Emodin induces apoptosis of concanavalin A-stimulated murine splenocytes

被引：5

作者：

An, Subin ^{[1
]}

Bing, So Jin ^{[1
]}

Cho, Jinhee ^{[1
]}

Herath, Kalahe Hewage Iresha Nadeeka Madushani ^{[1
,2
]}

Kim, Areum ^{[1
,2
]}

Chang, Hyeun Wook ^{[3
]}

Jee, Youngheun ^{[1
,2
,4
]}

机构：

[1] Jeju Natl Univ, Coll Vet Med, Jeju 63243, South Korea

[2] Jeju Natl Univ, Interdisciplinary Grad Program Adv Convergence Te, Jeju 63243, South Korea

[3] Yeungnam Univ, Coll Pharm, Gyongsan 38541, Gyeongbuk, South Korea

[4] Jeju Natl Univ, Vet Med Res Inst, Jeju 63243, South Korea

来源：

FOOD SCIENCE AND BIOTECHNOLOGY | 2016年 / 25卷 / 06期

关键词：

emodin; apoptosis; autoimmune disease; concanavalin A; immune cells; T-CELL APOPTOSIS; NF-KAPPA-B; DENDRITIC CELLS; CANCER CELLS; LYMPHOCYTES; ACTIVATION; MECHANISM; KINASE; PROLIFERATION;

D O I：

10.1007/s10068-016-0260-y

中图分类号：

TS2 [食品工业];

学科分类号：

0832 ;

摘要：

Emodin, one of the major compounds in the herb Reynoutria elliptica, is known to maintain immunosuppressive, anti-allergic, anti-cancer, and anti-inflammatory effects. In this study, we assessed the possibility of using emodin to induce apoptosis in stimulated immune cells in vitro. After treatment with emodin and concanavalin A (Con A), we observed DNA damage-induced apoptosis in splenocytes. Moreover, treatment with emodin and Con A increased the number of apoptotic splenocytes compared with untreated controls. Emodin also diminished the size of CD45R/B220(+) cells, CD19(+)CD69(+) cells, and cDC populations. These results indicate that emodin-induced apoptosis was involved in attenuating the immune activity promoted by DNA damage and in decreasing the number of CD45R/B220(+) B cells and CD19(+)CD69(+) activating B cells. This demonstration of emodin inducing apoptosis of Con A-stimulated immune cells indicates its potential utility as a therapy for diseases caused by abnormally activated immune cells.

引用

页码：1693 / 1700

页数：8

共 21 条

[11] Emodin, a naturally occurring anthraquinone derivative, suppresses IgE-mediated anaphylactic reaction and mast cell activation [J].