Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
Vol. 9, No. 1, 2010, pp. 19-26
Bioline Code: pr10003
Full paper language: English
Document type: Research Article
Document available free of charge
Tropical Journal of Pharmaceutical Research, Vol. 9, No. 1, 2010, pp. 19-26
© Copyright © 2010 - Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, 300001 Nigeria.
Study of the Molecular Mechanism of Anti-inflamma-tory Activity of Bee venom in Lipopolysaccharide Stimulated RAW 264.7 Macrophages|
Lam, Pham Duy; Mandal, Prabhat Kumar; Hak, Seung Yang & Hwang, Seong-Gu
Bee venom (BV) is traditionally used in many inflammatory chronic conditions but its mechanism of action at molecular level is not fully understood. This study was undertaken to elucidate the mechanism of action of bee venom at the molecular level
We used lipopolysaccharide (LPS) stimulation in Raw 264.7 macrophage (RM) cells and studied the effect of BV on cell proliferation, inflammation related protein expression by western blotting and RNA expression by reverse transcriptase polymerase chain reaction (RT-PCR).
Bee venom was toxic to RM cells above10 µg/ml but reduced the production of nitric oxide (NO) at 2–10 µg/ml in LPS stimulated RM cells by inhibiting the expression of inducible nitric oxide synthase (iNOS) and cyclooxigenase (COX)-2 via nuclear factor (NF)-κB. However, bee venom also induced the pro-inflammatory cytokine, interleukin (IL)-1β via p38 mitogen activated protein kinase (MAPK) which is known to stimulate inflammatory activity.
It seems that NFκB and p38 MAPK signal pathways are involved in triggering the functional activation of LPS-stimulated macrophage. We suggest that some components of bee venom can cause inflammation by inducing IL-1β via p38 MAPK while others act as anti-inflammatory by suppressing iNOS and COX2 via NFκB.
Bee venom, Cyclooxygenase-2, Interleukin 1beta, Inducible nitric oxide synthase, Lipopolysaccharide, Macrophage, Mitogen activated protein kinase, Nuclear factor kappa-B
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