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<p>Diclofenac (DFC), a nonsteroidal anti-inflammatory drug (NSAID), has long been associated with gastrointestinal damage secondary to oxidative stress, inflammation, and disordered mucosal defense mechanisms. Salvianolic acid B (Sal B), a polyphenol compound extracted from <i>Salvia miltiorrhiza</i>, exhibits robust antioxidative, tissue regenerative, and anti-inflammatory activities. The present work was planned to explore the antiulcerogenic impact of Sal B against DFC-driven gastric ulceration in rats. Thirty-two male Wistar rats were randomly classified into four categories (<i>n</i> = 8 per group): Group 1 (Control): Received dimethyl sulfoxide (DMSO) for 14 days. Group 2 (DFC): Administered DMSO for 14 days, followed by oral DFC administration (100&#xa0;mg/kg). Group 3 (Sal B): Received Sal B for 14&#xa0;days before DFC exposure. Group 4 (EMP): Received esomeprazole (EMP) for 14&#xa0;days prior to DFC administration. Pretreatment with Sal B dramatically attenuated stomach ulcerative symptoms, as reflected by apparent decrements in HCl-promoting elements, namely α1ATP, gastric juice volume, pepsin amount, and ADMA, while strengthening stomach pH and digestive mucosal defense factors (PGE2 and COX-1). Sal B also mitigated oxidative damage as reflected by significant decrements in malondialdehyde (MDA) and lipid peroxidation (LPO) production together with strengthened activity of antioxidative elements, namely superoxide dismutase (SOD) and catalase (CAT). Moreover, Sal.B substantially downregulated inflammatory mediators like interleukin-6 (IL-6) and upregulated IL-10 and markedly boosted amounts of angiogenic markers like hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF), and reversed DFC-exacerbated stomach histopathological damage. Sal B demonstrated strong gastroprotective actions towards DFC-evoked stomach ulcers via antioxidative, anti-inflammatory, and pro-angiogenic actions.</p>

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Gastroprotective effect of salvianolic acid B on rat model of diclofenac-induced gastric ulceration

  • 期刊论文

  • 发表日期：

    2026年2月11日

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  • Samer Jaffar Sharif,
  • Haitham Mahmood Kadhim,
  • Hayder Ridha-Salman,
  • Ali Hasson Hussein

摘要

Diclofenac (DFC), a nonsteroidal anti-inflammatory drug (NSAID), has long been associated with gastrointestinal damage secondary to oxidative stress, inflammation, and disordered mucosal defense mechanisms. Salvianolic acid B (Sal B), a polyphenol compound extracted from Salvia miltiorrhiza, exhibits robust antioxidative, tissue regenerative, and anti-inflammatory activities. The present work was planned to explore the antiulcerogenic impact of Sal B against DFC-driven gastric ulceration in rats. Thirty-two male Wistar rats were randomly classified into four categories (n = 8 per group): Group 1 (Control): Received dimethyl sulfoxide (DMSO) for 14 days. Group 2 (DFC): Administered DMSO for 14 days, followed by oral DFC administration (100 mg/kg). Group 3 (Sal B): Received Sal B for 14 days before DFC exposure. Group 4 (EMP): Received esomeprazole (EMP) for 14 days prior to DFC administration. Pretreatment with Sal B dramatically attenuated stomach ulcerative symptoms, as reflected by apparent decrements in HCl-promoting elements, namely α1ATP, gastric juice volume, pepsin amount, and ADMA, while strengthening stomach pH and digestive mucosal defense factors (PGE2 and COX-1). Sal B also mitigated oxidative damage as reflected by significant decrements in malondialdehyde (MDA) and lipid peroxidation (LPO) production together with strengthened activity of antioxidative elements, namely superoxide dismutase (SOD) and catalase (CAT). Moreover, Sal.B substantially downregulated inflammatory mediators like interleukin-6 (IL-6) and upregulated IL-10 and markedly boosted amounts of angiogenic markers like hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF), and reversed DFC-exacerbated stomach histopathological damage. Sal B demonstrated strong gastroprotective actions towards DFC-evoked stomach ulcers via antioxidative, anti-inflammatory, and pro-angiogenic actions.