Microbial pathogenesis · 2025
Qihuang decoction inhibits bacterial translocation by modulating macrophage M1 polarisation via negative regulation of miR-146a by lncRNA MALAT1.
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Zhou Fuhai, Li Ziyi, Lu Erguang, Peng Hui, Yu Qingsheng
Аннотация
OBJECTIVE: This study aimed to investigate whether Qihuang decoction prevents bacterial lipopolysaccharide (LPS) translocation by modulating macrophage M1 polarisation.
METHODS: A rat model of sleeve gastrectomy was established. Haematoxylin-eosin staining and electron microscopy were used to observe changes in small intestinal structures. Polymerase chain reaction (PCR), Western blotting and enzyme-linked immunosorbent assay (ELISA) were employed to detect expression levels of proteins and genes related to the TLR4/NF-κB pathway. Detection of phosphorylated NF-κB (p-NF-κB) was included to directly evaluate pathway activation. The expression levels of lncMALAT1 and miR-146a were also assessed by PCR. In addition, fluorescein isothiocyanate-labelled dextran (FD4), ELISA and a D-lactate assay kit were used to measure FD4 clearance, LPS levels and lactate concentrations. Macrophage polarisation was evaluated by flow cytometry and immunohistochemistry for iNOS, and CD206 was performed to visualise M1/M2 macrophage distribution in intestinal tissues.
RESULTS: The small intestine remained structurally intact, and inflammatory cell infiltration was reduced in the Qihuang decoction treatment group compared with the model group. There was a substantial decrease in the proportion of M1-polarised macrophages, as confirmed by both flow cytometry and immunohistochemistry. Qihuang decoction treatment resulted in substantial downregulation of lncRNA MALAT1, increased expression of miR-146a and reduced expression of TLR4/NF-κB pathway-related genes and proteins, including p-NF-κB. Lactate concentration, FD4 clearance and LPS levels were also reduced.
CONCLUSION: These findings suggest that Qihuang decoction negatively regulates miR-146a via lncRNA MALAT1, thereby reducing macrophage M1 polarisation induced by the TLR4/NF-κB pathway to inhibit bacterial translocation.
METHODS: A rat model of sleeve gastrectomy was established. Haematoxylin-eosin staining and electron microscopy were used to observe changes in small intestinal structures. Polymerase chain reaction (PCR), Western blotting and enzyme-linked immunosorbent assay (ELISA) were employed to detect expression levels of proteins and genes related to the TLR4/NF-κB pathway. Detection of phosphorylated NF-κB (p-NF-κB) was included to directly evaluate pathway activation. The expression levels of lncMALAT1 and miR-146a were also assessed by PCR. In addition, fluorescein isothiocyanate-labelled dextran (FD4), ELISA and a D-lactate assay kit were used to measure FD4 clearance, LPS levels and lactate concentrations. Macrophage polarisation was evaluated by flow cytometry and immunohistochemistry for iNOS, and CD206 was performed to visualise M1/M2 macrophage distribution in intestinal tissues.
RESULTS: The small intestine remained structurally intact, and inflammatory cell infiltration was reduced in the Qihuang decoction treatment group compared with the model group. There was a substantial decrease in the proportion of M1-polarised macrophages, as confirmed by both flow cytometry and immunohistochemistry. Qihuang decoction treatment resulted in substantial downregulation of lncRNA MALAT1, increased expression of miR-146a and reduced expression of TLR4/NF-κB pathway-related genes and proteins, including p-NF-κB. Lactate concentration, FD4 clearance and LPS levels were also reduced.
CONCLUSION: These findings suggest that Qihuang decoction negatively regulates miR-146a via lncRNA MALAT1, thereby reducing macrophage M1 polarisation induced by the TLR4/NF-κB pathway to inhibit bacterial translocation.