کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5859883 | 1133138 | 2015 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Lead exposure induced microgliosis and astrogliosis in hippocampus of young mice potentially by triggering TLR4-MyD88-NFκB signaling cascades
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کلمات کلیدی
PBSTNFαTLR4LPSGFAPDcxIL-1βAstrogliosis - استرولیوزیسInterleukin-1β - اینترلوکین-1βBrdU - بروموداکسی اوریدینlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP tumor necrosis factor-alpha - تومور نکروز عامل آلفاdoublecortin - دوچرخهLead toxicity - سمیت سربdentate gyrus - شکنج دندانه دارPhosphate buffered saline - فسفات بافر شورlipopolysaccharide - لیپوپلی ساکاریدmicrogliosis - میکروگلویوزیسNeurogenesis - نوروژنزHippocampus - هیپوکامپ Glial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالToll-like receptor-4 - گیرنده سفارشی -4
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
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چکیده انگلیسی
Proper proliferation and differentiation of neural stem cells or progenitors in hippocampus is critical to learn and memory functions, which might be disturbed by lead toxicity particularly in young individuals. While astroglial and microglial cells are known to play an important role in regulating neurogenesis of hippocampus, their abnormal response and influence on hippocampal neurogenesis remains unclear. In this study, therefore, glial response including microgliosis, astrogliogenesis and mediating involvement of TLR4-MyD88-NFκB signaling cascades were observed in hippocampus of young mice by animal model with lead (plumbum, Pb) exposure. It revealed that (1) significant microglial activation occurred in hippocampus soon following Pb exposure; (2) increased levels of TLR4, MyD88, NFκB expression were concomitantly detected; (3) BrdU-incorporated progenitor cells were observed in dentate gyrus with significantly-increased numbers at d28 in Pb insult group; (4) obvious astrogliogenesis was observed while these doublecortin-labeled differentiated neurons were not significantly changed in hippocampus; (5) administration of MyD88 inhibitory peptide attenuated or relieved above effects; (6) enhanced expression levels of IL-1β, TNFα, p38MAPK and ERK1/2 were also detected in hippocampus, indicating potential implication of inflammatory response and MAPK signaling activation in lead-induced microgliosis and astrogliosis. Data of this study overall have indicated that lead exposure could trigger or induce abnormal microgliosis and astrogliogenesis in the hippocampus of young mice through triggering TLR4-MyD88-NFκB signaling cascades, which might possibly thereafter disturb hippocampal neurogenesis and functional plasticity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology Letters - Volume 239, Issue 2, 3 December 2015, Pages 97-107
Journal: Toxicology Letters - Volume 239, Issue 2, 3 December 2015, Pages 97-107
نویسندگان
Jin-Tao Liu, Bei-Yu Chen, Jie-Qiong Zhang, Fang Kuang, Liang-Wei Chen,