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Mouse microglial cells (BV2) were cultured using DMEM/F12 media.
In the present research, we studied whether DHMEQ would inhibit the activation of mouse microglial cells.
A partially neutralizing IgG monoclonal antibody (MAb) CL55, specific for MV H protein, at 10 μg/ml enhanced MV infection in mouse microglial cells by 13 14-fold 13 14-fold
Here we report the synthesis of a number of non-steroidal anti-inflammatory drug (NSAID) conjugates, and the evaluation of their anti-inflammatory effects in lipopolysaccharide (LPS -stimulated BV-2 microgLPS -stimulatedprimary mouse microglial cells.
In primary mouse microglial cells exposure to IFN-γ (5 and 10 ng/ml; 48 h) or TNF-α (20 ng/ml; 48 h) alone were unable to induce iNOS expression; however, when cells were exposed to both cytokines together, the expression of this enzyme and the NO production in culture media were found significantly increased.
Similarly, in BV-2 mouse microglial cells, ibudilast had an inhibitory effect on Tat-induced TNFα production.
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It also inhibited LPS-induced secretions of TNF-α and IL-6 from mouse microglial cell line 6-1 cells.
Long et al. [84, 85] demonstrated that TiO2 NPs increased the levels of ROS, H2O2, and O2 − in BV2 cells (an immortalized mouse microglial cell line).
Mouse microglial cell line BV-2 was a kind gift from Dr. Steve Levison, University of Medicine and Dentistry, New Jersey, USA.
Mouse microglial cell line (BV2 cells) were cultured in similar culture medium, but using 10% heat-inactivated FBS instead.
The mouse microglial cell line EOC-20 was obtained from the American Type Culture Collection (ATCC CRL-2469; ATCC, Manassas, VA, USA).
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