1403/01/30
شهرام قاسمی میر

شهرام قاسمی میر

مرتبه علمی: دانشیار
ارکید:
تحصیلات: دکترای تخصصی
اسکاپوس:
دانشکده: دانشکده شیمی
نشانی:
تلفن: 01135302388

مشخصات پژوهش

عنوان
Acute administration of sulfur-doped g-C3N4 induces cognitive deficits and exacerbates the levels of glial activation in mouse hippocampus
نوع پژوهش
JournalPaper
کلیدواژه‌ها
Sulfur-doped g-C3N4, Neurotoxicity, Spatial memory, Hippocampus, Neuronal loss
سال
2021
مجله BRAIN RESEARCH BULLETIN
شناسه DOI
پژوهشگران Farangis Ramezani ، Maryam Ghasemi-Kasman ، Nasrin Nosratiyan ، Shahram Ghasemi ، farideh feizi

چکیده

During the last decades, graphitic carbon nitride (g-C3N4) has attracted increasing attention in several biomedical fields. In this study, the effects of sulfur-doped g-C3N4 (TCN) on cognitive function and histopathology of hippocampus were investigated in mice. The characteristics of synthetized sample were evaluated by X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR), Raman spectroscopy, transmission electron microscopy (TEM), field emission scanning electron microscopy (FESEM), and energy dispersive X-ray (EDX). Twenty-four male NMRI mice received vehicle, TCN at doses of 50, 150, or 500 mg/kg via gavage for one week. Morris water maze test was done to assess the cognitive function at day 14 post TCN administration. Nissl staining was used to determine the number of dark cells in the hippocampus. Immunostaining against NeuN, GFAP, and Iba1 was done to evaluate the neuronal density and levels of glial activation, respectively. Behavioral tests indicated that TCN reduces the spatial learning and memory in a dose-dependent manner. Histological evaluations showed an increased level of neuronal loss and glial activation in the hippocampus of TCN treated mice at doses of 150 and 500 mg/kg. Overall, our data indicate that TCN induces the cognitive impairment that is partly mediated via its exacerbating impacts on neuronal loss and glial activation.