电针对热损伤大鼠胃动力障碍的机制研究。

Journal of translational gastroenterology Pub Date : 2024-07-01 Epub Date: 2024-09-25 DOI:10.14218/jtg.2024.00026
Haixia Li, Jieyun Yin, Zhaohui Zhang, Hanaa S Sallam, Jiande D Z Chen
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引用次数: 0

摘要

背景和目的:胃肠道运动障碍常伴随热损伤,如烧伤。本研究旨在探讨电针(EA)对大鼠烧伤致胃运动障碍的影响及其机制。方法:将Sprague-Dawley大鼠分为60%烫伤假伤组和热伤组。拮抗剂,包括β-阻断剂(普萘洛尔),α-阻断剂(酚妥拉明),或选择性环氧化酶(COX)-2抑制剂(尼苏列特),用于验证所涉及的途径。烧伤6小时后,评估动物胃排空和心率变异性。采集血液和胃组织,检测细胞因子、激素和COX-2水平。在双侧ST36(足三里)穴行EA穴45 m。结果:烧伤后胃排空延迟61% (P < 0.01),尼舒利特和心得安能使胃排空恢复正常,酚妥拉明不能。EA能改善烧伤大鼠胃排空87% (P = 0.03)。心率变异性和血浆激素(去甲肾上腺素和胰多肽)分析显示烧伤大鼠交感神经亢进;EA通过增强迷走神经活动改善烧伤引起的交感神经不平衡。胃底和胃窦COX-2蛋白和mRNA的表达随烧伤升高,但经心得安后恢复正常。EA降低了烧伤引起的胃底COX-2表达的增加,但在胃窦中没有。EA还降低了烧伤引起的血浆白细胞介素(IL)-6和IL-10的升高。胃排空与血浆IL-6水平呈负相关,胃排空与COX-2 mRNA水平呈负相关。结论:这些发现表明,烧伤引起的胃运动障碍是通过自主cox -2途径介导的。ST36穴EA通过自主神经通路下调COX-2和促炎细胞因子,改善烧伤引起的胃排空延迟。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Autonomic-cyclooxygenase-2 Mechanisms of Electroacupuncture on Thermal Injury-induced Gastric Dysmotility in Rats.

Autonomic-cyclooxygenase-2 Mechanisms of Electroacupuncture on Thermal Injury-induced Gastric Dysmotility in Rats.

Autonomic-cyclooxygenase-2 Mechanisms of Electroacupuncture on Thermal Injury-induced Gastric Dysmotility in Rats.

Autonomic-cyclooxygenase-2 Mechanisms of Electroacupuncture on Thermal Injury-induced Gastric Dysmotility in Rats.

Background and objectives: Gastrointestinal dysmotility commonly follows thermal injuries, such as burns. This study aimed to investigate the effects and mechanisms of electroacupuncture (EA) on burn-induced gastric dysmotility in rats.

Methods: Sprague-Dawley rats were divided into sham and thermal injury groups subjected to a 60% scald burn. Antagonists, including β-blockade (propranolol), α-blockade (phentolamine), or a selective cyclooxygenase (COX)-2 inhibitor (nimsulide), were administered to verify the pathways involved. Six hours after the burn, the animals were evaluated for gastric emptying and heart rate variability. Blood and gastric tissues were collected for assays of cytokines, hormones, and COX-2 levels. EA was performed at bilateral ST36 (Zusanli) acupoints for 45 m.

Results: Burn injury delayed gastric emptying by 61% (P < 0.01), which was normalized by nimsulide or propranolol but not by phentolamine. EA improved gastric emptying by 87% (P = 0.03) in burned rats. Heart rate variability and plasma hormone (noradrenaline and pancreatic polypeptide) analyses indicated sympathetic hyperactivity in burned rats; EA improved burn-induced sympathovagal imbalance by enhancing vagal activity. Protein and mRNA expressions of COX-2 in the gastric fundus and antrum increased with burn but were normalized by propranolol. EA reduced the burn-induced increase in COX-2 expression in the gastric fundus but not in the antrum. EA also decreased burn-induced elevations in plasma interleukin (IL)-6 and IL-10. Negative correlations were found between gastric emptying and plasma IL-6 levels, as well as between gastric emptying and COX-2 mRNA levels.

Conclusions: These findings suggest that burn-induced gastric dysmotility is mediated via autonomic-COX-2 pathways. EA at acupoint ST36 improves burn-induced delays in gastric emptying by down-regulating COX-2 and pro-inflammatory cytokines through the autonomic nervous pathway.

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