细胞凋亡
内质网
标记法
TLR4型
炎症
炎症体
氧化应激
红景天苷
内分泌学
肠道菌群
内科学
呋喃
化学
脂多糖
生物
生物化学
免疫学
药理学
医学
有机化学
作者
Ziyue Wang,Lu Li,Haiyang Yan,Wenliang Li,Yong Pang,Yuan Yuan
标识
DOI:10.1021/acs.jafc.3c06587
摘要
Furan is a heat-induced food contaminant, and it causes damage to visceral organs, including the testis. To determine the mechanism of the damage to the testis, a mouse model treated with furan (8 mg/kg bw/day) and salidroside (SAL, 10/20/40 mg/kg bw/day) was established, and levels of testicular functional markers and changes of morphology were investigated in furan-induced mice treated with SAL. The change in related proteins and genes suggested that SAL restored the furan-mediated leaky tight junction and triggered the TLR4/MyD88/NF-κB pathway and NLRP3 inflammasome together with inflammation. To find out the gut-testis axis, microbiota PICRUSt analysis and correlation analysis were conducted to investigate the core microbiota and metabolites. The endoplasmic reticulum stress (ERS)-related key protein levels and the result of transmission electron microscopy suggested that SAL inhibited the furan-induced intestinal ERS. The result of TUNEL and levels of apoptosis-related proteins suggested that furan-induced intestinal apoptosis was alleviated by SAL. Collectively, SAL inhibited furan-induced ERS-mediated intestinal apoptosis through modulation of intestinal flora and metabolites, thus strengthening the gut barrier. It inhibited LPS from entering the circulatory system and suppressed the testicular TLR4/MyD88/NF-κB pathway and NLRP3 inflammasome, which alleviated testicular inflammation.
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