CAJ | 학술논문

目的采用鸡Ⅱ型胶原诱导性关节炎(CIA)小鼠模型,观察(-)-表没食子儿茶素没食子酸酯(EGCG)的治疗作用,并探讨其作用机制.方法给予CIA小鼠EGCG治疗,以磷酸盐缓冲液(PBS)作为阴性对照,观察各组小鼠发病情况.通过对CIA小鼠关节评分和关节病灶病理学检测[苏木素-伊红(HE)染色] 判断EGCG的疗效;通过,3H-胸腺嘧啶核苷(TdR)掺入实验、流式细胞术及Western-blot方法阐明EGCG的免疫学作用机制.结果 ①EGCG能够改善CIA的关节评分、减少病变关节组织炎性细胞浸润;② EGCG能抑制CIA小鼠C Ⅱ反应性脾细胞的增殖[EGCG组每分钟脉冲数(cpm)值3366±199;PBS组cpm值5342+112,P<0.05]和细胞因子白细胞介素(IL)-17的分泌(EGCG组IL-17阳性细胞数占CD4+T细胞0.41%;PBS组占4.05%);③EGCG能提高CIA小鼠淋巴结细胞中IKB的表达,降低磷酸化IKB蛋白水平的表达.结论 EGCG能显著减轻CIA严重程度.EGCG通过抑制CIA小鼠C Ⅱ反应性脾细胞的增殖和炎症因子IL-17的分泌;以及通过抑制CⅡ反应性淋巴结细胞中IKB的磷酸化,增强IKB的表达从而抑制核因子(NF)-κB的活性来治疗CIA.
목적 채용계Ⅱ형효원유도성관절염(CIA)소서모형,관찰(-)-표몰식자인다소몰식자산지(EGCG)적치료작용,병탐토기작용궤제.방법 급여CIA소서EGCG치료,이린산염완충액(PBS)작위음성대조,관찰각조소서발병정황.통과대CIA소서관절평분화관절병조병이학검측[소목소-이홍(HE)염색] 판단EGCG적료효;통과,3H-흉선밀정핵감(TdR)참입실험、류식세포술급Western-blot방법천명EGCG적면역학작용궤제.결과 ①EGCG능구개선CIA적관절평분、감소병변관절조직염성세포침윤;② EGCG능억제CIA소서C Ⅱ반응성비세포적증식[EGCG조매분종맥충수(cpm)치3366±199;PBS조cpm치5342+112,P<0.05]화세포인자백세포개소(IL)-17적분비(EGCG조IL-17양성세포수점CD4+T세포0.41%;PBS조점4.05%);③EGCG능제고CIA소서림파결세포중IKB적표체,강저린산화IKB단백수평적표체.결론 EGCG능현저감경CIA엄중정도.EGCG통과억제CIA소서C Ⅱ반응성비세포적증식화염증인자IL-17적분비;이급통과억제CⅡ반응성림파결세포중IKB적린산화,증강IKB적표체종이억제핵인자(NF)-κB적활성래치료CIA.
Objective The therapeutic effect of epigallocatechin-3-gallate (EGCG) on the collageninduced arthritis model (CIA) was observed and its immunological mechanism was analyzed. Methods EGCG was administered to CIA mice and PBS was admitted as negative control. The severity of CIA was evaluated by clinical scores and histopathological assessment (H-E staining). Immunological mechanisms inv-suppressive effect on IL-17 secretion of CD4+T cells (EGCG group: 0.41%; PBS group: 4.05% ) and inhibitive activity of C Ⅱ -reactive splenocytes proliferation. There was statistical significant difference between IKB expression and down-regulate phosphorylated IKB expression in lymph node cells of CIA mice.Conclusion EGCG can significantly ameliorate the severity of CIA. The therapeutic mechanisms may be related to inhibition of C Ⅱ -reactive splenocyte proliferation and IL-17 secretion and via inhibiting the activity of NF-κB by inducing the expression of IKB and by suppressing the expression of phosphorylated IKB in CIA mice.