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Aspirin-triggered lipoxin A4 attenuates LPS-induced pro-inflammatory responses by inhibiting activation of NF-κB and MAPKs in BV-2 microglial cells.
J Neuroinflammation 2011; 8:95JN

Abstract

BACKGROUND

Microglial activation plays an important role in neurodegenerative diseases through production of nitric oxide (NO) and several pro-inflammatory cytokines. Lipoxins (LXs) and aspirin-triggered LXs (ATLs) are considered to act as 'braking signals' in inflammation. In the present study, we investigated the effect of aspirin-triggered LXA4 (ATL) on infiammatory responses induced by lipopolysaccharide (LPS) in murine microglial BV-2 cells.

METHODS

BV-2 cells were treated with ATL prior to LPS exposure, and the effects of such treatment production of nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) were analysed by Griess reaction, ELISA, western blotting and quantitative RT-PCR. Moreover, we investigated the effects of ATL on LPS-induced nuclear factor-κB (NF-κB) activation, phosphorylation of mitogen-activated protein kinases (MAPKs) and activator protein-1 (AP-1) activation.

RESULTS

ATL inhibited LPS-induced production of NO, IL-1β and TNF-α in a concentration-dependent manner. mRNA expressions for iNOS, IL-1β and TNF-α in response to LPS were also decreased by ATL. These effects were inhibited by Boc-2 (a LXA4 receptor antagonist). ATL significantly reduced nuclear translocation of NF-κB p65, degradation of the inhibitor IκB-α, and phosphorylation of extracellular signal-regulated kinase (ERK) and p38 MAPK in BV-2 cells activated with LPS. Furthermore, the DNA binding activity of NF-κB and AP-1 was blocked by ATL.

CONCLUSIONS

This study indicates that ATL inhibits NO and pro-inflammatory cytokine production at least in part via NF-κB, ERK, p38 MAPK and AP-1 signaling pathways in LPS-activated microglia. Therefore, ATL may have therapeutic potential for various neurodegenerative diseases.

Authors+Show Affiliations

Department of Anesthesiology and Critical Care, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21831303

Citation

Wang, Yan-Ping, et al. "Aspirin-triggered Lipoxin A4 Attenuates LPS-induced Pro-inflammatory Responses By Inhibiting Activation of NF-κB and MAPKs in BV-2 Microglial Cells." Journal of Neuroinflammation, vol. 8, 2011, p. 95.
Wang YP, Wu Y, Li LY, et al. Aspirin-triggered lipoxin A4 attenuates LPS-induced pro-inflammatory responses by inhibiting activation of NF-κB and MAPKs in BV-2 microglial cells. J Neuroinflammation. 2011;8:95.
Wang, Y. P., Wu, Y., Li, L. Y., Zheng, J., Liu, R. G., Zhou, J. P., ... Yao, S. L. (2011). Aspirin-triggered lipoxin A4 attenuates LPS-induced pro-inflammatory responses by inhibiting activation of NF-κB and MAPKs in BV-2 microglial cells. Journal of Neuroinflammation, 8, p. 95. doi:10.1186/1742-2094-8-95.
Wang YP, et al. Aspirin-triggered Lipoxin A4 Attenuates LPS-induced Pro-inflammatory Responses By Inhibiting Activation of NF-κB and MAPKs in BV-2 Microglial Cells. J Neuroinflammation. 2011 Aug 10;8:95. PubMed PMID: 21831303.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Aspirin-triggered lipoxin A4 attenuates LPS-induced pro-inflammatory responses by inhibiting activation of NF-κB and MAPKs in BV-2 microglial cells. AU - Wang,Yan-Ping, AU - Wu,Yan, AU - Li,Long-Yan, AU - Zheng,Jin, AU - Liu,Ren-Gang, AU - Zhou,Jie-Ping, AU - Yuan,Shi-Ying, AU - Shang,You, AU - Yao,Shang-Long, Y1 - 2011/08/10/ PY - 2011/03/24/received PY - 2011/08/10/accepted PY - 2011/8/12/entrez PY - 2011/8/13/pubmed PY - 2012/2/24/medline SP - 95 EP - 95 JF - Journal of neuroinflammation JO - J Neuroinflammation VL - 8 N2 - BACKGROUND: Microglial activation plays an important role in neurodegenerative diseases through production of nitric oxide (NO) and several pro-inflammatory cytokines. Lipoxins (LXs) and aspirin-triggered LXs (ATLs) are considered to act as 'braking signals' in inflammation. In the present study, we investigated the effect of aspirin-triggered LXA4 (ATL) on infiammatory responses induced by lipopolysaccharide (LPS) in murine microglial BV-2 cells. METHODS: BV-2 cells were treated with ATL prior to LPS exposure, and the effects of such treatment production of nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) were analysed by Griess reaction, ELISA, western blotting and quantitative RT-PCR. Moreover, we investigated the effects of ATL on LPS-induced nuclear factor-κB (NF-κB) activation, phosphorylation of mitogen-activated protein kinases (MAPKs) and activator protein-1 (AP-1) activation. RESULTS: ATL inhibited LPS-induced production of NO, IL-1β and TNF-α in a concentration-dependent manner. mRNA expressions for iNOS, IL-1β and TNF-α in response to LPS were also decreased by ATL. These effects were inhibited by Boc-2 (a LXA4 receptor antagonist). ATL significantly reduced nuclear translocation of NF-κB p65, degradation of the inhibitor IκB-α, and phosphorylation of extracellular signal-regulated kinase (ERK) and p38 MAPK in BV-2 cells activated with LPS. Furthermore, the DNA binding activity of NF-κB and AP-1 was blocked by ATL. CONCLUSIONS: This study indicates that ATL inhibits NO and pro-inflammatory cytokine production at least in part via NF-κB, ERK, p38 MAPK and AP-1 signaling pathways in LPS-activated microglia. Therefore, ATL may have therapeutic potential for various neurodegenerative diseases. SN - 1742-2094 UR - https://www.unboundmedicine.com/medline/citation/21831303/Aspirin_triggered_lipoxin_A4_attenuates_LPS_induced_pro_inflammatory_responses_by_inhibiting_activation_of_NF_κB_and_MAPKs_in_BV_2_microglial_cells_ L2 - https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-8-95 DB - PRIME DP - Unbound Medicine ER -