Fan Hong-cui, Ren Xiao-rong, Yu Jie-zhong, Guo Min-fang, Ji Ning, Sun Yong-sheng, Liang Li-yun, Ma Cun-gen
Institute of Brain Science, Shanxi Datong University, Datong, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2009 Mar;25(3):222-5.
To explore the therapeutic effectivity and the possible mechanism of triptolide (Tri) on experimental autoimmune encephalomyelitis (EAE).
All female C57BL/6 mice were randomly divided into EAE group (28), Tri treated group (20) and adjuvant group (18). Mice in EAE and treated groups were immunized with myelin oligodendrocyte glycoprotein peptides 35-55 (MOG(35-55);), adjuvant group was injected at the same time, but instead of MOG(35-55); with normal saline. Tri was intraperitoneally injected in the dosage of 100 microg/(kg.d) in treated group on day 5 post-immunization (p.i.), and mice in EAE and adjuvant group injected with normal saline as control. The clinical feature and pathological changes were observed and the splenic lymphocytes were prepared on days 18-20 p.i. The cell cultures were divided into the control group (only 200 microL of cell suspension) and the experimental group (cell suspension in the presence of 10 mg/L MOG(35-55);). Then all of them were inoculated in 96-well flat-bottom plates under 37 degrees Celsius, 50 mL/L CO(2);. After 48 h, the proliferation assay was determined by MTT, and the supernatants were harvested for the detection of INF-gamma, IL-17, IL-10 and IL-4 by ELISA.
Tri treatment showed an significantly protective action on EAE. After the intervention of Tri, the levels of IL-10 were increased (P<0.05), but the secretion of INF-gamma and proliferation response of splenic lymphocytes induced by MOG(35-55); were statistically significantly inhibited(P<0.05 and P<0.01, respectively). There were no influences on the amount of IL-17 and IL-4 by Tri.
Tri is an effective drug in suppressing murine EAE. This suppression is supposed to be related to downregulation of INF-gamma and upregulation of IL-10 secretion in splenic lymphocytes.
探讨雷公藤甲素（Tri）对实验性自身免疫性脑脊髓炎（EAE）的治疗效果及可能机制。
将所有雌性C57BL/6小鼠随机分为EAE组（28只）、Tri治疗组（20只）和佐剂组（18只）。EAE组和治疗组小鼠用髓鞘少突胶质细胞糖蛋白肽35 - 55（MOG(35 - 55)）免疫，佐剂组同时注射，但用生理盐水代替MOG(35 - 55)。免疫后第5天，治疗组小鼠腹腔注射Tri，剂量为100μg/(kg·d)，EAE组和佐剂组小鼠注射生理盐水作为对照。观察免疫后18 - 20天的临床特征和病理变化，并制备脾淋巴细胞。细胞培养分为对照组（仅200μL细胞悬液）和实验组（存在10mg/L MOG(35 - 55)的细胞悬液）。然后将它们全部接种于96孔平底培养板中，置于37℃、50mL/L CO₂条件下培养。48小时后，用MTT法测定增殖情况，收集上清液，用ELISA法检测INF -γ、IL - 17、IL - 10和IL - 4。
Tri治疗对EAE具有显著的保护作用。Tri干预后，IL - 10水平升高（P<0.05），但MOG(35 - 55)诱导的脾淋巴细胞INF -γ分泌和增殖反应受到统计学显著抑制（分别为P<0.05和P<0.01）。Tri对IL - 17和IL - 4的量无影响。
Tri是抑制小鼠EAE的有效药物。这种抑制作用可能与脾淋巴细胞中INF -γ的下调和IL - 10分泌的上调有关。
