期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 820, 期 -, 页码 106-112出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2017.12.030
关键词
Cafestol; Endothelial cells; Urotensin II, interleukin-8; Heme oxygenase-1; Nuclear factor erythroid 2-related factor 2
资金
- Ministry of Science and Technology Grants [MOST 104-2314-B-016-044, MOST105-2320-B-038-030, MOST 106-2314-B-038-068-MY3]
- Tri-Service General Hospital Grants, Taipei, Taiwan, R.O.C [TSGH-C103-029, TSGH-C105-028, TSGH-C106-021]
Cafestol, a diterpene molecule found in the berries of Coffea arabica L. (Rubiaceae), has been shown to exercise anti-angiogenic and anti-tumorigenic effects. However, cafestol's cellular mechanism has yet to be fully investigated. We previously demonstrated that urotensin II enhanced interleukin-8 secretion by endothelial cells, thereby increasing endothelial cell proliferation. Urotensin II may also participate in angiogenesis and tumor infiltration by macrophages. However, the effects of cafestol on urotensin II-induced interleukin-8 expression and cellular proliferation have not been determined. Here, we showed that pretreatment with cafestol inhibited urotensin II-stimulated endothelial cell proliferation. Further experiments demonstrated that cafestol increased translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and expression of enhanced heme oxygenase-1. Moreover, cafestol inhibited expression of urotensin II-induced interleukin-8. Cafestol's inhibitory effects on interleukin-8 expression and cellular proliferation induced by urotensin II were significantly abrogated by heme oxygenase-1 silencing, suggesting it may be involved in mediating the effects of cafestol. This study reports that cafestol inhibits urotensin II-induced interleukin-8 expression and cell proliferation via Nrf2/heme oxygenase-1-dependent mechanism in endothelial cells. These findings provide novel insight into the signaling pathways that may be important in mediating the effects of cafestol.
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