Maslinic acid enhances immune responses in leukemic mice through macrophage phagocytosis and natural killer cell activities in vivo

Kuang Chi Lai, Shu Fen Peng, Chia Chi Liu, Jye Yu Huang, Jung Yu Kuo, Zheng Yu Cheng, Rick Sai Chuen Wu, Chin Chung Lin, Jr Kai Chen*, Jing Gung Chung

*此作品的通信作者

研究成果: 期刊稿件文章同行評審

10 引文 斯高帕斯(Scopus)

摘要

Background/Aim: Maslinic acid (MA), a pentacyclic triterpene extracted from wax-like coatings of olives, has been shown to reduce cancer cell number through induction of autophagy and apoptosis in many human cancer cells including human leukemia HL-60 cells. In the present study, we investigated whether or not MA affects immune responses in a leukemia mouse model. Materials and Methods: WEHI-3 cells were intraperitonealIy (i.p.) injected into normal BALB/c mice to develop leukemia. Mice were then treated by i.p. injection with MA at different doses (0, 8, 16 and 32 mg/kg) for 2 weeks. After treatment, all animals were weighed and blood, liver and spleen tissues were weighed. Blood or spleen both were used for determination of cell markers or phagocytosis, natural killer (NK) cell activities and T- and B-cell proliferation, respectively, by using a flow cytometric assay. Results: MA did not significantly affect body, liver, and spleen weights. However, MA increased markers of T-cells (at 16 mg/kg treatment) and monocytes (at 32 mg/kg treatment), but reduced B-cell markers (at 8 mg/kg treatment); MA did not significantly affect cell marker of macrophages. Furthermore, MA increased phagocytosis by macrophages from peripheral blood mononuclear cells and peritoneal cavity at 32 mg/kg treatment and increased NK cell activity at target cell:splenocyte ratio of 25:1 but did not affect B- and T-cell proliferation. Conclusion: MA increased immune responses by enhancing macrophage phagocytosis and NK cell activities in leukemic mice.

原文英語
頁(從 - 到)65-73
頁數9
期刊In Vivo
33
發行號1
DOIs
出版狀態已出版 - 01 01 2019
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Publisher Copyright:
© 2019 International Institute of Anticancer Research. All rights reserved.

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