Colonic inflammatory response in a D-galactose-induced aging model: elevated IL-1β expression

Aging is a long-term and complex process characterized by cellular changes, including cell cycle arrest, increased production of the senescence-associated secretory phenotype (SASP), and nuclear membrane disintegration. To accelerate the aging process, various animal models are made using chemical inducers, such as D-galactose (D-Gal). D-Gal has been extensively applied to induce aging in experimental animals; however, its effects on the gastrointestinal system, particularly the colon, remain underexplored. Observation of molecular aging markers will provide a valuable approach to assess these cellular changes. This study aimed to observe the expression of genes related to cell cycle arrest (p53 and Cdkn1a), SASP production (Il-6 and Il-1β), nuclear membrane disintegration (Lmnb1), as well as histological inflammation process in the colon of D-Gal-induced aging rat models. Twelve-week-old male Sprague-Dawley rats (n = 12) were divided into the control and D-Gal (100 mg/kg/day for 6 weeks) groups. The expression levels of aging-related genes (p53, Cdkn1a, Il-6, Il-1β, and Lmnb1) were assessed by reverse-transcription quantitative polymerase chain reaction. The D-Gal group exhibited inflammatory cell infiltration. Il-1β immunohistochemical score along with Il-1β expression was significantly elevated in D-Gal group (p < 0.01), suggesting SASP activation and pro-inflammatory signaling. No statistically significant differences were observed in the expression levels of p53, Il-6, Cdkn1a, or Lmnb1 expression. Molecular and histological results demonstrated that D-Gal administration induces colonic inflammation, characterized by increased Il-1β expression, which subsequently promotes potential cellular senescence.