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Neuroprotective effects of cyclooxygenase-2 inhibitor celecoxib against toxicity of LPS-stimulated macrophages toward motor neurons

	author = {Yong Huang and Jing Liu and Li-zhen Wang and Wei-yu Zhang and Xing-zu Zhu},
	title = {Neuroprotective effects of cyclooxygenase-2 inhibitor celecoxib against toxicity of LPS-stimulated macrophages toward motor neurons},
	journal = {Acta Pharmacologica Sinica},
	volume = {26},
	number = {8},
	year = {2016},
	keywords = {},
	abstract = {Aim: To establish an in vitro injured motor neuronal model and investigate the neuroprotective effects and possible mechanism of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, on this model.
Methods: After macrophages were stimulated with lipopolysaccharide (LPS)+interferon-gamma (IFN-gamma) in the presence or absence of celecoxib for 24 h, the cell-free supernatant of LPS-stimulated macrophages was transferred to the culture of NSC34 cells. Viability of NSC34 cells was assessed by MTT assay after a further 24 h and 72 h incubation. After macrophages were stimulated by LPS+IFN-gamma for 12 h or 24 h, the release of prostaglandin E2 (PGE2), nitric oxide (NO), reactive oxygen species (ROS), tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) from macrophages was measured by radioimmunoassay, Griess assay, fluorescence assay and enzyme-linked immunosorbent assay, respectively. The mRNA levels of COX-2, inducible nitric oxide synthase (iNOS), TNF-alpha and IL-1beta in macrophages were determined by reverse transcription-polymerase chain reaction after macrophages were stimulated for 6 h and 12 h.
Results: The supernatant of LPS-stimulated mouse macrophages induced the death of NSC34 cells and celecoxib protected the NSC34 cells against this toxicity. The LPS-induced increases in the release of PGE2, NO, TNF-alpha and IL-1beta from macrophages were attenuated by pre-treatment with celecoxib. However, celecoxib showed no effect on the ROS levels upregulated by LPS+IFN-gamma in the macrophage supernatant. The mRNA levels of COX-2, iNOS, TNF-alpha and IL-1beta were increased in LPS-activated macrophages and, except COX-2, reduced by pre-treatment with celecoxib.
Conclusion: An in vitro injured motor neuronal model was established by using the toxicity of LPS-stimulated mouse macrophages toward motor neuronal NSC34 cells. In this model, celecoxib exerted neuroprotective effects on motor neurons via an inhibition of the neurotoxic secretions from activated macrophages.},
	issn = {1745-7254},	url = {}