- 作者: Ben-Ching Liao; Rolis Chien-Wei Hou; Jen-Shu Wang; Kee-Ching G. Jeng
- 作者服務機構: 1 Institute of Biomedical Science, National Chung Hsing University, Taichung, ROC; ; 2 Jen-Teh Junior College of Medical and Nursing Management, Miaoli, Taiwan, ROC; ; 3 Department of Chinese Medicine, China Medical University, Taichung, ROC;; 4 Department of Chinese Medicine, Taichung Veterans General Hospital, Taichung, Taiwan, ROC; ; 5 Department of Education and Research, Taichung Veterans General Hospital, Taichung, Taiwan, 40705, ROC
- 中文摘要: --
- 英文摘要: Substance P (SP), a neurotransmitter, may play an important role in neurogenic inflammation. Ginseng has been used extensively in traditional medicine; however, few studies were focused on their anti-allergic effect. Therefore, the effect and mechanism of ginsenoside Rb1 on the SP enhancement of allergic mediators were explored. In this study, SP and dinitrophenyl-bovine serum albumin (DNP-BSA) were used to activate rat basophilic leukemia (RBL)-2H3 cells. The cultured supernatants were assayed for histamine, leukotriene C4(LTC4) and interleulin-4 (IL-4) production. The mitogen-activated protein kinases (MAPKs) signaling pathway was determined by Western blotting analysis. We found that IgE/DNP-BSA, SP, ginsenoside Rb1, or MAPK specific inhibitors had no effect on cell viability and cytotoxicity. SP (30 μΜ) alone, did not induce histamine and LTC4 release, but it enhanced allergen-induced histamine and LTC4 release. In addition, SP significantly induced and enhanced allergen-activated IL-4. Ginsenoside Rbl dose-dependently inhibited these effects. SP enhanced the allergen-activated ERK pathway in RBL-2H3 cells, and Rbl effectively inhibited the ERK pathway activation. Although MAPK specific inhibitors suppressed LTC4 and IL-4, only U0126 inhibited the SP enhanced histamine release. These results demonstrate that Rbl dose-dependently inhibited SP enhanced allergen-induced mediator release and its mechanism was through the inhibition of the ERK pathway.
- 中文關鍵字: --
- 英文關鍵字: allergen, ginsenoside Rb1, histamine, interleukin-4, leukotriene C4, mitogen-activated protein kinases, RBL-2H3 cells, substance P