[Electroacupuncture of "Shangjuxu"(ST37) and "Tianshu"(ST25) reduces colonic injury by suppressing NF-κB/NLRP3 signaling in rats with ulcerative colitis].

To observe the effect of electroacupuncture (EA) of "Shangjuxu"(ST37) and "Tianshu"(ST25) on colonic mucosal injury and activities of nuclear factor-κB (NF-κB)/Nod-like receptor family，pyrin domain-containing 3 (NLRP3) inflammasome signaling in the colonic tissue in rats with ulcerative colitis (UC), so as to explore its mechanisms underlying improvement of UC.Male SD rats were randomly divided into blank, model, medication and EA groups, with 12 rats in each group. The UC model was established by enema of 2-4-6 trinitrobenzene sulfonic acid +50% ethanol (2.5 mL). EA (10 Hz/50 Hz) was applied to bilateral ST37 and ST25 for 20 min, once a day, for a total of 10 days. Rats of the medication group received gavage of mesalazine suspension (2 mL：0.2 g/kg+0.9% saline) once a day, for 10 days. The rats' general conditions were recorded for calculating the disease activity index (DAI) score (0-4 points). The colonic tissue was sampled for giving colonic mucosa damage index (CMDI, 0-5 points) score and for observing histopathological changes after hematoxylin-eosin (HE) staining, and for detecting expression levels of NF-κB and NLRP3 by using immunohistochemistry and Western blot, separately. The contents of serum interleukin-1β (IL-1β), NLRP3 and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay.Compared with the blank group, the DAI and CMDI scores, contents of serum IL-1β, NLRP3, and TNF-α, as well as the immunoactivity and expression of NF-κB and NLRP3 proteins were significantly increased in the model group (P<0.05). Relevant to the model group, modeling-induced increases of DAI and CMDI scores, serum IL-1β, NLRP3 and TNF-α contents, and NF-κB and NLRP3 expression were reversed in both medication and EA groups (P<0.05), the effect of EA was apparently superior to that of mesalazine in down-regulating CMDI score and serum IL-1β level (P<0.05). No significant diffe-rences were found between the medication and EA groups in down-regulating DAI score, serum TNF-α and NLRP3 contents, and expression of NF-κB and NLRP3 proteins (P>0.05). The rats' general conditions including arch back sloth, anorexia, loss of fur gloss, weight loss, lethargy and loose of stool, and histopathological changes such as necrosis of intestinal mucosa, formation of obvious ulcerative surface, with many neutrophils and pus cells and inflammatory cell infiltration were obvious in the model group, which were relative milder in both medication and EA groups.EA can relieve colonic injury in UC rats, which may be related to its functions in down-regulating serum IL-1β, TNF-α and NLRP3 levels by suppressing colonic NF-κB / NLRP3 inflammasome signaling.目的：观察电针“上巨虚”“天枢”对2-4-6三硝基苯磺酸(TNBS)/乙醇诱导的溃疡性结肠炎(UC)大鼠核转录因子-κB(NF-κB)/NOD样受体热蛋白结构域3(NLRP3)炎性小体信号通路相关蛋白表达的影响，探讨电针治疗UC的部分作用机制。方法：SD大鼠随机分成空白组、模型组、美沙拉嗪组和电针组，每组12只。采用TNBS/乙醇灌肠法制备UC大鼠模型。电针组予电针双侧“上巨虚”“天枢”穴，每日1次，每次20 min，共10次；美沙拉嗪组予美沙拉嗪混悬液(0.2 g/kg)灌胃，每日1次，共10次。观察大鼠一般情况，计算大鼠疾病活动指数(DAI)；肉眼结合HE染色观察结肠黏膜损伤情况及结肠组织形态学变化，并评估结肠形态损伤指数(CMDI)；酶联免疫吸附法检测血清白细胞介素-1 β(IL-1β)、NLRP3及肿瘤坏死因子-α(TNF-α)的含量；分别采用免疫组织化学法、Western blot法检测结肠组织中NF-κB及NLRP3表达水平。结果：与空白组比较，模型组一般情况较差，肠黏膜坏死，形成明显溃疡面，并有大量炎细胞浸润，DAI及CMDI评分显著升高(P<0.05)，血清IL-1β、NLRP3、TNF-α含量及结肠组织NF-κB、NLRP3相对表达量均显著升高(P<0.05)。与模型组比较，美沙拉嗪组和电针组一般情况明显好转，肠黏膜坏死、炎细胞浸润程度明显减轻，DAI及CMDI评分显著降低(P<0.05)，血清IL-1β、NLRP3、TNF-α含量及结肠组织NF-κB、NLRP3相对表达量显著降低(P<0.05)。与美沙拉嗪组比较，电针组CMDI评分及血清IL-1β含量显著降低(P<0.05)。结论：电针对UC具有一定的治疗作用，其作用机制可能与下调NF-κB/NLRP3信号通路IL-1β、TNF-α、NF-κB及NLRP3炎性小体的表达有关。.