Dr. Weeks’ Comment: I was a beekeeper before I became a medical doctor, so understandably, I remain very interested in the therapeutic aspects of apitherapy (therapies using honey bee products). Propolis is the sticky substances which bees under to sterilize the inside of their hive – it hardens into something like a varnish. It is the bees’ first line of defense (“pro” “polis” derives from the Latin: “before the city” – or barrier). Well known and scientifically validated medicinal uses of propolis include lowering cholesterol, topical and systemic anti-viral, anti-bacterial and anti-fungal and dental hygiene. Now we see more of what aspects of propolis are so effective.
Effect of propolis and caffeic acid phenethyl ester (CAPE) on NFÎºB activation by HTLV-1 Tax.
Department of Virology and Developmental Genetics, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva 84105, Israel.
HTLV-1 is the etiological agent of aggressive malignancy of the CD4(+) T-cells, adult T-cell leukemia (ATL), and other severe clinical disorders. The viral Tax protein is a key factor in HTLV-1 pathogenicity. A major part of Tax oncogenic potential is accounted for by its capacity of inducing the transcriptional activity of the NFÎºB factors, which regulate the expression of numerous cellular genes. Propolis (PE), a natural product produced by honeybees, has been used for a long time in folk medicine. One of PE active components, caffeic acid phenylethyl ester (CAPE), was well characterized and found to be a potent inhibitor of NFÎºB activation. Therefore, the aim of this study was to pursue the possibility of blocking Tax oncogenic effects by treatment with these natural products. Human T-cell lines were used in this study since these cells are the main targets of HTLV-1 infections. We tried to determine which step of Tax-induced NFÎºB activation is blocked by these products. Our results showed that both tested products substantially inhibited the activation of NFÎºB-dependent promoter by Tax. However, only PE could efficiently inhibit also the Tax-induced activation of SRF- and CREB-dependent promoters. Our results showed also that PE and CAPE strongly prevented both Tax binding to IÎºBÎ± and its induced degradation by Tax. However, both products did not interfere in the nuclear transport of Tax or NFÎºB proteins.
Effects of the Schisandra fructus water extract on cytokine release from a human mast cell line.
, Chae HS
, Choi JH
, Choi HJ
, Park PS
, Cho SH
, Lee GH
, So HY
, Choo YK
, Kweon OH
, Kwon DY
Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.
Schisandra fructus has been used for treatment of cough and thirst in Korea. However, its therapeutic mechanisms remain largely unclear. To investigate the biological effect of Schisandra fructus water extract (SFWE), we examined the effect of SFWE on the phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187-induced pro-inflammatory cytokine secretion in the human mast cell line HMC-1. HMC-1 cells were stimulated with PMA plus A23187 in the presence or absence of SFWE. Tumor necrosis factor (TNF)-alpha, interleukin 6 (IL-6), and granulocyte-macrophage colony-stimulating factor (GM-CSF) productions were measured by enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction. Inhibitory IkappaB/nuclear factor-kappaB (NF-kappaB) expression was assessed by western blot. SFWE suppressed PMA plus A23187-induced TNF-alpha, IL-6, and GM-CSF production in dose-dependent manners. Furthermore, SFWE inhibited IkappaB degradation and NF-kappaB nuclear translocation. These results suggest that SFWE inhibits the secretion of pro-inflammatory cytokines in HMC-1 cells through blockade of IkappaB degradation and NF-kappaB activation. Taken together, these findings may help elucidate the mechanism of action of this medicine in the modulation of mast cell activation in inflammatory conditions.