High‐fat diets (HFDs) can trigger lipid accumulation, insulin resistance, and inflammatory responses in the body, causing glucose and lipid metabolism dysfunction. This study aimed to explore the role of nuciferine on HFD‐induced disorders of glucose and lipid metabolism in obesity mice models, and further to identify the possible underlying mechanisms. In our experiments, nuciferine effectively ameliorated HFD‐induced insulin resistance by IRS/PI3K/AKT pathway, and alleviated HFD‐induced lipid accumulation via AMPK‐mediated regulation of FAS and ATGL expression. Nuciferine also suppressed HFD‐induced intestinal pathological damage, as evidenced by the improvement of intestinal barrier integrity and the increasing in expressions of tight junction proteins of claudin, ZO‐1, and occludin. In addition, 16S rRNA gene sequencing of the fecal microbiota suggested that nuciferine changed the diversity and the composition of gut microbiota in HFD‐fed mice. Nuciferine decreased the ratio of Firmicutes/Bacteroidetes, the relative abundance of LPS‐producing genus Desulfovibrio and the bacteria which involved in lipid metabolism. In summary, nuciferine ameliorated the disorders of glucose and lipid metabolism in obese mice via balancing the gut–liver axis.
Cadmium (Cd) is a heavy metal toxic that can cause health problems including lung injury. This study was set out to meet the growing demand for effective treatment of lung diseases and explore the mechanism of caffeic acid phenethyl ester (CAPE, a natural phenolic acid) protect against Cd‐caused lung damage. In this study, CAPE significantly increased mice body weight, decreased lung W/D ratio, and alleviated histomorphological injury. CAPE mitigated CdCl2‐induced oxidative stress through Nrf2/HO‐1/NQO1 pathway, suppressed inflammation via MyD88/NF‐κB pathway, and alleviated apoptosis by modulating apoptosis mediators. CAPE also inhibited the CdCl2‐caused decreasing of TLR4 level and the increasing of miR‐182‐5p level, which is achieved by miR‐182‐5p sponging TLR4. Collectively, miR‐182‐5p is involved in CAPE against CdCl2‐caused lung damage by targeting TLR4. MiR‐182‐5p/TLR4 is a new pathway for inhibiting oxidative stress, apoptosis, and inflammation in CAPE‐mediated lung protection, which provides a novel avenue for treatment therapies.
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