Background/Aims. The aim of this study is to examine the protective effect of the cholinergic anti-inflammatory pathway (CAP) in experimental esophagitis in rats. Methods. A total of 40 male Sprague-Dawley (SD) rats were randomly divided into five groups as follows: control group, sham + saline group, sham + acid group, operation + saline group, and operation + acid group. Two weeks after the dorsal motor nucleus of the vagus (DMV) destruction, hydrochloric acid with pepsin was perfused into the lower part of the esophagus for 90 min. The rats were sacrificed 60 min after perfusion. The esophagus was prepared for hematoxylin and eosin (HE) staining, and the degree of inflammation and NF-κB activation in the esophagus was measured. Inflammatory cytokines (TNF-α, IL-6, IL-1β, and PGE2) in the esophagus were measured by ELISA. The brain was removed and processed for c-fos immunohistochemistry staining. The c-fos-positive neurons were counted and analyzed. Results. The TNF-α, IL-1β, IL-6, and PGE2 concentrations in the esophageal tissue increased after acid perfusion. The microscopic esophagitis scores and the activation of NF-κB p65 in the esophagus were significantly higher in the operation + acid group than in the operation + saline group. c-fos-positive neurons significantly increased in rats receiving acid perfusion in the amygdala (AM), the paraventricular nucleus of the hypothalamus (PVN), the parabrachial nucleus (PBN), the nucleus of the solitary tract (NTS)/DMV, the nucleus ambiguous (NA), the reticular nucleus of the medulla (RNM), and the area postrema (AP). After DMV destruction, c-fos expression was reduced in the AM, PVN, PBN, NTS/DMV, NA, RNM, and AP, especially in the AM, PVN, NTS/DMV, RNM, and AP. Conclusions. The DMV is an important nucleus of the CAP. The DMV lesion can aggravate esophageal inflammation and injury from acid-induced acute esophagitis in a rat model. The CAP has a protective effect on the acute esophagitis rat model and could be a new therapy for reflux esophagitis (RE).

中文翻译：

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在大鼠模型中，迷走神经背侧运动核的破坏加剧了酸诱导的急性食管炎的炎症和损伤。

背景/目标。本研究的目的是检查胆碱能抗炎通路 (CAP) 在大鼠实验性食管炎中的保护作用。方法。将40只雄性Sprague-Dawley(SD)大鼠随机分为5组：对照组、假手术+生理盐水组、假手术+酸液组、手术+生理盐水组、手术+酸液组。迷走神经背侧运动核 (DMV) 破坏两周后，将含有胃蛋白酶的盐酸灌注到食道下部，持续 90 分钟。灌注后60分钟处死大鼠。准备食道用于苏木精和伊红（HE）染色，并测量食道中的炎症程度和NF-κB活化程度。炎症细胞因子（TNF-通过ELISA测量食道中的α、IL-6、IL-1β和PGE2)。取出大脑并进行 c-fos 免疫组织化学染色处理。对 c-fos 阳性神经元进行计数和分析。结果。酸灌注后食管组织中的TNF - α、IL- 1β、IL-6和PGE2浓度增加。显微镜下食管炎评分和 NF- κ的激活手术+酸组食管中B p65明显高于手术+生理盐水组。在接受酸灌注的大鼠杏仁核 (AM)、下丘脑室旁核 (PVN)、臂旁核 (PBN)、孤束核 (NTS)/DMV、模糊核（NA）、延髓网状核（RNM）和后区（AP）。DMV破坏后，c-fos在AM、PVN、PBN、NTS/DMV、NA、RNM和AP中的表达降低，尤其是在AM、PVN、NTS/DMV、RNM和AP中。结论。DMV 是 CAP 的一个重要核心。DMV 损伤可加重大鼠模型中酸诱导的急性食管炎的食管炎症和损伤。CAP对急性食管炎大鼠模型具有保护作用，可能成为反流性食管炎（RE）的新疗法。