15,16-Dihydrotanshinone I suppresses the activation of BV-2 cell, a murine microglia cell line, by lipopolysaccharide

2006 ◽  
Vol 48 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Pyeongjae Lee ◽  
Jinyoung Hur ◽  
Jongseok Lee ◽  
Jeongmin Kim ◽  
Jueun Jeong ◽  
...  
2017 ◽  
Vol 111 ◽  
pp. 174-181 ◽  
Author(s):  
Hua Zhao ◽  
Aihua Liu ◽  
Yuhui Cui ◽  
Zhang Liang ◽  
Bingxue Li ◽  
...  

2013 ◽  
Vol 10 (1-2) ◽  
pp. 87-92 ◽  
Author(s):  
M. A. Miah ◽  
S. S. Choi ◽  
S. H. Lee

Microglia activation plays a pivotal role in varying stress conditions including oxidation, inflammation and certain neurodegenerative diseases. iNOS and PrxI are known to up regulate in LPS-activated microglia in vitro. Natural fruits including various berries containing both antioxidants and anti-inflammatory polyphenols may attenuate such stress conditions. We investigated the effects of blueberry extracts (BBE) on the LPS-activated stress related genes up regulation using BV-2 microglia cells in vitro. BV-2 cells were cultured in DMEM with 10% FBS, were pre-incubated with 50 µg/ml BBE for 0, 1 h and 12 h, and treated with 1µg/ml LPS for 24 h . The levels of mRNA and protein expression showed significant differences in iNOS and PrxI among the treatment groups. Hoechst and PI staining showed that BBE protects cells from activation induced death. Intracellular levels of ROS were increased by LPS stimulation over the level in the control cells whereas BBE treatment significantly lowered the LPS stimulated ROS levels at a time dependent manner. High expressions of iNOS and PrxI are indication of microglia activation and treatment with BBE in LPS-activated BV-2 cells cause down regulation of stress-related genes expression and protect the cells from over activation and death. DOI: http://dx.doi.org/10.3329/bjvm.v10i1-2.15651


2014 ◽  
Vol 96 (9) ◽  
pp. 1414-1427
Author(s):  
Yamato Sakamoto ◽  
Yumi Nakamoto ◽  
Tetsuyuki Wada ◽  
Seiji Ichida ◽  
Takeshi Minami

2004 ◽  
Vol 367 (1) ◽  
pp. 10-13 ◽  
Author(s):  
Rolis Chien-Wei Hou ◽  
Chia-Chuan Wu ◽  
Chia-Hung Yang ◽  
Kee-Ching G Jeng

2020 ◽  
Author(s):  
Mai Fukasawa ◽  
Yoshihiro Kudo ◽  
Anna Nishihara ◽  
Kensuke Nishio ◽  
Tomoka Itou ◽  
...  

Abstract Allograft inflammatory factor-1 (AIF-1) is a marker for activated microglia. Unilateral common carotid artery occlusion (UCCAO) was conducted to elucidate mechanisms that regulate AIF-1 expression in C57BL/6 male mice. Immunohistochemical reactivity of microglia against anti-AIF-1 antibody was increased significantly in the brain of this model. The increased AIF-1 production was further confirmed by ELISA using brain homogenate. Real-time PCR demonstrated that the increased AIF-1 production was regulated at the transcriptional level. Serum AIF-1 levels were further examined by ELISA and marked increase was observed on Day 1 of UCCAO. To examine the influence of AIF-1, immunohistochemical staining was performed and revealed that the immunoreactivity against anti-Iba-1 antibody was significantly increased in various organs. Among them, the accumulation of Iba-1+ cells were observed prominently in the spleen. Intraperitoneal injection of minocycline, a potent microglia inhibitor, reduced the number of Iba-1+ cells suggesting microglia activation-dependent accumulation. Based on these results, AIF-1 expression was further examined in the murine microglia cell line MG6. AIF-1 mRNA expression and secretion were up-regulated when the cells were cultured under hypoxic condition. Importantly, stimulation of the cells with recombinant AIF-1 induced the expression of AIF-1 mRNA. These results suggest that increased AIF-1 production by microglia in cerebral ischemia regulate the AIF-1 mRNA expression at least in part by an autocrine manner.


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