Bee Venom Decreases LPS-Induced Inflammatory Responses in Bovine Mammary Epithelial Cells
Author(s) -
Chang Hee Jeong,
Wei Cheng,
Hyojin Bae,
Kyung-Woo Lee,
Sang Mi Han,
Michael C. Petriello,
HongGu Lee,
Han Geuk Seo,
Sung Gu Han
Publication year - 2017
Publication title -
journal of microbiology and biotechnology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 64
eISSN - 1738-8872
pISSN - 1017-7825
DOI - 10.4014/jmb.1706.06003
Subject(s) - inflammation , oxidative stress , tumor necrosis factor alpha , reactive oxygen species , immunology , biology , chemistry , pharmacology , microbiology and biotechnology , biochemistry
The world dairy industry has long been challenged by bovine mastitis, an inflammatory disease, which causes economic loss due to decreased milk production and quality. Attempts have been made to prevent or treat this disease with multiple approaches, primarily through increased abuse of antibiotics, but effective natural solutions remain elusive. Bee venom (BV) contains a variety of peptides ( e.g. , melittin) and shows multiple bioactivities, including prevention of inflammation. Thus, in the current study, it was hypothesized that BV can reduce inflammation in bovine mammary epithelial cells (MAC-T). To examine the hypothesis, cells were treated with LPS (1 μg/ml) to induce an inflammatory response and the anti-inflammatory effects of BV (2.5 and 5 μg/ml) were investigated. The cellular mechanisms of BV against LPS-induced inflammation were also investigated. Results showed that BV can attenuate expression of an inflammatory protein, COX2, and pro-inflammatory cytokines such as IL-6 and TNF-α. Activation of NF-κB, an inflammatory transcription factor, was significantly downregulated by BV in cells treated with LPS, through dephosphorylation of ERK1/2. Moreover, pretreatment of cells with BV attenuated LPS-induced production of intracellular reactive oxygen species ( e.g. , superoxide anion). These results support our hypothesis that BV can decrease LPS-induced inflammatory responses in bovine mammary epithelial cells through inhibition of oxidative stress, NF-κB, ERK1/2, and COX-2 signaling.
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