[目的]观察β-内啡肽(β-endorphin,β-END)腹腔注射对慢性炎性痛大鼠的治疗作用,探究其对外周局部致炎性细胞因子前列腺素E2(prostag landin E2,PGE2)、白细胞介素1-β(interleukin 1-β,IL-1β)、肿瘤坏死因子-α(tamor necrosis factor-α,TNF-α)的基因和蛋白表达的干预作用。[方法]建立大鼠完全弗化佐剂(Complete Freund's Adjuvant,CFA)诱导的炎性痛模型,随机分为模型对照组和β-END腹腔注射组。造模后1~13 d进行β-END腹腔注射,隔日1次。观察热缩腿阈(Thermal-PWLs)变化,检测足爪炎症组织PGE2、IL-1β、TNF-α的mRNA表达和蛋白水平。[结果]β-END腹腔注射能显著提高慢性炎性痛大鼠的痛阈;能显著抑制局部炎症组织PGE2、IL-1β和TNF-αmRNA表达;能显著降低IL-1β和TNF-α的蛋白水平,对PGE2蛋白水平有下调趋势。[结论]除了经典的外周阿片受体机制外,β-END外周抗慢性炎性痛作用,可能还与其有效抑制局部炎性因子的表达有关。
[Objective]To observe the effect of β-endorphin(β-END) intraperitoneally(i.p.) injected on rats with complete freund's adjuvant-induced chronic inflammatory pain and its influence in regulating the protein levels and gene expressions of PGE2,1L-1 β, TNF-a in local inflammatory tissue. [Methods] Rat inflammatory pain model was established by i.p. injecting 0.1 ml Complete Freund's Adjuvant(CFA) into the right hind paw. Rats were randomly divided into CFA group and i.p. β-END group. β-END was administered i.p. every other day from ld to 13d after CFA injection. The thermal paw withdrawal latency(Thermal-PWLs), the gene expressions and protein levels of PGE2, IL-1 β, TNF-a in the inflammatory paws were measured. [Results]β-END administered i.p. significantly increased the thermal PWLs of rats with chronic inflammatory pain. It significantly inhibited the mRNA levels of PGE2, IL-1 β, TNF-et in the inflammatory paws. In hne with this, it significantly reduced the protein levels of IL-1 β, TNF-a, and showed a down-regulating trend of PGE2 level in the inflammatory paws. [Conclusion]Besides the mechanism that reducing the activities of sensory nerves by acting with peripheral opioid receptors, the therapeutic effects of β-END applied peripherally on chronic inflammatory pain may also be related to its inhibitory action on inflammatory cytokines in the local inflammatory tissue.