalase were decreased significantly by MCA occlusion. The neurobehavioral activities (spontaneous motor activity and motor coordination) were also decreased significantly in MCA occlusion group. All the alternations induced by ischemia were significantly attenuated by 15 days pretreatment of NJ (250 mg/kg po) and correlated well with histopathology by decreasing the neuronal cell death following MCA occlusion and reperfusion. The study provides first evidence of effectiveness of NJ in focal ischemia most probably by virtue of its antioxidant property. (C) 2002 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:481 / 486
页数:6
相关论文
共 55 条
[1]  
Arora R B, 1965, Spec Rep Ser Indian Counc Med Res, V51, P1
[2]  
BENVENISTE H, 1991, CEREBROVAS BRAIN MET, V3, P213
[3]  
BIANS JS, 1997, SOC NEUR ABSTR, V23, P1761
[4]   POLYAMINES ANTAGONIZE N-METHYL-D-ASPARTATE EVOKED DEPOLARIZATIONS, BUT REDUCE MG2+ BLOCK [J].
BOWE, MA ;
NADLER, JV .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1995, 278 (01) :55-65
[5]   CENTRAL NERVOUS-SYSTEM TRAUMA AND STROKE .1. BIOCHEMICAL CONSIDERATIONS FOR OXYGEN RADICAL FORMATION AND LIPID-PEROXIDATION [J].
BRAUGHLER, JM ;
HALL, ED .
FREE RADICAL BIOLOGY AND MEDICINE, 1989, 6 (03) :289-301
[6]   HORIZONTAL SPREAD OF SYNCHRONIZED ACTIVITY IN NEOCORTEX AND ITS CONTROL BY GABA-MEDIATED INHIBITION [J].
CHAGNACAMITAI, Y ;
CONNORS, BW .
JOURNAL OF NEUROPHYSIOLOGY, 1989, 61 (04) :747-758
[7]  
Chang M, 1987, Arch Biochem Biophys, V259, P536, DOI 10.1016/0003-9861(87)90520-0
[8]   GLUTAMATE NEUROTOXICITY AND DISEASES OF THE NERVOUS-SYSTEM [J].
CHOI, DW .
NEURON, 1988, 1 (08) :623-634
[9]  
Claiborne A., 1985, CRC HDB METHODS OXYG, P283
[10]   GLUTATHIONE AND ASCORBATE DURING ISCHEMIA AND POST-ISCHEMIC REPERFUSION IN RAT-BRAIN [J].
COOPER, AJL ;
PULSINELLI, WA ;
DUFFY, TE .
JOURNAL OF NEUROCHEMISTRY, 1980, 35 (05) :1242-1245