Low dose of resveratrol enhanced immune response of mice

To study the immune modulating effect of low dose of resveratrol. Concanavalin A (ConA) and Staphylococcus aureus Cowan (Sac) were used to induce the activation of T lymphocyte and antigen presenting cell and cytokine production. [3H]-Thymidine incorporation was used to evaluate the proliferation of...

Full description

Saved in:
Bibliographic Details
Published inActa pharmacologica Sinica Vol. 23; no. 10; p. 893
Main Authors Feng, Yong-Hong, Zhou, Wen-Liang, Wu, Qing-Li, Li, Xiao-Yu, Zhao, Wei-Min, Zou, Jian-Ping
Format Journal Article
LanguageEnglish
Published United States 01.10.2002
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:To study the immune modulating effect of low dose of resveratrol. Concanavalin A (ConA) and Staphylococcus aureus Cowan (Sac) were used to induce the activation of T lymphocyte and antigen presenting cell and cytokine production. [3H]-Thymidine incorporation was used to evaluate the proliferation of lymphocyte. Cytokine production was detected by ELISA method. Dinitrofluorobenzene (DNFB) was used to induce mice delayed type hypersensitivity (DTH, delayed hypersensitivity) response and ear swelling was used as an evaluating indicator. Changes of lymphocyte subtypes were detected by flow cytometry. Resveratrol (0.75-6 micromol/L) concentration-dependently promoted lymphocyte proliferation and IL-2 production induced by ConA. Sac induced IL-12 and IFN-gamma (interferon type II) production were also concentration-dependently enhanced by resveratrol, while IL-10 production was inhibited. Resveratrol (4 mg/kg, ig) promoted DTH response of mouse, which was suppressed by ethanol (16 %, w/v) consumption. Resveratrol treatment had no significant influence on lymphocyte subtypes in mice, however it could reverse the suppressive effect of ethanol both on macrophage percentage and on macrophage MHC-II molecule expression. Low dose resveratrol enhanced cell-mediate immune response. Promoting Th1 cytokine production and influencing on macrophage function might be its mechanisms.
ISSN:1671-4083
1745-7254