کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5737852 | 1614733 | 2017 | 36 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
NLRP3 inflammasome activation contributes to long-term behavioral alterations in mice injected with lipopolysaccharide
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کلمات کلیدی
TNFαLPSASCNLRP3Tail suspension test - آزمون تعلیق دمforced swim test - آزمون شناور اجباریDepression - افسردگیNLRP3 inflammasome - التهاب NLRP3interleukin - اینترلوکینELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاtumor necrosis factor α - تومور نکروز عامل αRecognition memory - حافظه تشخیص یا شناختlipopolysaccharide - لیپوپلی ساکاریدapoptosis-associated speck-like protein - وابسته به پروپوفون وابسته به آپوپتوز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Lipopolysaccharide (LPS) might affect the central nervous system by causing neuroinflammation, which subsequently leads to brain damage and dysfunction. In this study, we evaluated the role of nod-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome activation in long-term behavioral alterations of 8-week-old male C57BL/6 mice injected intraperitoneally with LPS (5 mg/kg). At different time points after injection, we assessed locomotor function with a 24-point neurologic deficit scoring system and the rotarod test; assessed recognition memory with the novel object recognition test; and assessed emotional abnormality (anhedonia and behavioral despair) with the tail suspension test, forced swim test, and sucrose preference test. We also assessed protein expression of NLRP3, apoptosis-associated speck-like protein (ASC), and caspase-1 p10 in hippocampus by Western blotting; measured levels of interleukin (IL)-1β, IL-18, tumor necrosis factor α (TNFα), and IL-10 in hippocampus; measured TNFα and IL-1β in serum by ELISA; and evaluated microglial activity in hippocampus by Iba1 immunofluorescence. We found that LPS-injected mice displayed long-term depression-like behaviors and recognition memory deficit; elevated expression of NLRP3, ASC, and caspase-1 p10; increased levels of IL-1β, IL-18, and TNFα; decreased levels of IL-10; and increased microglial activation. These effects were blocked by the NLRP3 inflammasome inhibitor Ac-Tyr-Val-Ala-Asp-chloromethylketone. The results demonstrate proof of concept that NLRP3 inflammasome activation contributes to long-term behavioral alterations in LPS-exposed mice, probably through enhanced inflammation, and that NLRP3 inflammasome inhibition might alleviate peripheral and brain inflammation and thereby ameliorate long-term behavioral alterations in LPS-exposed mice.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 343, 20 February 2017, Pages 77-84
Journal: Neuroscience - Volume 343, 20 February 2017, Pages 77-84
نویسندگان
Wei Zhu, Feng-Sheng Cao, Jun Feng, Hua-Weng Chen, Jie-Ru Wan, Qing Lu, Jian Wang,