Anti-Inflammatory Potential of Newly Synthesized 4-[(Butylsulfinyl)methyl]-1,2-benzenediol in Lipopolysaccharide-Stimulated BV2 Microglia

Molecules

Guk-Heui Jo⁷  Il-Whan Choi²  Jin-Woo Jeong⁵  Gi-Young Kim¹  Jinwoo Kim⁶  Hongsuk Suh⁶  Chung-Ho Ryu⁴  Wun-Jae Kim³  Yung Hyun Choi⁷ 

[1] Department of Marine Life Sciences, Jeju National University, Jeju 690-756, Korea; E-Mail:;Department of Microbiology, College of Medicine, Inje University, Busan 608-756, Korea; E-Mail:;Department of Urology, College of Medicine, Chungbuk National University, Cheongju 361-763, Korea; E-Mail:;Division of Applied Life Science, Gyeongsang National University, Jinju 660-701, Korea; E-Mail:;Division of Applied Life Science (BK21 Plus), Gyeongsang National University, Jinju 660-701, Korea; E-Mail:;Department of Chemistry and Chemistry Institute for Functional Materials, Pusan National University, Busan 609-735, Korea; E-Mails:;Department of Biochemistry, College of Korean Medicine, Dongeui University, Busan 614-052, Korea; E-Mail:

关键词: 4-[(butylsulfinyl)methyl]-1;    2-benzenediol;    BV2 microglia;    anti-inflammation;    NF-κB;    MAPKs;    PI3K/Akt;   

DOI  :  10.3390/molecules191016609

来源: mdpi

【 摘 要 】

In this study, we investigated the anti-inflammatory effects of newly synthesized 4-[(butylsulfinyl)methyl]-1,2-benzenediol (SMBD) in lipopolysaccharide (LPS)-stimulated BV2 microglia and the subsequent signaling events. Following stimulation with LPS, elevated production of nitric oxide (NO) and prostaglandin E₂ (PGE₂) was detected in BV2 cells; however, SMBD pretreatment inhibited the production of NO and PGE₂ through suppressing gene expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), respectively, at non-toxic concentrations. LPS-stimulated gene expression and production of interleukin (IL)-1β and tumor necrosis factor (TNF)-α were also significantly reduced by SMBD. The anti-inflammatory effects of SMBD were associated with suppression of LPS-induced nuclear translocation of nuclear factor-kappa B (NF-κB), and phosphorylation of mitogen-activated protein kinases (MAPKs) and Akt, a phosphatidylinositol 3-kinase (PI3K) downstream effector. Therefore, the present results demonstrate that SMBD down-regulates inflammatory gene expression by inhibiting the activation of NF-κB through interference with the activation of MAPKs and PI3K/Akt signaling. Taken together, our data suggest that SMBD may have potential to be developed into an effective anti-inflammatory agent.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.