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<p>Ulcerative colitis (UC) is a long-term inflammatory condition affecting the colon’s lining starting from the rectum and extending throughout the colon. Interplay between UC, diabetes, and a liver complication involves complex interactions between inflammation, the immune system, and metabolic processes, which can complicate their management. Thus, the present study aims to investigate the in vivo effectiveness of sodium orthovanadate (SOV) in attenuating dextran sulfate sodium salt (DSS)-induced colitis and the associated liver injury in diabetic BALB/c mice, with particular emphasis on diabetes-related pathophysiological alterations and the underlying molecular mechanisms. 55 BALB/c male mice were allocated randomly into seven distinct groups (n = 7 − 8. The diabetes was induced with STZ; 40&#xa0;mg/kg; i.p. for five days successively and UC was instigated using 2.5% w/v DSS in three alternating cycles, each lasting seven days. SOV orally was given at 5 and 10&#xa0;mg/kg doses, along with the standard 5-aminosalicylic acid at dose 100&#xa0;mg/kg and metformin at 50&#xa0;mg/kg dose, in the beginning of the DSS second cycle and continuing until the end of the study. In diabetic mice, DSS-induced colitis was significantly more severe, with elevated glucose levels, worsened disease activity index (DAI) scores, heightened oxidative stress, and altered liver biomarkers, confirming that diabetes exacerbates colitis onset and progression. Oral administration of SOV at 5 and 10&#xa0;mg/kg, beginning with the second DSS cycle and continuing until the study’s end, significantly mitigated these diabetes-aggravated effects. SOV improved glycemic control, reduced DAI scores, oxidative stress, and normalized liver biomarkers. Histopathological the intervention helped maintain normal pancreatic architecture and mitigate diabetes-induced histological damage. Immunohistochemical analysis revealed that SOV enhanced Nrf2/Keap1 expression while suppressing NF-κB and IL-6, confirming its anti-inflammatory mechanism. The diabetes exacerbated DSS-induced colitis, while SOV (5 and 10&#xa0;mg/kg) significantly mitigated disease severity, oxidative stress, and metabolic and hepatic disturbances. These findings establish that SOV effectively counteracts the exacerbating impact of diabetes on colitis, highlighting its therapeutic potential in diabetes-associated intestinal inflammation.</p> Graphical Abstract <p></p>

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Investigate sodium orthovanadate molecular mechanisms in diabetes-aggravated ulcerative colitis, focusing on Nrf2/Keap1 antioxidant and NF-κB/IL-6 inflammatory pathways

  • 期刊论文

  • 发表日期：

    2026年3月12日

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  • Gurpreet Kaur,
  • Ajay Singh Kushwah

摘要

Ulcerative colitis (UC) is a long-term inflammatory condition affecting the colon’s lining starting from the rectum and extending throughout the colon. Interplay between UC, diabetes, and a liver complication involves complex interactions between inflammation, the immune system, and metabolic processes, which can complicate their management. Thus, the present study aims to investigate the in vivo effectiveness of sodium orthovanadate (SOV) in attenuating dextran sulfate sodium salt (DSS)-induced colitis and the associated liver injury in diabetic BALB/c mice, with particular emphasis on diabetes-related pathophysiological alterations and the underlying molecular mechanisms. 55 BALB/c male mice were allocated randomly into seven distinct groups (n = 7 − 8. The diabetes was induced with STZ; 40 mg/kg; i.p. for five days successively and UC was instigated using 2.5% w/v DSS in three alternating cycles, each lasting seven days. SOV orally was given at 5 and 10 mg/kg doses, along with the standard 5-aminosalicylic acid at dose 100 mg/kg and metformin at 50 mg/kg dose, in the beginning of the DSS second cycle and continuing until the end of the study. In diabetic mice, DSS-induced colitis was significantly more severe, with elevated glucose levels, worsened disease activity index (DAI) scores, heightened oxidative stress, and altered liver biomarkers, confirming that diabetes exacerbates colitis onset and progression. Oral administration of SOV at 5 and 10 mg/kg, beginning with the second DSS cycle and continuing until the study’s end, significantly mitigated these diabetes-aggravated effects. SOV improved glycemic control, reduced DAI scores, oxidative stress, and normalized liver biomarkers. Histopathological the intervention helped maintain normal pancreatic architecture and mitigate diabetes-induced histological damage. Immunohistochemical analysis revealed that SOV enhanced Nrf2/Keap1 expression while suppressing NF-κB and IL-6, confirming its anti-inflammatory mechanism. The diabetes exacerbated DSS-induced colitis, while SOV (5 and 10 mg/kg) significantly mitigated disease severity, oxidative stress, and metabolic and hepatic disturbances. These findings establish that SOV effectively counteracts the exacerbating impact of diabetes on colitis, highlighting its therapeutic potential in diabetes-associated intestinal inflammation.

Graphical Abstract