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Synergistic Effect of Natural Killer Cells and Bee Venom on Inhibition of NCI-H157 Cell Growth
Author(s) -
Hee Jin Sung,
Ho Sueb Song
Publication year - 2016
Publication title -
the acupuncture
Language(s) - English
Resource type - Journals
eISSN - 2287-7797
pISSN - 1229-1137
DOI - 10.13045/acupunct.2016005
Subject(s) - bee venom , venom , chemistry , cell growth , immunology , biology , zoology , biochemistry
Objectives : This study examined the effects of Bee venom on apoptosis in NCI-H157 human lung cancer cells and for promoting the apoptosis effects of Natural killer cell. Methods :Bee venom and Natural killer-92 cells were cultured either separately from or together with NCI-H157 cells for 24 hours. To figure out whether Bee venom enhances the cytotoxic effect of Natural Killer-92 cells, a cell viability assay was conducted. To observe the changes in Death receptors, apoptotic regulatory proteins and Nuclear factor-κB, western blot analysis was conducted. To observe the effect of Bee venom through an extrinsic mechanism, a transfection assay was conducted. Results : 1. Natural killer-92 cells and Bee venom significantly inhibited the growth of NCI-H157 cells and co-culture had more inhibitory effect than the separate culture. 2. Expressions of Fas, DR3, DR6, Bax, caspase-3, caspase-8, cleaved caspase-3, cleaved caspase-8 were increased, and expressions of Bcl-2 and cIAP were decreased. More efficacy was observed in co-culture than in separate culture. 3. Nuclear Factor-κB activation was clearly decreased. And co-culture showed much less activation than separate culture. 4. As a result of treatment for DR-siRNA, the reduced cell viability of NCI-H157 cells and the activity of Nuclear factor-κB were increased. With this, it can be seen that Bee venom and Natural killer-92 cells have an effect on the cancer cells through the extrinsic mechanism. Conclusion : Bee venom is effective in inhibiting the growth of human lung cancer cells. Furthermore Bee venom effectively enhances the functions of Natural killer cells.

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