ArticlePhysiological reports2025
Dextran sodium sulfate-induced colitis in male BALB/c mice leads to albuminuria and increased markers of inflammation and tissue damage in the kidney.
Article in Physiological reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Protective effects of watercress (Nasturtium officinale) leaf methanolic extract against dextran sodium sulfate induced colon inflammation in rats.Inflammopharmacology · 2026Article
- The Intestinal Barrier: A Multilayered Gatekeeper Against Systemic Disease.International journal of microbiology · 2026Review
- Optimization of dextran sulfate sodium-induced colitis and associated mortality in BALB/c mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Article
- Dextran sodium sulfate-induced colitis in male BALB/c mice leads to albuminuria and increased markers of inflammation and tissue damage in the kidney.Physiological reports · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Inflammatory molecules originating from an inflamed gut can promote systemic inflammation. We studied how acute intestinal injury affects the kidneys and the kallikrein-kinin system in mice with dextran sodium sulfate (DSS)-induced colitis. Seven-week-old male BALB/c mice were treated with 5% DSS for 7 days and either sacrificed immediately (DSS7, n = 6) or given fresh water for 4 more days (DSS11, n = 6). Untreated mice (n = 6) served as controls. Colitis and kidney damage was assessed using histochemical and immunohistochemical staining, ELISA, and RT-qPCR. Markers of kidney injury correlated with markers of colitis. Colitis increased albuminuria, reduced kidney weight, and induced transcription of lipocalin 2, kidney injury molecule-1, and interleukin-1beta, as well as increased immunostaining signal of c-Jun and NF-κB p65 in the kidneys. Colitis caused strong induction of colonic kininogen 2 transcription and bradykinin receptor B1-positive cells in the disrupted mucosa. In the kidney, colitis induced localization of tubular bradykinin receptor B2 to the nuclear envelope and increased kininogen 2 transcription. Disruption of the intestinal barrier by DSS promotes markers of kidney injury and inflammation, and the degree of kidney injury correlates with the severity of colitis. Colitis is associated with increased expression of kallikrein-kinin components in both the colon and kidneys.
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