目的 探究微小RNA（miRNA, miR）-155-5p调控TLR4/MAPK/NF-κB通路对川崎病小鼠炎症反应、冠状动脉病变及免疫功能的影响。 方法 将60只雄性BALB/C小鼠采用随机数字表法分为健康组、川崎病（Kawasaki disease, KD）组、miR-155-5p agomir（激动剂）组、agomir-NC（激动剂阴性对照）组、miR-155-5p antagomir（拮抗剂）组、antagomir-NC（拮抗剂阴性对照）组，每组10只。采用干酪乳杆菌细胞壁提取物腹腔注射法建立KD小鼠模型。采用ELISA法检测白细胞介素（interleukins, IL）-6、IL-1β、肿瘤坏死因子（tumor necrosis factor, TNF）-α水平，流式细胞术检测淋巴细胞亚群CD3⁺、CD4⁺、CD8⁺ T百分率及CD4⁺/CD8⁺比值，高频小动物超声成像法检测冠状动脉内径，苏木精-伊红染色观察冠状动脉组织病理形态，TUNEL染色观察冠状动脉组织内皮细胞凋亡情况，免疫印迹法检测核因子κB（nuclear factor kappa-B, NF-κB）p65、磷酸化NF-κB p65 （phosphorylated NF-κB p65, p-NF-κB p65）、Toll样受体4（Toll-like receptor 4, TLR4）、p38丝裂原激活的蛋白激酶（p38 mitogen-activated protein kinase, MAPK）蛋白表达水平。 结果 与健康组相比，KD组冠状动脉管壁增厚、内皮脱落，大量炎性细胞浸润，平滑肌层排列紊乱，伴血管扩张及管腔狭窄；miR-155-5p agomir组冠脉炎性浸润、管壁增厚及管腔狭窄较KD组显著加重；miR-155-5p antagomir组冠状动脉炎性浸润减少、管壁增厚减轻，平滑肌排列较规整，管腔狭窄明显改善。与健康组相比，KD组IL-6、IL-1β、TNF-α水平与CD4⁺百分率、CD4⁺/CD8⁺比值、冠状动脉内径、内皮细胞凋亡率及p-NF-κB p65、TLR4、p38 MAPK蛋白表达水平升高（P<0.05），CD3⁺、CD8⁺百分率降低（P<0.05）。与KD组相比，miR-155-5p agomir组IL-6、IL-1β、TNF-α水平与CD4⁺百分率、CD4⁺/CD8⁺比值、冠状动脉内径、内皮细胞凋亡率及p-NF-κB p65、TLR4、p38 MAPK蛋白表达水平升高（P<0.05），CD3⁺、CD8⁺百分率降低（P<0.05）；miR-155-5p antagomir组IL-6、IL-1β、TNF-α水平与CD4⁺百分率、CD4⁺/CD8⁺比值、冠状动脉内径、内皮细胞凋亡率及p-NF-κB p65、TLR4、p38 MAPK蛋白表达水平降低（P<0.05），CD3⁺、CD8⁺百分率升高（P<0.05）。 结论 川崎病模型小鼠中过表达miR-155-5p可加重炎症反应、冠状动脉病变及内皮细胞凋亡，诱发免疫功能紊乱，其机制可能与调控TLR4/MAPK/NF-κB通路相关；抑制miR-155-5p表达则可逆转上述病理改变。

Objective To investigate the effect of miR-155-5p regulation of the TLR4/MAPK/NF-κB pathway on inflammatory response, coronary artery lesion, and immune function in mice with Kawasaki disease (KD). Methods Sixty male BALB/C mice were randomly assigned to six groups (n=10 each): healthy, KD, miR-155-5p agomir, agomir-negative control (agomir-NC), miR-155-5p antagomir, and antagomir-negative control (antagomir-NC). KD models were established by intraperitoneal injection of Lactobacillus casei cell wall extract in all groups except the healthy group. Levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α were measured by ELISA. Flow cytometry was used to determine the proportions of CD3⁺, CD4⁺, and CD8⁺ T lymphocyte subsets and the CD4⁺/CD8⁺ ratio. Coronary artery diameter was assessed by high-frequency ultrasound, and histopathological changes were observed by hematoxylin-eosin staining. Endothelial cell apoptosis in coronary tissue was detected with TUNEL staining. Expression levels of nuclear factor kappa-B (NF-κB) p65, phosphorylated NF-κB p65 (p-NF-κB p65), Toll-like receptor 4 (TLR4), and p38 mitogen-activated protein kinase (MAPK) proteins were analyzed by Western blot. Results Compared with the healthy group, the KD group showed coronary arterial wall thickening, endothelial shedding, extensive inflammatory cell infiltration, disordered smooth muscle layer arrangement, vascular dilation, and lumen stenosis. The miR-155-5p agomir group exhibited aggravated coronary inflammation, wall thickening, and lumen stenosis versus the KD group, whereas the miR-155-5p antagomir group showed attenuated inflammation and wall thickening, improved smooth muscle arrangement, and reduced stenosis. The KD group demonstrated increased IL-6, IL-1β, TNF-α, CD4⁺ T cell percentage, CD4⁺/CD8⁺ ratio, coronary artery diameter, endothelial apoptosis rate, and p-NF-κB p65, TLR4, and p38 MAPK protein expression compared to the healthy group (all P<0.05), with decreased CD3⁺ and CD8⁺ T cell percentages (P<0.05). No significant differences were observed among the KD, agomir-NC, and antagomir-NC groups. Compared with the KD group, the miR-155-5p agomir group showed further increased inflammatory cytokines (IL-6, IL-1β, and TNF-α), CD4⁺ T cell percentage, CD4⁺/CD8⁺ ratio, coronary diameter, endothelial apoptosis, and protein expression of p-NF-κB p65, TLR4, and p38 MAPK, while reduced CD3⁺ and CD8⁺ T cell percentages (all P<0.05). Conversely, the miR-155-5p antagomir group showed significant reductions in inflammatory cytokines, protein expression of p-NF-κB p65, TLR4, and p38 MAPK, CD4⁺ T cell percentage, CD4⁺/CD8⁺ ratio, coronary artery diameter, and endothelial apoptosis, as well as significant increases in CD3⁺ and CD8⁺ T cell percentages (all P<0.05). Conclusions Overexpression of miR-155-5p exacerbates inflammatory response, coronary artery lesions, endothelial cell apoptosis, and immune dysfunction in KD, potentially through modulation of the TLR4/MAPK/NF-κB pathway. Inhibition of miR-155-5p may reverse these pathological changes.