期刊
CURRENT ISSUES IN MOLECULAR BIOLOGY
卷 43, 期 1, 页码 93-106出版社
MDPI
DOI: 10.3390/cimb43010008
关键词
bromelain; inflammation; pro-inflammatory cytokines; NF-kappa B; MAPKs
资金
- Kasetsart University
- National Research Council of Thailand (NRCT) [70/2562]
The study found that bromelain can inhibit LPS-induced inflammatory responses, reduce the production of inflammatory cytokines, and achieve anti-inflammatory effects by regulating the expression of iNOS and COX-2, with purified rhizome bromelain showing stronger inhibitory effects than crude bromelain in RAW264.7 cells.
Bromelain is a mixture of proteolytic enzymes derived from pineapple (Ananas comosus) fruit and stem possessing several beneficial properties, particularly anti-inflammatory activity. However, the molecular mechanisms underlying the anti-inflammatory effects of bromelain are unclear. This study investigated the anti-inflammatory effects and inhibitory molecular mechanisms of crude and purified rhizome bromelains on lipopolysaccharide (LPS)-induced inflammation in RAW 264.7 macrophage cells. RAW264.7 cells were pre-treated with various concentrations of crude bromelain (CB) or purified bromelain (PB), and then treated with LPS. The production levels of pro-inflammatory cytokines and mediators, including nitric oxide (NO), interleukin (IL)-6, and tumor necrosis factor (TNF)-alpha were determined by Griess and ELISA assays. The expressions of inducible nitric oxide synthetase (iNOS), cyclooxygenase (COX)-2, nuclear factor kappa B (NF-kappa B), and mitogen-activated protein kinases (MAPKs)-signaling pathway-related proteins were examined by western blot analysis. The pre-treatment of bromelain dose-dependently reduced LPS-induced pro-inflammatory cytokines and mediators, which correlated with downregulation of iNOS and COX-2 expressions. The inhibitory potency of PB was stronger than that of CB. PB also suppressed phosphorylated NF-kappa B (p65), nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha, extracellular signal-regulated kinases, c-Jun amino-terminal kinases, and p38 proteins in LPS-treated cells. PB then exhibited potent anti-inflammatory effects on LPS-induced inflammatory responses in RAW264.7 cells by inhibiting the NF-kappa B and MAPKs-signaling pathways.
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