The Influence on Immunological Status of Experimental Allergic Neuritis by Intervention of Tripterygium Polyglucoside

Objective To investigate the effect of Tripterygium polyglucoside (TPG) on immunological status of experimental allergic neuritis (EAN). Methods TPG was administrated for 14 days in EAN model rats after the symptom emerging. The alterations of lymphocyte proliferation, lymphocyte K~+ channel mRNA and serum antibodies in rats were observed, along with their correlations with the clinical presentation. Results On day 23 after immunization, lymphocyte proliferation on baseline and that induced by LPS and bovine peripheral myelin (BPM) in EAN group increased prominently compared with control group [(8.77 ± 0.56)% vs. (4.67 ± 0.39)%, (8. 07 ± 0. 74)% vs. (7. 24±0. 30) % , (9. 24±0. 72) % vs. (7.22 ± 0.67)%], mRNA levels of voltage- gated K~+ channel (Kv1. 3) and intermediate-conductance calcium-activated K~+ channel (IKCa1) and serum level of anti-BPM antibody also elevated significantly (0.56 ± 0.03 vs. 0.35 ± 0.02, 0.71 ± 0.05 vs. 0.44 ± 0.04, 1 489.67±153.08 vs. 15.00 ± 2.85). Compared with EAN group, baseline lymphocyte proliferation and that induced by BPM decreased notablely in TPG treatment group [(7. 96 ± 0. 45) % vs. (8. 77 ± 0. 56) % , (8. 09 ± 0. 52)% vs. (9.24 ± 0. 72)%], mRNA expression of Kv1. 3 and IKCa1 came down (0. 51 ± 0.04 vs. 0. 56 ± 0. 03, 0.64 ± 0.04 vs. 0. 71 ± 0. 05), but anti-BPM antibody level had no noticeable change (1 341.08 ± 346.42 vs. 1 489.67 ± 153.08). Conclusions TPG interfered in the cellular immunity in EAN by suppressing the antigen specific lymphocyte proliferation which was partially attributed to the decrease of expression of lymphocyte K~+ channels. TPG may be supposed to be a potentially potent agent for therapy agaist Guillain-Barre syndrome.