Tags

Type your tag names separated by a space and hit enter

A novel synthetic HTB derivative, BECT inhibits lipopolysaccharide-mediated inflammatory response by suppressing the p38 MAPK/JNK and NF-κB activation pathways.
Pharmacol Rep 2014; 66(3):471-9PR

Abstract

Activated microglia cells are well recognized as mediators of neuroinflammation, as they release nitric oxide and pro-inflammatory cytokines in various neuroinflammatory diseases. Thus, suppressing microglial activation may alleviate neuroinflammatory and neurodegenerative processes. In the present study, we synthesized and investigated the anti-neuroinflammatory effect of a novel HTB (2-hydroxy-4-trifuoromethylbenzoic acid) derivative in lipopolysaccharide (LPS)-stimulated microglial cells. Among the synthesized derivatives, the BECT [But-2-enedioic acid bis-(2-carboxy-5-trifluoromethyl-phenyl) ester] significantly decreased production of nitric oxide and other pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-1β, and interleukin-6 in microglial cells. BECT also mitigated the expression of inducible nitric oxide synthase and cyclooxygenase-2 at both the mRNA and protein levels. Further mechanistic studies demonstrated that the HTB derivative inhibited phosphorylation of JNK and p38 mitogen-activated protein kinase and nuclear translocation of nuclear factor kappa-B in LPS-stimulated BV-2 microglial cells. Thus BECT, our novel synthesized compound have anti-inflammatory activity in microglial cells, and may have therapeutic potential for treating neuroinflammatory diseases.

Authors+Show Affiliations

Department of Biotechnology, Research Institute for Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of Korea.Department of Biotechnology, Research Institute for Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of Korea.Department of Molecular Science and Technology, Ajou University, Suwon 443-749, Republic of Korea.Department of Biotechnology, Research Institute for Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of Korea.Department of Biotechnology, Research Institute for Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of Korea.Department of Molecular Science and Technology, Ajou University, Suwon 443-749, Republic of Korea.Department of Biotechnology, Research Institute for Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of Korea. Electronic address: choidk@kku.ac.kr.

Pub Type(s)

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

Language

eng

PubMed ID

24905526

Citation

Kang, Seong-Mook, et al. "A Novel Synthetic HTB Derivative, BECT Inhibits Lipopolysaccharide-mediated Inflammatory Response By Suppressing the P38 MAPK/JNK and NF-κB Activation Pathways." Pharmacological Reports : PR, vol. 66, no. 3, 2014, pp. 471-9.
Kang SM, More SV, Park JY, et al. A novel synthetic HTB derivative, BECT inhibits lipopolysaccharide-mediated inflammatory response by suppressing the p38 MAPK/JNK and NF-κB activation pathways. Pharmacol Rep. 2014;66(3):471-9.
Kang, S. M., More, S. V., Park, J. Y., Kim, B. W., In, P. J., Yoon, S. H., & Choi, D. K. (2014). A novel synthetic HTB derivative, BECT inhibits lipopolysaccharide-mediated inflammatory response by suppressing the p38 MAPK/JNK and NF-κB activation pathways. Pharmacological Reports : PR, 66(3), pp. 471-9. doi:10.1016/j.pharep.2013.08.015.
Kang SM, et al. A Novel Synthetic HTB Derivative, BECT Inhibits Lipopolysaccharide-mediated Inflammatory Response By Suppressing the P38 MAPK/JNK and NF-κB Activation Pathways. Pharmacol Rep. 2014;66(3):471-9. PubMed PMID: 24905526.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A novel synthetic HTB derivative, BECT inhibits lipopolysaccharide-mediated inflammatory response by suppressing the p38 MAPK/JNK and NF-κB activation pathways. AU - Kang,Seong-Mook, AU - More,Sandeep Vasant, AU - Park,Ju-Young, AU - Kim,Byung-Wook, AU - In,Park Jeong, AU - Yoon,Sung-Hwa, AU - Choi,Dong-Kug, Y1 - 2014/03/06/ PY - 2013/02/07/received PY - 2013/08/01/revised PY - 2013/08/20/accepted PY - 2014/6/7/entrez PY - 2014/6/7/pubmed PY - 2015/2/11/medline KW - HTB derivative KW - Lipopolysaccharide KW - Microglia KW - Neurodegenerative disease KW - Neuroinflammation SP - 471 EP - 9 JF - Pharmacological reports : PR JO - Pharmacol Rep VL - 66 IS - 3 N2 - Activated microglia cells are well recognized as mediators of neuroinflammation, as they release nitric oxide and pro-inflammatory cytokines in various neuroinflammatory diseases. Thus, suppressing microglial activation may alleviate neuroinflammatory and neurodegenerative processes. In the present study, we synthesized and investigated the anti-neuroinflammatory effect of a novel HTB (2-hydroxy-4-trifuoromethylbenzoic acid) derivative in lipopolysaccharide (LPS)-stimulated microglial cells. Among the synthesized derivatives, the BECT [But-2-enedioic acid bis-(2-carboxy-5-trifluoromethyl-phenyl) ester] significantly decreased production of nitric oxide and other pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-1β, and interleukin-6 in microglial cells. BECT also mitigated the expression of inducible nitric oxide synthase and cyclooxygenase-2 at both the mRNA and protein levels. Further mechanistic studies demonstrated that the HTB derivative inhibited phosphorylation of JNK and p38 mitogen-activated protein kinase and nuclear translocation of nuclear factor kappa-B in LPS-stimulated BV-2 microglial cells. Thus BECT, our novel synthesized compound have anti-inflammatory activity in microglial cells, and may have therapeutic potential for treating neuroinflammatory diseases. SN - 1734-1140 UR - https://www.unboundmedicine.com/medline/citation/24905526/A_novel_synthetic_HTB_derivative_BECT_inhibits_lipopolysaccharide_mediated_inflammatory_response_by_suppressing_the_p38_MAPK/JNK_and_NF_κB_activation_pathways_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1734-1140(14)00047-4 DB - PRIME DP - Unbound Medicine ER -