Acupuncture in medicine : journal of the British Medical Acupuncture Society · 2026
Electroacupuncture inhibits the NLRP3/caspase-1/ASC signaling pathway in a mouse model of inflammatory bowel disease.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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.
Jia Lv, Cao Sihui, Chen Lin, Li Zuqiang, Lu Penghui, Liu Qiong, Liu Mi
Аннотация
OBJECTIVE: Intestinal inflammatory responses are a key pathological feature of inflammatory bowel disease (IBD) and the nucleotide oligomerization domain (NOD)-like receptor protein 3/cysteine aspartate protease-1/apoptosis-associated speck-like protein (NLRP3/caspase-1/ASC) signaling pathway plays a key role in mediating these responses. The aim of this study was to investigate how electroacupuncture (EA) affects inflammation-related protein levels, including NLRP3, caspase-1 and ASC, in a mouse model of IBD and explore the underlying mechanisms of action.
METHODS: Forty-eight mice were randomly assigned to control, model, EA and NLRP3 inhibitor groups. IBD was induced using dextran sodium sulfate (DSS). After 1 week of EA treatment, fecal occult blood tests were performed and disease activity index (DAI) scores were recorded. In addition, hematoxylin-eosin staining was performed to evaluate the histopathological changes in the colon. Serum interleukin (IL)-1β, IL-18 and tumor necrosis factor (TNF)-α levels were measured using enzyme-linked immunosorbent assay, and protein expression of NLRP3, caspase-1, ASC, gasdermin D (GSDMD), N-terminal GSDMD (N-GSDMD), IL-1β and IL-18 in colonic tissues was assessed using Western blotting.
RESULTS: IBD resulted in alterations in general condition and colonic morphology, a significant increase in serum IL-1β, IL-18 and TNF-α levels, and a significant increase in protein expression of NLRP3, caspase-1, ASC, GSDMD, N-GSDMD, IL-1β and IL-18 in the colonic tissues (p < 0.01 or p < 0.001). EA and NLRP3 inhibition reversed these pathological changes and reduced the expression of inflammatory proteins induced by intestinal inflammatory responses (p < 0.05 or p < 0.01).
CONCLUSION: The NLRP3/caspase-1/ASC signaling pathway appears to play a role in mediating the therapeutic effects of EA in IBD.
METHODS: Forty-eight mice were randomly assigned to control, model, EA and NLRP3 inhibitor groups. IBD was induced using dextran sodium sulfate (DSS). After 1 week of EA treatment, fecal occult blood tests were performed and disease activity index (DAI) scores were recorded. In addition, hematoxylin-eosin staining was performed to evaluate the histopathological changes in the colon. Serum interleukin (IL)-1β, IL-18 and tumor necrosis factor (TNF)-α levels were measured using enzyme-linked immunosorbent assay, and protein expression of NLRP3, caspase-1, ASC, gasdermin D (GSDMD), N-terminal GSDMD (N-GSDMD), IL-1β and IL-18 in colonic tissues was assessed using Western blotting.
RESULTS: IBD resulted in alterations in general condition and colonic morphology, a significant increase in serum IL-1β, IL-18 and TNF-α levels, and a significant increase in protein expression of NLRP3, caspase-1, ASC, GSDMD, N-GSDMD, IL-1β and IL-18 in the colonic tissues (p < 0.01 or p < 0.001). EA and NLRP3 inhibition reversed these pathological changes and reduced the expression of inflammatory proteins induced by intestinal inflammatory responses (p < 0.05 or p < 0.01).
CONCLUSION: The NLRP3/caspase-1/ASC signaling pathway appears to play a role in mediating the therapeutic effects of EA in IBD.