International immunopharmacology · 2025
Electroacupuncture alleviates intestinal ischemia-reperfusion-induced acute lung injury via the vagus-sympathetic nerve pathway.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lv Shihua, Ma Can, Fu Wenchao, Hu Cong, Han Xiao, Chen Jiahui, Tan Xin, Liu Tianhua, Li Wenzhi
Аннотация
AIMS: Intestinal ischemia-reperfusion (II/R) injury predominantly causes acute lung injury (ALI), and in severe instances, acute respiratory distress syndrome, both associated with high mortality. Electroacupuncture (EA) excels in regulating autonomic nervous system balance and safeguarding organ function. This study delved into EA's impacts and mechanisms on II/R-induced ALI.
METHODS AND RESULTS: A rat II/R model was created by occluding the superior mesenteric artery for 1 h followed by reperfusion, with EA stimulation applied 30 min before reperfusion. Vagotomy and chemical sympathectomy explored EA's link with the autonomic nervous system. Findings revealed EA mitigated II/R-induced intestinal and lung pathological damage and edema, increased Claudin-5 and ZO-1 expression, inhibited local and systemic inflammation. Additionally, EA reduced the total protein concentration in bronchoalveolar lavage fluid while increasing the levels of pulmonary surfactant related proteins SP-A and SP-D, and decreased the low/high frequency ratio of heart rate variability. EA enhanced central parasympathetic activity, peripheral acetylcholine, vasoactive intestinal peptide in mesenteric lymph nodes, and lung α7nAChR expression, while reducing hypothalamic-pituitary-adrenal axis substances and peripheral blood glutamic acid/γ-aminobutyric acid ratio. However, the protective effect of EA disappeared after vagotomy in rats and partially weakened after sympathetic nerve chemical resection.
CONCLUSION: EA alleviates II/R-ALI via the vagus-sympathetic nerve pathway, highlighting its therapeutic potential.
METHODS AND RESULTS: A rat II/R model was created by occluding the superior mesenteric artery for 1 h followed by reperfusion, with EA stimulation applied 30 min before reperfusion. Vagotomy and chemical sympathectomy explored EA's link with the autonomic nervous system. Findings revealed EA mitigated II/R-induced intestinal and lung pathological damage and edema, increased Claudin-5 and ZO-1 expression, inhibited local and systemic inflammation. Additionally, EA reduced the total protein concentration in bronchoalveolar lavage fluid while increasing the levels of pulmonary surfactant related proteins SP-A and SP-D, and decreased the low/high frequency ratio of heart rate variability. EA enhanced central parasympathetic activity, peripheral acetylcholine, vasoactive intestinal peptide in mesenteric lymph nodes, and lung α7nAChR expression, while reducing hypothalamic-pituitary-adrenal axis substances and peripheral blood glutamic acid/γ-aminobutyric acid ratio. However, the protective effect of EA disappeared after vagotomy in rats and partially weakened after sympathetic nerve chemical resection.
CONCLUSION: EA alleviates II/R-ALI via the vagus-sympathetic nerve pathway, highlighting its therapeutic potential.