【摘要】 目的:通过结肠张力测定，观察水溶性蜂胶（WSP）对右旋葡聚糖硫酸钠（DSS）诱导的溃疡性结肠炎（UC）小鼠损伤的缓解作用，并探讨其可能作用机制。方法:采用SPF级C57小鼠24只，随机分为正常组（CTRL组）、模型组（DSS组）、蜂胶干预组（WSP组）和柳氮磺胺吡啶组（SASP组）,每组6只。除CTRL组外，其余各组均通过自由饮用2.5%DSS 7 d复制急性UC小鼠模型。对各组小鼠进行疾病活动指数（DAI）评分，测量结肠长度，HE法检测结肠形态学变化，ELISA法检测血清中白介素-6（IL-6）、白介素-1β（IL-1β）及肿瘤坏死因子-α（TNF-α）的水平，经PowerLab生物信号处理系统测定各组小鼠结肠张力及其Ca²⁺量效收缩度。结果:与CTRL组相比较，DSS组小鼠体质量降低，DAI评分升高，结肠明显缩短，结肠黏膜损伤明显，炎症细胞浸润较多，血清中IL-6、IL-1β及TNF-α水平升高（P<0.05）,结肠平滑肌收缩力下降、频率加快（P<0.01）,对ACh和KCl刺激的敏感性降低，Ca²⁺量效收缩度降低（P<0.01）;与DSS组相比较，WSP组和SASP组小鼠体质量升高，DAI评分下降，结肠长度增加，结肠黏膜损伤减少，炎症细胞浸润减少，血清中IL-6、IL-1β及TNF-α水平下降（P<0.05）,结肠平滑肌收缩力及频率趋于恢复（P<0.01）,对ACh和KCl刺激时结肠敏感性增强，CaCl₂量效收缩度亦上升（P<0.01）。结论:DSS诱导的急性UC小鼠结肠损伤明显，收缩张力下降，频率增快，CaCl₂量效收缩度减弱，WSP干预后明显缓解UC小鼠结肠损伤，可能机制为通过降低UC小鼠血清中的促炎细胞因子水平，减轻肠黏膜损伤，使其收缩力及频率趋于恢复，从而提高其CaCl₂量效收缩度。更多还原

【Abstract】 Objective:To observe the alleviating effect of water-soluble propolis（WSP） on dextran sodium sulfate（DSS） induced ulcerative colitis（UC） in mice by measuring colonic tone and explore its possible mechanism.Methods:Twenty-four SPF C57 mice were randomly and equally divided into control group（CTRL group）,dextran sodium sulfate group（DSS group）,water-soluble propolis group（WSP group） and salicylazosulfapyridine group（SASP group）.Except for the CTRL group, 2.5% DSS was applied ad libitum in the mice in all groups for 7 days to induce an acute UC model.Disease activity index（DAI） and colon length were measured.Hematoxylin & eosin（HE） staining was performed to evaluate morphological changes of the colon.Enzyme-linked immunosorbent assay（ELISA） was used to detect the serum levels of pro-inflammatory cytokines interleukin-6（IL-6）,interleukin-1β（IL-1β） and tumor necrosis factor alpha（TNF-α）.The colonic tone and Ca²⁺ dose-effect contraction were measured by PowerLab biological signal processing system.Results:Compared with the CTRL group, mice in the DSS group had lower body weight, higher DAI scores, shorter colon, significantly damaged colon mucosa, more inflammatory cell infiltration, higher serum levels of IL-6,IL-1β and TNF-α（P<0.05）,decreased muscle contractibility and increased contraction frequency（P<0.01）.The sensitivity to ACh and KCl stimulation and the Ca²⁺ dose-effect contraction were decreased（P <0.01）.Compared with the DSS group, mice in the WSP group and SASP group had higher body weight, lower DAI scores, longer colon, less damaged colon mucosa and inflammatory cell infiltration, lower serum levels of IL-6,IL-1β and TNF-α（P<0.05）,more normal contractibility and contraction frequency of colon smooth muscle（P<0.01）.Colon sensitivity to ACh and KCl was increased and CaCl₂ dose-effect contraction activity was enhanced（P<0.01）. Conclusion:The colon damage of DSS-induced acute UC mice is significant, with decreased contractibility and increased frequency, and CaCl₂ dose-effect contraction activity is reduced. WSP can significantly alleviate colon damage in UC mice, possibly by lowering serum levels of pro-inflammatory cytokines, reducing intestinal mucosal damage, restoring their contractility and frequency, and thereby enhancing CaCl₂ dose-effect contraction activity.更多还原