کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6493330 | 1418052 | 2018 | 34 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neuroprotective effect of Annona glabra extract against ethanol-induced apoptotic neurodegeneration in neonatal rats
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کلمات کلیدی
Annona glabraDTNBTBARSMDAGPXGSHTCASDSFACS5,5′-dithiobis-2-nitrobenzoic acid - 5،5'-dithiobis-2-nitrobenzoic acidAChE - آهیEthanol - اتانولacetylcholine esterase - استیل کولین استرازtrichloroacetic acid - اسید ترشکلراکتیکTerminal deoxynucleotidyl transferase dUTP nick end labeling - ترمینال deoxynucleotidyl transferase dUTP نام نهایی پایان نامهNeurodegeneration - تولید نوروژنیکTUNEL - تونلApoptosis - خزان یاختهایfluorescence-activated cell sorting - دسته بندی سلول های فعال فلورسنسSOD - سدsodium dodecyl sulfate - سدیم دودسیل سولفاتAge - سنSuperoxide dismutase - سوکسوکس دیسموتازmalondialdehyde - مالون دی آلدهیدNeonatal Rats - موش نوزادPropidium iodide - پروتئین یدیدreduced glutathione - کاهش گلوتاتیونglutathione peroxidase - گلوتاتیون پراکسیدازthiobarbituric acid reactive species - گونه های واکنشی اسید تیوباربیتوریک
موضوعات مرتبط
مهندسی و علوم پایه
مهندسی شیمی
بیو مهندسی (مهندسی زیستی)
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
The present study aimed to investigate the neuroprotective effect of Annona glabra extract (AGE) against ethanol-induced neurodegeneration in neonatal rats. AGE is known to contain various pharmacological and therapeutic properties. Phytochemical analysis of AGE was performed to understand the presence of vital therapeutic components. Neonatal rats were assigned to the following groups: group I (normal control rats receiving normal saline), group II (control rats receiving ethanol), and group III (treated rats receiving ethanol-AGE). The lipid peroxidation, reduced glutathione (GSH), glutathione peroxidase (Gpx), superoxide dismutase (SOD), catalase, and acetylcholine esterase (AChE) levels were determined. Behavioral parameters, histological features, neuronal cell viability, and apoptosis were also investigated. The presence of flavonoids, terpenoid, glycosides, steroids, saponins, tannins, anthraquinones, and acidic compounds was noted in the AGE. Ethanol supplementation drastically increased the malondialdehyde (MDA) content to 52.17â¯nmol/g in the control rats (group II). However, the MDA content was reduced to 27.34â¯nmol/g in ethanol-AGE-treated neonatal rats (group III) compared with control rats. The GSH content was substantially reduced, to 33.68â¯mg/g, in control rats compared with in normal control rats. However, the GSH content was significantly increased, to 59.32â¯mg/g, following ethanol-AGE supplementation. Gpx, SOD, catalase, and AChE enzyme activities were increased in treated neonatal rats compared with their respective controls. Locomotor activities, such as crossing, grooming, rearing, and sniffing, were increased in ethanol-AGE-treated neonatal rats compared with controls. Reduced levels of intact pyramidal cells and cells with degenerative alterations appeared in the control rats. However, ethanol-AGE supplementation reduced degenerative alterations and hippocampal damage. Reduced cultured hippocampal neuron cell viability and increased apoptosis were noted in the control rats, whereas these impacts were significantly recovered following ethanol-AGE supplementation. Based on all these data, we concluded that the supplementation of AGE was very effective against ethanol-induced neurodegeneration in neonatal rats.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Photochemistry and Photobiology B: Biology - Volume 181, April 2018, Pages 106-114
Journal: Journal of Photochemistry and Photobiology B: Biology - Volume 181, April 2018, Pages 106-114
نویسندگان
Hongru Ma, Jianfeng Han, Qinchuan Dong,