中文摘要：

[目的]观察足爪注射beta-endorphin（Beta-END）对慢性炎性痛大鼠的治疗作用,探讨其对外周局部致炎性细胞因子Prostaglandin E2（PGE2）、Interleukin-1 beta（IL-1 beta）、Tumor Necrosis Factor-alpha（TNF-alpha）的基因和蛋白表达的干预作用。[方法]建立大鼠Complete Freund＇s Adju-vant（CFA）诱导的炎性痛模型,随机分为模型对照组和beta-END足爪局部注射组。Beta-END注射从模后1d至13d,隔日1次。观察痛阈（PWLs）变化,检测足爪炎症组织PGE2、IL-1 beta、TNF-alpha的mRNA和蛋白水平。[结果]与模型对照组比较,足爪局部注射beta-END能显著提高慢性炎性痛大鼠的痛阈,能显著降低IL-1 beta和TNF-alpha的蛋白水平,并对PGE2蛋白水平和PGE2、IL-1 beta、TNF-alpha mRNA表达呈现下调趋势。[结论]Beta-END足爪局部注射对慢性炎性痛大鼠具有良好的治疗作用,除传统的外周阿片受体机制外,其外周治疗慢性炎性痛的作用可能还与其有效抑制局部炎性因子的表达有关。

英文摘要：

[Objective] To observe the effect of＂ beta-endorphin（beta-END） intraplantarly（i.pl.） injected on rats with complete freund＇s adjuvant-induced chronic inflammatory pain and its influence in regulating the protein levels ,and gene expressions of PGE2, IL-1 beta.TNF-alpha in local inflammatory tissue. [Methods] Rat inflammatory pain model＇ was established by i.pl. injecting 0.1 ml Complete Freund＇s Adjuvant（CFA） into the right hind paw. Rats were randomly divided into CFA group and i.pl.beta=END group. Beta-END was administered i.pl. every＂ other day from d I to d 13 after CFA injection. The thermal paw withdrawal latency （PWEs）,the gene expressions and protein levels of PGE2, IL-1 beta, TNF-alpha In the inflammatory paws were measured. [Results]Beta-END administered i.pl. significantly increased the thermal PWLs of rats with chronic inflammatory pain. It significantly reduced the protein levels of IL-1 beta, TNF-alpha, and showed a down-regulating trend of PGE2 protein level and the mRNA levels of PGE2, IL-1 beta, TNF-alpha in the inflammatory paws. [Conclusion] Besides the mechanism of peripheral opioid receptors, the therapeutic effects of beta-END i.pl. apphed on chronic inflammatory pain may also be associated with its inhibitory action on inflammatory cytokines in the local inflammatory tissue.