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<p>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 (<i>p53</i> and <i>Cdkn1a</i>), SASP production (<i>Il-6</i> and <i>Il-1β</i>), nuclear membrane disintegration (<i>Lmnb1</i>), as well as histological inflammation process in the colon of D-Gal-induced aging rat models. Twelve-week-old male Sprague-Dawley rats (<i>n</i> = 12) were divided into the control and D-Gal (100&#xa0;mg/kg/day for 6 weeks) groups. The expression levels of aging-related genes (<i>p53</i>, <i>Cdkn1a</i>, <i>Il-6</i>, Il-1β, and <i>Lmnb1</i>) 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 (<i>p</i> &lt; 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 <i>Il-1β</i> expression, which subsequently promotes potential cellular senescence.</p>

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

  • 期刊论文

  • 发表日期：

    2026年3月18日

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  • Cherry Azaria,
  • Rina Susilowati,
  • Yustina Andwi Ari Sumiwi,
  • Dewajani Purnomosari

摘要

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.