穴位埋线抑制血管性痴呆大鼠神经炎症反应

目的 观察穴位埋线对血管性痴呆(VD)大鼠环氧化酶2 (COX-2)/前列腺素E2 (PGE2)信号通路中炎症因子表达的影响，探讨穴位埋线对VD大鼠脑部神经炎性反应抑制作用的机制。 方法 采用改良Pulsinelli’s 4血管阻断法建立VD模型，148只雄性SD大鼠随机分为VD模型组、非穴位埋线组、穴位埋线组，另设置假手术组为对照。术后第7天2个治疗组分别施行穴位埋线和非穴位埋线治疗，15 d后取材。Western blotting检测COX-2和PGE2的表达；Real-time PCR检测大鼠海马肿瘤坏死因子α（TNF-α）、细胞间黏附分子1（ICAM-1）、白细胞介素（IL）-6、巨噬细胞炎性蛋白2（MIP-2）、IL-1β和单核细胞趋化蛋白1（MCP-1）的mRNA表达。 结果 与假手术组相比，其他3组大鼠海马组织COX-2、PGE2、TNF-α、ICAM-1、IL-6、MIP-2、IL-1β和MCP-1因子的表达均显著性升高（P＜0.01）。与模型组相比，穴位埋线组和非穴位埋线组海马组织COX-2、PGE2蛋白及TNF-α、ICAM-1、IL-6、MIP-2、IL-1β和 MCP-1 mRNA表达均下降（P＜0.01），且穴位埋线组下降最为明显（P＜0.01）。 结论 穴位埋线可通过下调 COX-2/PGE2信号通路中相关炎症因子的表达，降低VD大鼠引起的炎症反应，起到保护脑炎免受损伤的作用。

Acupoint catgut embedding inhibiting neuroinflammation in vascular dementia rats

Objective To observe the effect of acupoint catgut embedding on the expression of inflammatory factor mRNA in cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) signal pathway of vascular dementia (VD) rats, and to explore the protective mechanism of acupoint catgut embedding on the brain inflammatory response of VD rats. Methods VD model was established by the modified Pulsinelli’s four vessel blocking method . Totally 148 male rats were randomly divided into VD model group, non acupoint catgut embedding group and acupoint catgut embedding group. On the 7th day after operation, catgut embedding at acupoints and catgut embedding at non acupoints were performed in the two treatment groups respectively, and materials were taken out 15 days later. Western blotting was used to detect the expression of COX-2 and PGE2, and real-time PCR was used to detect the mRNA expression of tumor necrosis factor α(TNF-α), intercellular cell adhesion molecule 1 (ICAM-1), interleukin(IL)-6, macrophage inflammatory protein 2 (MIP-2), IL-1β, and monocyte chemotactic protein 1 (MCP-1) in rat hippocampus. Results Compared with the sham group, the expressions of COX-2, PGE2, TNF-α, ICAM-1, IL-6, MIP-2, IL-1β and MCP-1 in hippocampus of the other three groups were significantly higher (P<0.01). Compared with the model group, the expressions of COX-2, PGE2 protein and TNF-α, ICAM-1, IL-6, MIP-2, IL-1β, MCP-1 mRNA in the hippocampus of the acupoint catgut embedding group and the non acupoint catgut embedding group decreased significantly (P<0.01). Conclusion Acupoint catgut embedding can protect the brain from inflammatory injury by down-regulating the expression of related inflammatory factors in COX-2/PGE2 signaling pathway and reducing the inflammatory response induced by VD rats.