MC-LR induces and exacerbates Colitis in mice through the JAK1/STAT3 pathway DOI

Xiaodie Zhou,

Yue Yang,

Canqun Yan

et al.

Journal of Toxicology and Environmental Health, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 11

Published: Jan. 26, 2025

Inflammatory bowel disease (IBD) is a complex gastrointestinal disorder attributed to genetic and environmental factors. Microcystin-leucine-arginine (MC-LR) an toxin that accumulates in the gut produces intestinal damage. The aim of this study was investigate effects exposure MC-LR on development progression IBD as well examine underlying mechanisms microcystin-initiated tissue Male C57BL/6 mice were treated with either alone or concurrently dextran-sulfate sodium (DSS). Mice divided into 4 groups (1): PBS gavage (control, CT) (2); 200 μg/kg (3); 3% DSS Drinking Water (DSS); (4) + (DSS MC-LR). each experimental group exhibited reduced body weight, shortened colon length, increased activity index (DAI) score, disrupted barrier, elevated levels proinflammatory cytokines compared control. Compared alone, colitis symptoms exacerbated following combined both MC-LR. Subsequent experiments confirmed protein phosphorylation Janus Kinase1 (JAK1) Signal Transducer Activator Transcription3 (STAT3). treatment also significantly upregulated expression related proteins. In conclusion, our indicates MC-LR-induced involves activation JAK1/STAT3 signaling pathway exacerbates DSS-induced through same pathway.

Language: Английский

MC-LR induces and exacerbates Colitis in mice through the JAK1/STAT3 pathway DOI

Xiaodie Zhou,

Yue Yang,

Canqun Yan

et al.

Journal of Toxicology and Environmental Health, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 11

Published: Jan. 26, 2025

Inflammatory bowel disease (IBD) is a complex gastrointestinal disorder attributed to genetic and environmental factors. Microcystin-leucine-arginine (MC-LR) an toxin that accumulates in the gut produces intestinal damage. The aim of this study was investigate effects exposure MC-LR on development progression IBD as well examine underlying mechanisms microcystin-initiated tissue Male C57BL/6 mice were treated with either alone or concurrently dextran-sulfate sodium (DSS). Mice divided into 4 groups (1): PBS gavage (control, CT) (2); 200 μg/kg (3); 3% DSS Drinking Water (DSS); (4) + (DSS MC-LR). each experimental group exhibited reduced body weight, shortened colon length, increased activity index (DAI) score, disrupted barrier, elevated levels proinflammatory cytokines compared control. Compared alone, colitis symptoms exacerbated following combined both MC-LR. Subsequent experiments confirmed protein phosphorylation Janus Kinase1 (JAK1) Signal Transducer Activator Transcription3 (STAT3). treatment also significantly upregulated expression related proteins. In conclusion, our indicates MC-LR-induced involves activation JAK1/STAT3 signaling pathway exacerbates DSS-induced through same pathway.

Language: Английский

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