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咖啡酸苯乙酯减轻吲哚美辛诱导的大鼠胃溃疡。

Caffeic acid phenethyl ester attenuates indomethacin-induced gastric ulcer in rats.

作者信息

Neamatallah Thikryat

机构信息

Department of Pharmacology and Toxicology, Faculty of Pharmacy, King Abdulaziz University, 21589, Jeddah, Saudi Arabia.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 2024 Mar;397(3):1791-1801. doi: 10.1007/s00210-023-02730-z. Epub 2023 Sep 23.

DOI:10.1007/s00210-023-02730-z
PMID:37740773
Abstract

Gastric ulcer is one of the most frequent gastrointestinal ailments worldwide. Indomethacin, one of the most potent NSAIDs, suffers undesirable ulcerogenic activity. Caffeic acid phenethyl ester (CAPE) has known health benefits. The current study examined the potential of CAPE to combat indomethacin-induced gastric ulcers in rats. Animals were randomized into 5 groups: control, Indomethacin (50 mg/kg) mg/kg), Indomethacin + CAPE (5 mg/kg/day), Indomethacin + CAPE (10 mg/kg), and Indomethacin + Omeprazole (30 mg/kg). CAPE prevented the rise in ulcer index, attenuated histopathological changes and preserved gastric mucin concentration. CAPE efficiently significantly prevented accumulation of malondialdehude (MDA) and prevented exhaustion of the enzymatic activities of catalase (CAT) and superoxide dismutase (SOD). Further, CAPE prevented the rise in the expression of tumor necrosis factor-α (TNF-α), cyclo-oxygenase-2 (COX-2) and nuclear factor kapp-B (NFκB). This was associated with down-regulation of Bax and up-regulation of Bcl-2 mRNA. Finally, CAPE prevented induced indomethacin-induced decrease in heat shock protein 70 (HSP70) in gastric tissues. In conclusion, CAPE possesses the ability to prevent indomethacin-induced gastric ulcer in rats. This involves, at least partially, antioxidation, anti-inflammation, anti-apoptosis and enhancement of HSP70 expression.

摘要

胃溃疡是全球最常见的胃肠道疾病之一。吲哚美辛是最强效的非甾体抗炎药之一,具有不良的致溃疡活性。咖啡酸苯乙酯(CAPE)已知对健康有益。本研究考察了CAPE对抗吲哚美辛诱导的大鼠胃溃疡的潜力。将动物随机分为5组:对照组、吲哚美辛组(50 mg/kg)、吲哚美辛+CAPE组(5 mg/kg/天)、吲哚美辛+CAPE组(10 mg/kg)和吲哚美辛+奥美拉唑组(30 mg/kg)。CAPE可防止溃疡指数升高,减轻组织病理学变化,并维持胃黏液浓度。CAPE能有效显著地防止丙二醛(MDA)的积累,并防止过氧化氢酶(CAT)和超氧化物歧化酶(SOD)的酶活性耗竭。此外,CAPE可防止肿瘤坏死因子-α(TNF-α)、环氧化酶-2(COX-2)和核因子κB(NFκB)表达的升高。这与Bax的下调和Bcl-2 mRNA的上调有关。最后,CAPE可防止吲哚美辛诱导的胃组织中热休克蛋白70(HSP70)的减少。总之,CAPE具有预防吲哚美辛诱导的大鼠胃溃疡的能力。这至少部分涉及抗氧化、抗炎、抗凋亡和增强HSP70表达。

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