SPB-201 Alleviates Indomethacin-Induced Gastric Damage in Rats through Its Antioxidant, Anti-inflammatory, and Pro-angiogenic Properties.

Seonghyun Ho, Seon Hee Kim, Su-Jin Park
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Abstract

Background/aims: The inhibition of prostaglandin (PG) synthesis by indomethacin causes gastric ulceration by inducing oxidative stress and inflammation.

Methods: This study investigated the protective effects of an Artemisia annua extract powder (SPB-201) on gastric damage and its underlying mechanisms by analyzing various molecular biological markers in indomethacin-induced gastric ulceration rats and AGS human gastric cancer cells.

Results: The oral administration of SPB-201 augmented the gastroprotective PGE2 and NO contents by increasing COX-1, COX-2, and eNOS expression, resulting in the improvement of gastric damage and ulcerative hyperemia in rats. In addition, elevated levels of mucin and pro-angiogenic factors, including EGF, bFGF, VEGF, and TGF-β1, were observed in the gastric tissue of rats treated with SPB-201. Furthermore, SPB-201 induced the SOD and CAT activities in rats but reduced the protein and mRNA levels of TNF-α, IL-1β, and IL-6. In addition, the SPB-201 treatment showed a dose-dependent and statistically significant increase in COX-1, COX-2, and PGE2 production in AGS cells exposed to indomethacin.

Conclusions: SPB-201 might be an excellent candidate for developing anti-ulcer agents that prevent or treat gastric injury caused by NSAIDs, through antioxidant, anti-inflammatory, and pro-angiogenic mechanisms.

SPB-201通过其抗氧化、抗炎和促血管生成特性减轻吲哚美辛引起的大鼠胃损伤。
背景/目的:吲哚美辛抑制前列腺素(PG)的合成,通过诱导氧化应激和炎症引起胃溃疡。方法:通过分析吲哚美辛致大鼠胃溃疡和AGS人胃癌细胞的各种分子生物学标志物,探讨青蒿提取物粉(SPB-201)对胃损伤的保护作用及其机制。结果:口服SPB-201可通过增加COX-1、COX-2、eNOS表达,增强胃保护性PGE2、NO含量,改善大鼠胃损伤及溃疡性充血。此外,SPB-201处理后大鼠胃组织中黏液蛋白和促血管生成因子EGF、bFGF、VEGF、TGF-β1水平升高。此外,SPB-201还能诱导大鼠SOD和CAT活性,降低TNF-α、IL-1β和IL-6的蛋白和mRNA水平。此外,SPB-201处理显示暴露于吲哚美辛的AGS细胞中COX-1、COX-2和PGE2的产生呈剂量依赖性且具有统计学意义。结论:SPB-201可能是开发抗溃疡药物的理想候选者,通过抗氧化、抗炎和促血管生成机制预防或治疗非甾体抗炎药引起的胃损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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