DGIST Scholar: Caffeine reduces LPS-induced pro-inflammatory microglial response and autophagic suppression by inducing autophagy.

Title: Caffeine reduces LPS-induced pro-inflammatory microglial response and autophagic suppression by inducing autophagy.

Citation: Kim, Eun Jung. (2016). Caffeine reduces LPS-induced pro-inflammatory microglial response and autophagic suppression by inducing autophagy. doi: 10.22677/thesis.2294169

Subject: Autophagy ; Microglia ; Caffeine ; Neuroinflammation ; Lipopolysaccharide ; 미세아교세포 ; 카페인 ; 뇌염증 ; 자가소화작용

Abstract: Background Microglia are the resident immune cells in the brain that are sensitive to changes in their local environment. They respond to pathogen or danger signals by triggering brain immune response. Many drugs working on the nervous system can target microglia as well as neurons. Caffeine is the most widely consumed psychoactive drug across various age groups worldwide. However, little is known whether caffeine can affect microglia function. This study is aimed to examine whether caffeine regulates microglia functions and autophagy is involved in the action of caffeine on microglia, since autophagy plays a critical role in cellular immune response. ⓒ 2016 DGIST

Table Of Contents: 1. Introduction 1 --
2. Materials and methods 4 --
2.1 Antibodies and reagents 4 --
2.2 Cell culture 4 --
2.3 plasmids and magnetofection 5 --
2.4 Sh-RNA Lentiviral production 5 --
2.5 Western blotting 5 --
2.6 Immunocytochemistry 6 --
2.7 qRT-PCR 6 --
2.8 Enzyme-linked immunosorbent assay (ELISA) 7 --
2.9 Statistical analysis 7 --
3. Results 8 --
3.1 LPS suppressed autophagic flux in BV-2 and primary microglia 8 --
3.2 Caffeine induced autophagy in BV-2 and primary microglia 10 --
3.3 Autophagy inhibition blocked caffeine-induced autophagy and anti-apoptotic effect 11 --
3.4 Caffeine rescued LPS-induced autophagic suppression and ameliorated LPS-induced inflammation 12 --
3.5 Ablation of autophagy blocked caffeine’s anti-inflammatory effect 13 --
4. Discussion 15 --
5. Figure legends 17 --
6. Figures 19 --
Reference 27

URI: http://dgist.dcollection.net/jsp/common/DcLoOrgPer.jsp?sItemId=000002294169
http://hdl.handle.net/20.500.11750/1431

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