Histopathological and Stereological Study of the Effects of Gallic Acid Administration on Hippocampal Neuronal Density after Trimethyltin Toxication
الموضوعات :
Report of Health Care
heydar aqababa
1
,
Mona Ghezelbash
2
,
Mohamad Amin Edalatmanesh
3
,
Shirin Dehghan
4
1 - Department of Biology, Arsanjan Branch, Islamic Azad University, Arsanjan, Iran
2 - Department of Biology, Shiraz Branch, Islamic Azad University, Shiraz, Iran
3 - Department of Biology, Shiraz Branch, Islamic Azad University, Shiraz, Iran
4 - Department of Biology, Arsanjan Branch, Islamic Azad University, Arsanjan, Iran
تاريخ الإرسال : 16 الأحد , ذو القعدة, 1439
تاريخ التأكيد : 23 الأحد , ذو القعدة, 1439
تاريخ الإصدار : 17 الجمعة , رمضان, 1439
الکلمات المفتاحية:
Rat,
Hippocampus,
Gallic Acid,
Trimethyltin,
ملخص المقالة :
Introduction: Trimethyltin is a methylated organotin, which induces selective damage and neuronal death in human and rodents’ CNS. On the other hand, the neuroprotective effects of Gallic acid can prevent toxicity of trimethyltin. In the current study, the repairing effect of Gallic acid in cell injury caused by trimethyltin in rats was evaluated. Also, this study assessed the effects of Gallic acid on neuronal density of the different hippocampal areas of intoxicated rats with trimethyltin. Methods: 30 rats were divided in three groups: the no treatment control group, the control group, and the experimental group with intraperitoneal injection of trimethyltin (8 mg/kg) and Gallic acid solvent for 14 days. In the experimental group, after the administration of trimethyltin, 50 mg/kg of Gallic acid was injected. It was continued for 14 days. Finally, the rats were killed with transcardial perfusion. Histopathological and stereological analysis was performed on the rats. In this research, Kolmogorov-Smirnov test, one-way analysis of variance, and Tukey’s post-hoc test were used. Results: The results of this study showed that neuronal density of different hippocampal areas of the no treatment control group was significantly increased compared to the rats of the control and experimental groups (P<0.05), while chronic administration of Gallic acid could prevent apoptosis and protect hippocampal cells. Conclusions: According to the results, it is suggested that chronic administration of Gallic acid decreases the effects of trimethyltin and therefore, it prevents the reduction of hippocampal cells.
المصادر:
Besser JM, Brumbaugh WG, Brunson EL, Ingersoll CG. Acute and chronic toxicity of lead in water and diet to the amphipod hyalellaazteca. Environ Toxicol Chem. 2005; 24: 1807- 1815.
Hajipour S, Sarkaki A. Effect of gallic acid on dementia type of alzheimer disease in rats: electrophysiological and histological studies. BCNJ. 2016; 7 (2): 97- 106.
Sarkaki A, Mansouri SM. Gallic acid improves cognitive, hippocampal long term induced by chronic cerebral hypoperfusion in rats. US National Library Med National Inst Health. 2014: 17 (8): 978- 990.
Farbood Y, Sarkaki A, Hashemi SH. The effects of gallic acid on pain and memory following transient global ischemia/ reperfusion in Wistar rats. Avicenna J. 2013; 25: 1- 12.
Corvino V, Marchese E, Michetti F. Neuroprotectivestrantegics in hippocampal neuro degeneration induced by the neurotoxicant trimethylyin. Neurochem Res. 2012; 10: 1- 14.
Shuto M, Seko K, Kuramoto N, Sugiyama C, Kawada K, Yoneyama M. Activation of c-Jun N- terminal kinase cascades is involved in part of the neuronaldegeneration induced by trimethyltin in cortical neurons of mice. J Pharmacol Sci. 2009; 109: 60- 70.
Mignini F, Nasuti C, Artico M, Giovannetti F, Fabrizi C, Fumagalli L, et al. Effects of trimethyltin on hippocampal dopaminergic markers and cognitive behaviour. Int J Immunopathol Pharmacol. 2012; 25 (4): 1107- 1119.
Park HJ, Shim HS, Ahn YH, Kim KS, Park KJ, Choi WK, et al. Tremellafuciformis enhances the neurite outgrowth of PC12 cells and restores trimethyltin- induced impairment of memory in rats via activation of CREB transcription and cholinergic systems. Behav Brain Res. 2012; 229 (1): 82- 90.
Ogita K, Nishiyama N, Sugiyama C, Higuchi K, Yoneyama M, Yoneda Y. Regeneration of granule neurons after lesioning of hippocampal dentate gyrus: evaluation using adult mice treated with trimethyltin chloride as a model. J Neurosci Res. 2005; 82 (5): 609- 621.
Lattanzi W, Corvino V, Di Maria V, Michetti F, Geloso MC. Gene expression profiling as a tool to investigate the molecular machinery activated during hippocampal neurodegeneration induced by trimethyltin (TMT) administration. Int J Mol Sci. 2013; 14 (8): 16817- 16835.
Kikuta M, Shiba T, Yoneyama M, Kawada K, Yamaguchi T, Hinoi E, et al. Invivo and invitro treatment with edaravone promotes proliferation of neural progenitor cells generated following neuronal loss in the mouse dentate gyrus. J Pharmacol Sci. 2013; 121 (1): 74- 83.
Lee S, Yang M, Kim J. Trimethyltin- induced hippocampal neural generation: A mechanism-based review. US National Library Med National Inst Health. 2016; 125: 187- 199.
Funk JA, Gohlke J, Kraft AD, McPherson CA, Collins JB, Jean Harry G. Voluntary exercise protects hippocampal neurons from trimethyltin injury: possible role of Interlukin-6 to modulate tumor necrosis factor receptor- mediated neurotoxicity. Brain Behav Immun. 2011; 25 (6): 1063- 1077.
Mansouri TM, Farbood Y, Sameri MJ, Sarkaki A, Naghizadeh B, Rafeirad M. Neuroprotective effects of oral gallic acid against oxidative stress induced by 6-hydroxydopamine in rats. Food Chem. 2013; 138: 1028- 1033.
Abdel A, Yousef AJ. Gallic acid and p- comaric acid attenuate type 2 diabetes-induced neurodegeneration in rats. US National Library Med National Inst Health. 2017; 7 (2): 97- 106.