摘要
目的:观察雷公藤甲素对细菌脂多糖(LPS)诱导的急性葡萄膜炎(LIU)的抗炎作用。方法:BALB/c小鼠24只,随机分为空白对照组、模型组和雷公藤甲素组,每组8只,雷公藤甲素组给予0.05%雷公藤甲素滴眼液,空白对照组和模型组均给予等体积的生理盐水。连续给药30 d后,除空白对照组外各组小鼠于玻璃体腔内注射125 mg/L的LPS建立LIU模型。分别在造模后12、24、48和72 h后,对各组小鼠眼前节进行裂隙灯检查,并对眼组织进行病理学观察,同时提取眼组织蛋白,ELISA法检测眼组织中细胞间黏附分子1(ICAM-1)、白细胞介素1β(IL-1β)和单核细胞趋化蛋白1(MCP-1)的水平。结果:造模24 h后,与模型组相比,雷公藤甲素组能明显减轻LIU引起的炎症反应并降低炎症临床评分,差异有统计学意义(P<0.01)。组织病理学也表明雷公藤甲素对小鼠前房、玻璃体腔内的炎症细胞浸润以及视网膜水肿增厚有明显的抑制作用。同时,ELISA结果显示雷公藤甲素显著下调眼组织中ICAM-1、IL-1β和MCP-1的表达,差异有统计学意义(P<0.05)。结论:雷公藤甲素可能通过下调炎症细胞因子表达,从而减轻葡萄膜炎的眼部组织损伤,为葡萄膜炎的治疗提供了新的免疫疗法。
AIM：To observe the anti-inflammatory effect of triptolide（TP） on lipopolysaccharide（LPS）-induced uveitis（LIU）.METHODS：BALB/c mice（n = 24） were randomly divided into 3 groups：blank control group（treated with normal saline）,model group（treated with normal saline） and triptolide treatment group（treated with0.05% triptolide eye drops）,with 8 mice in each group.The mice in model group and triptolide treatment group were intravitreally injected with LPS after 30 d of drug treatment.The anterior chamber was assessed by slit-lamp examination at different time points after modeling.Ocular tissues were collected for histological examination.The protein levels of intercellular adhesion molecule-1（ICAM-1）,interleukin-1β（IL-1β） and monocyte chemotactic protein-1（MCP-1） in iridial and retinal samples were tested by ELISA.RESULTS：Compared with model group,the inflammatory reaction and clinical score were obviously decreased in triptolide treatment group at 24 h after modeling（P 〈 0.01）.The histopathological observation indicated that infiltrating inflammatory cells were dramatically reduced in the anterior and posterior segments by triptolide eye drops.In addition,the expression levels of ICAM-1,IL-1β and MCP-1 were significantly decreased in the ocular tissues by treatment with triptolide（P 〈 0.05）.CONCLUSION：Triptolide prevents the injury of LIU by downregulating inflammatory cytokines,and may be a new immune therapy for uveitis.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2017年第11期2099-2102,2109,共5页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.81500739)
广东省中医药局科研项目(No.20151168)
广东省医学科学技术研究基金资助项目(No.A2015170)
