Protective effect of Khamira Abresham Uood Mastagiwala against free radical induced damage in focal cerebral ischemia

被引:31
作者
Yousuf, S [1 ]
Salim, S [1 ]
Ahmad, M [1 ]
Ahmed, AS [1 ]
Ansari, MA [1 ]
Islam, F [1 ]
机构
[1] Handard Univ, Neurotoxicol Lab, Dept Med Elementol & Toxicol, New Delhi 110062, India
关键词
cerebral ischemia; Khamira Abresham Uood Mastagiwala; free radicals antioxidant enzymes; Cook's climbing pole;
D O I
10.1016/j.jep.2004.12.035
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
The effect of Khamira Abresham Uood Mastagiwala (KAUM) (a preparation of Indian System of Unani Medicine) on the activity of antioxidant enzymes, glutathione reductase (GR), glutathione S-transferase (GST), glutathione peroxidase (GPx), catalase (CAT) and the content of glutathione (GSH) and thiobarbituric acid reactive substances (TBARS) was studied in the middle cerebral artery occluded (MCAO) rats after 15 days pretreatment (200 mg/kg body weight (b.wt.), orally) of Khamira Abresham Uood Mastagiwala. The rats were trained and assessed for neurobehavioral activity using Cook's climbing pole. The middle cerebral artery of adult male Wistar rats was occluded for 2 It and reperfused for 22 h. The activity of GPx, GST, GR, catalase and content of GSH was decreased significantly in MCAO group as compared with sham. The rats of MCAO + KAUM group have shown a significant protection in the activity of above-mentioned antioxidant enzymes and content of glutathione when compared with MCAO group. The significantly elevated level of TBARS in MCAO group was depleted significantly by the pretreatment of animals with KAUM in MCAO group. The neurobehavioral assessment has also strengthened the above biochemical data thereby indicating that the therapeutic intervention of KAUM, which is a potent cardiac and melancholic tonic, can be used to prevent or reduce the deterioration caused by free radicals thereby preventing subsequent pathological and biochemical changes which occur during cerebral ischemia. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:179 / 184
页数:6
相关论文
共 23 条
[11]  
KABEER U, 1951, BAYAAZE E KABEER 2, P66
[12]   Silk protein, sericin, inhibits lipid peroxidation and tyrosinase activity [J].
Kato, N ;
Sato, S ;
Yamanaka, A ;
Yamada, H ;
Fuwa, N ;
Nomura, M .
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY, 1998, 62 (01) :145-147
[13]   Free radical pathways in CNS injury [J].
Lewén, A ;
Matz, P ;
Chan, PH .
JOURNAL OF NEUROTRAUMA, 2000, 17 (10) :871-890
[14]  
LOWRY OH, 1951, J BIOL CHEM, V193, P265
[15]   Prevention of in vivo excitotoxicity by a family of trialkylglycines, a novel class of neuroprotectants [J].
Montoliu, C ;
Humet, M ;
Canales, JJ ;
Burda, J ;
Planells-Cases, R ;
Sánchez-Baeza, F ;
Carbonell, T ;
Pérez-Payá, E ;
Messeguer, A ;
Ferrer-Montiel, A ;
Felipo, V .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2002, 301 (01) :29-36
[16]   TEMPORAL PROFILE OF NEURONAL DAMAGE IN A MODEL OF TRANSIENT FOREBRAIN ISCHEMIA [J].
PULSINELLI, WA ;
BRIERLEY, JB ;
PLUM, F .
ANNALS OF NEUROLOGY, 1982, 11 (05) :491-498
[17]  
RAFIQUDDIN H, 1995, KUNZUL ADVIYA ALIGAR, P568
[18]   Protective effect of Nardostachys jatamansi in rat cerebral ischemia [J].
Salim, S ;
Ahmad, M ;
Zafar, KS ;
Ahmad, AS ;
Islam, F .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 2003, 74 (02) :481-486
[19]   Antioxidant/restorative effects of calcined gold preparations used in Indian systems of medicine against global and focal models of ischaemia [J].
Shah, ZA ;
Vohora, SB .
PHARMACOLOGY & TOXICOLOGY, 2002, 90 (05) :254-259
[20]  
SIFIUDDIN H, 1999, UNANI ADVIYA MAFARR, P65