Frontiers in microbiology · 2026
Zinc gluconate ameliorates antibiotics/PGN-induced intestinal injury via modulating the gut barrier, macrophages immunity and gut microbiota.
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.
Yang Xia, Wei Sumei, Su Shiqi, Su Ying, Lan Liancheng, Chen Xiuqi, Huang Ting, Shan Qingwen
Аннотация
OBJECTIVE: This study aimed to investigate the protective effects of zinc gluconate (ZnG) against antibiotics and peptidoglycan (PGN) induced intestinal injury by targeting gut barrier integrity, macrophage, and gut microbiota homeostasis.
METHODS: Twenty four C57BL/J mice were randomly divided into four groups: normal group (NC), antibiotic cocktail group (ABX), model group (ABX+PGN), and ZnG treatment group (ZnG+ABX/PGN). An antibiotic associated dysbiosis model was established via oral gavage of an antibiotic cocktail, followed by intraperitoneal injection of PGN (10 mg/kg) to simulate Gram positive (G+) bacteria associated challenge in antibiotic associated colitis (AAC) after microbiota disruption. Subsequently, ZnG was administered for therapeutic intervention. Parameters assessed included general condition of mice, intestinal permeability, barrier integrity, macrophage polarization, and gut microbiota composition.
RESULTS: The results indicated that ZnG significantly increased the body weight of the mice treated with ABX and PGN. It also markedly alleviated pathological and ultrastructural damage in the colon. ZnG improved intestinal permeability by reducing serum diamine oxidase (DAO) levels and restored intestinal integrity by upregulating tight junction proteins (TJs), including zonula occludens-1 (ZO-1), Occludin, and mucin 2 (MUC2). In addition, ZnG modulated the macrophage immunity by regulating the expression of polarization associated proteins (iNOS/ARG-1) and inhibited activation of the TLR2-NF-κB signaling pathway. Microbiota analysis revealed that ZnG increased gut microbial diversity while modulating the microbial community structure and its predicted functional potential in mice.
CONCLUSIONS: These findings demonstrate that ZnG exhibits therapeutic potential for AAC through modulation of gut microbiota, enhancement of gut barrier, and regulation of immune responses.
METHODS: Twenty four C57BL/J mice were randomly divided into four groups: normal group (NC), antibiotic cocktail group (ABX), model group (ABX+PGN), and ZnG treatment group (ZnG+ABX/PGN). An antibiotic associated dysbiosis model was established via oral gavage of an antibiotic cocktail, followed by intraperitoneal injection of PGN (10 mg/kg) to simulate Gram positive (G+) bacteria associated challenge in antibiotic associated colitis (AAC) after microbiota disruption. Subsequently, ZnG was administered for therapeutic intervention. Parameters assessed included general condition of mice, intestinal permeability, barrier integrity, macrophage polarization, and gut microbiota composition.
RESULTS: The results indicated that ZnG significantly increased the body weight of the mice treated with ABX and PGN. It also markedly alleviated pathological and ultrastructural damage in the colon. ZnG improved intestinal permeability by reducing serum diamine oxidase (DAO) levels and restored intestinal integrity by upregulating tight junction proteins (TJs), including zonula occludens-1 (ZO-1), Occludin, and mucin 2 (MUC2). In addition, ZnG modulated the macrophage immunity by regulating the expression of polarization associated proteins (iNOS/ARG-1) and inhibited activation of the TLR2-NF-κB signaling pathway. Microbiota analysis revealed that ZnG increased gut microbial diversity while modulating the microbial community structure and its predicted functional potential in mice.
CONCLUSIONS: These findings demonstrate that ZnG exhibits therapeutic potential for AAC through modulation of gut microbiota, enhancement of gut barrier, and regulation of immune responses.