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A multifunctional alanine-rich anti-inflammatory peptide BCP61 showed potent inhibitory effects by inhibiting both
Yun Hee Choi1, Yoon Seok Choi1, Young Kyun Kim1
1Department of Pharmacy, College of Pharmacy, Chosun University, Gwangju, 501-759, Korea.
Abstract:
The purified BCP61 was reported to be a unique low-molecular-weight (MW) anti-microbial peptide because of its non-identical alanine-rich N-terminal sequence. In this study, we investigated the anti-inflammatory effects of BCP61 on induction of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), pro-inflammatory cytokines, nuclear factor-kappa B (NF-κB), and mitogen-activated protein kinases (MAPKs) in lipopolysaccharide (LPS)-stimulated Raw 264.7 cells. The treatment with BCP61, with varying concentrations of 10, 50, and 100 μg/mL, inhibited levels of expression of LPS-induced NF-κB and MAPKs (extracellular signal-related kinases (ERKs), c-Jun NH2-terminal kinase (JNK), and mitogen-activated protein (p38)) as well as production of pro-inflammatory mediators, such as nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6). The results suggested that BCP61 prevents inhibitor of kappa B (IκBα) phosphorylation and degradation, thereby inhibiting the nuclear translocation of the p65 protein. We do report that the use of BCP61 in the treatment of inflammation as well as microbial infection could be a potent therapeutic candidate.
Insights
BCP61, an antimicrobial peptide, demonstrates significant anti-inflammatory effects by inhibiting key inflammatory pathways and mediators. This suggests BCP61
Area of Science:
- Biochemistry
- Immunology
- Pharmacology
Background:
- BCP61 is a unique low-molecular-weight antimicrobial peptide.
- Its N-terminal sequence is rich in alanine and non-identical.
Purpose of the Study:
- To investigate the anti-inflammatory effects of BCP61.
- To examine BCP61's impact on inflammatory mediators and signaling pathways in LPS-stimulated Raw 264.7 cells.
Main Methods:
- Treatment of Raw 264.7 cells with varying concentrations of BCP61 (10, 50, 100 μg/mL).
- Assessment of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), pro-inflammatory cytokines (TNF-α, IL-6), NF-κB, and MAPKs (ERK, JNK, p38) expression and production.
- Evaluation of IκBα phosphorylation and degradation, and p65 nuclear translocation.
Main Results:
- BCP61 inhibited LPS-induced NF-κB and MAPK signaling pathways.
- BCP61 reduced the production of pro-inflammatory mediators including nitric oxide (NO) and prostaglandin E2 (PGE2).
- BCP61 prevented IκBα phosphorylation and degradation, inhibiting p65 nuclear translocation.
Conclusions:
- BCP61 exhibits potent anti-inflammatory properties.
- BCP61 may serve as a therapeutic candidate for treating inflammation and microbial infections.
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