The neuroprotective role of boric acid on aluminum chloride-induced neurotoxicity

被引:37
作者
Colak, Suat [1 ]
Geyikoglu, Fatime [1 ]
Keles, Osman Nuri [2 ]
Turkez, Hasan [1 ]
Topal, Ahmet [3 ]
Unal, Bunyami [2 ]
机构
[1] Ataturk Univ, Fac Sci, Dept Biol, TR-25240 Erzurum, Turkey
[2] Ataturk Univ, Sch Med, Dept Histol & Embryol, TR-25240 Erzurum, Turkey
[3] Ataturk Univ, Fac Vet, Dept Physiol, TR-25240 Erzurum, Turkey
关键词
Boric acid; aluminum chloride; brain; stereology; histopathology; BLOOD-BRAIN-BARRIER; NF-KAPPA-B; CELL-CYCLE; UNBIASED ESTIMATION; OXIDATIVE STRESS; CEREBRAL-CORTEX; UBIQUITIN; PERMEABILITY; BORTEZOMIB; DISEASE;
D O I
10.1177/0748233710395349
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
This study was designed to investigate the qualitative and quantitative changes in brain tissue following aluminum chloride (AlCl3) administration and to determine whether boric acid (BA) has a protective effect against brain damage induced by AlCl3. For this aim, Sprague-Dawley rats were randomly separated into eight groups: (1) control, (2) AlCl3 (5 mg/kg/day), (3, 4 and 5) BA (3.25, 36 and 58.5 mg/kg/day), (6, 7 and 8) AlCl3 (5 mg/kg/day) plus BA (3.25, 36 and 58.5 mg/kg/day). After the animals were killed, the total numbers of neuron in the brain of all groups were determined using an unbiased stereological analysis. In addition to the stereological analysis, all brains were examined histopathologically by using light and electron microscopy. The stereological and histopathological results indicated a high damage of the rat brain tissues in the AlCl3 and AlCl3 + high dose BA (36 and 58.5) treatment groups. However, protective effects on neuron were observed in the AlCl3 + low dose BA (3.25) group when compared other AlCl3 groups. Our stereological and histopathological findings show that low-dose BA, as a proteasome inhibitor, can decrease the adverse effects of AlCl3 on the cerebral cortex.
引用
收藏
页码:700 / 710
页数:11
相关论文
共 44 条
[1]   Structure and function of the blood-brain barrier [J].
Abbott, N. Joan ;
Patabendige, Adjanie A. K. ;
Dolman, Diana E. M. ;
Yusof, Siti R. ;
Begley, David J. .
NEUROBIOLOGY OF DISEASE, 2010, 37 (01) :13-25
[2]   Astrocyte-endothelial interactions at the blood-brain barrier [J].
Abbott, NJ ;
Rönnbäck, L ;
Hansson, E .
NATURE REVIEWS NEUROSCIENCE, 2006, 7 (01) :41-53
[3]   Maintaining Blood-Brain Barrier Integrity: Pericytes Perform Better Than Astrocytes During Prolonged Oxygen Deprivation [J].
Al Ahmad, A. ;
Gassmann, M. ;
Ogunshola, O. O. .
JOURNAL OF CELLULAR PHYSIOLOGY, 2009, 218 (03) :612-622
[4]  
Albensi BC, 2000, SYNAPSE, V35, P151
[5]   17β-estradiol differentially regulates blood-brain barrier permeability in young and aging female rats [J].
Bake, S ;
Sohrabji, F .
ENDOCRINOLOGY, 2004, 145 (12) :5471-5475
[6]   Cellular changes in boric acid-treated DU-145 prostate cancer cells [J].
Barranco, WT ;
Eckhert, CD .
BRITISH JOURNAL OF CANCER, 2006, 94 (06) :884-890
[7]   Aluminum as a toxicant [J].
Becaria, A ;
Campbell, A ;
Bondy, SC .
TOXICOLOGY AND INDUSTRIAL HEALTH, 2002, 18 (07) :309-320
[8]   Bortezomib-mediated 26S proteasome inhibition causes cell-cycle arrest and induces apoptosis in CD-30+ anaplastic large cell lymphoma [J].
Bonvini, P. ;
Zorzi, E. ;
Basso, G. ;
Rosolen, A. .
LEUKEMIA, 2007, 21 (04) :838-842
[9]   Inflammation, neurodegenerative diseases, and environmental exposures [J].
Campbell, A .
PROTECTIVE STRATEGIES FOR NEURODEGENERATIVE DISEASES, 2004, 1035 :117-132
[10]  
Campbell A, 2006, J ALZHEIMERS DIS, V10, P165