MARATTO

article · Egyptian Journal of Basic and Applied Sciences

Vitamin D3 alleviates corticosteroid-mediated gastric damage in rats: targeting HMGB1/inflammation/apoptosis pathway, gastric angiogenesis and proliferation

2026Open accessMenoufia University

In plain language

Prolonged administration of synthetic corticosteroids often causes severe gastric damage. An experimental study evaluated the gastroprotective properties of vitamin D3 against prednisolone-induced stomach injury in male Wistar albino rats across four test groups. Rats co-treated with vitamin D3 showed reduced total gastric acidity alongside elevated mucous content and prostaglandin E2 levels. The supplement lowered tissue markers of oxidative stress and inflammation, specifically malondialdehyde, high mobility group box 1, tumour necrosis factor-alpha, and interleukin-1beta. In contrast, it boosted antioxidant defences including superoxide dismutase, catalase, and the anti-inflammatory cytokine interleukin-10. Microscopic analysis confirmed reduced structural damage in stomach tissue. Furthermore, vitamin D3 promoted blood vessel formation and cell proliferation by upregulating endothelial nitric oxide synthase and proliferating cell nuclear antigen, while suppressing programmed cell death through increased Bcl-2 expression. These outcomes indicate that vitamin D3 co-administration counteracts corticosteroid-induced stomach injury.

Key takeaways

  • Vitamin D3 reduced gastric acidity and increased protective mucous and prostaglandin E2 in rats receiving prednisolone.
  • Co-treatment lowered inflammatory cytokines, malondialdehyde, and HMGB1 levels while boosting antioxidant enzyme activity.
  • Histopathological evaluation showed that vitamin D3 mitigated corticosteroid-induced structural damage in gastric tissues.
  • The treatment upregulated markers associated with cell survival, proliferation, and blood vessel formation, including Bcl-2, PCNA, and e-NOS.

Why it matters

Synthetic corticosteroids are widely prescribed for inflammatory and autoimmune conditions, but their long-term use frequently causes severe stomach injury and ulceration. Demonstrating that vitamin D3 can mitigate this harm by curbing inflammation, boosting antioxidants, and promoting tissue repair offers a potential dietary or therapeutic co-treatment strategy to improve patient safety during prolonged steroid therapy.

Commercialisation angle

This research represents early-stage preclinical work in an animal model, pointing toward potential co-formulation or supportive supplement strategies alongside prescribed corticosteroids. Pharmaceutical developers or nutraceutical manufacturers could explore vitamin D3 as an adjuvant therapy to prevent gastrointestinal adverse effects in patients on long-term steroid regimens. However, moving this approach toward clinical adoption will require dedicated human trials to determine effective dosages, safety profiles, and real-world efficacy.

AI-generated from the published abstract. Always read the original work before citing.

Abstract

Long-term use of synthetic corticosteroids has a gastric damaging effect. This research examined the gastro-protective action of Vitamin D3 ‎against corticosteroid-induced gastric injury in rats. Forty male adults Wistar albino rats were allocated into control, Vitamin D3‎, prednisolone-induced gastric injury (PIGI) and Vitamin D3‎ + PIGI groups. Total acidity and mucous content, as well as prostaglandin E2 (PGE2), high mobility group box 1 (HMGB1), malondialdehyde (MDA), superoxide dismutase (SOD) activity, catalase and inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-10 (IL-10)] were measured in stomach tissues. Also, gastric tissues were histopathologically examined and evaluated for collagen, gastric B cell lymphoma-2 protein (Bcl-2), endothelial nitric oxide synthase (e-NOS) and proliferating cell nuclear antigen (PCNA) expression. Vitamin D3 reduced stomach acidity and increased gastric mucous secretion and gastric PGE2. It significantly decreased gastric HMGB1, MDA, TNF-α and IL-1β, while increased gastric SOD activity, catalase and IL-10. Moreover, Vitamin D3 mitigated the stomach histopathological abnormalities of corticosteroids. The expressions of Bcl-2, e-NOS and PCNA in stomach were apparently upregulated. Vitamin D3‎ co-administration could protect against the gastric injurious effect of corticosteroids. Vitamin D3 attenuated gastric inflammation and apoptosis through downregulation of HMGB1, while also improving gastric angiogenesis and proliferation.

Research topics

  • Helicobacter pylori-related gastroenterology studies
  • Advanced Glycation End Products research
  • Vitamin D Research Studies

Sustainable Development Goals

Read the original research

This page summarises published work. The authoritative version sits with the publisher.

DOI: 10.1080/2314808x.2026.2688707

Is something wrong with this record? Report it or request removal.

Discussion

Discuss this research

Have you built on this work, tried to replicate it, or seen it applied in practice? Share what you know. Verified researchers and MARATTO™ domain experts can open a discussion, and any member can reply. Contributions are reviewed before they appear.

No discussion yet. Open the first thread.