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Using the microglial cell line, BV-2, as well as primary murine microglial cells, we show here that the β-adrenergic agonist, isoproterenol, suppresses uptake of hydrophobic polystyrene microspheres.
Migration of BV-2 murine microglial cells was assessed with a transwell migration chamber.
T. gondii-infected WT murine microglial cells showed variable kinetics of pro-inflammatory cytokine expression dependent on the parasite strain [ 22].
The antioxidant and anti-inflammatory activities of AE-COS in murine microglial cells (BV-2) were investigated by Ngo et al. [ 97].
The agonists also decreased nitric oxide (NO) production by murine microglial cells and enhanced IL-4 production and suppressed IFN-γ secretion of cultured human T cells.
Of the 17 lignans, six were new and three were potent inhibitors of LPS-induced NO production in murine microglial cells.
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Le et al. reported that TGF-β1 inhibits lipopolysaccharide (LPS -induced phosphoryLPS -inducedth phosphorylationa murine microflial cell line [54].
The murine microglial cell-line (BV-2) was obtained from Dr. R. Donato (University of Perugia, Perugia, Italy).
To check whether B[a]P causes bystander neuronal death by activating microglia, we treated murine microglial cell BV-2 with varying doses of B[a]P, viz.
Cell-lines: The murine microglial cell-line (BV-2) and human embryonic kidney cell line (HEK 293) were obtained from Dr. R. Donato (University of Perugia, Perugia, Italy) and American Type Culture Collection (ATCC, Manassas, VA, USA) respectively.
To test this hypothesis, we performed survivality assay after addition of B[a]P to murine microglial cell line BV-2, in same doses as applied to neuroblastoma cells or primary neurons, and observed no significant decreases in cell survivality.
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