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Assessment of sinapic acid's protective effects against ethanol-induced gastric ulcers in rats.

作者信息

Akdemir Fazile Nur Ekinci, Güler Mustafa Can, Eraslan Ersen, Tanyeli Ayhan, Yildirim Serkan

机构信息

Department of Nutrition and Dietetics, Faculty of Health Science, Ağrı İbrahim Çeçen University, Ağrı, Turkey.

Department of Physiology, Faculty of Medicine, Atatürk University, 25240, Erzurum, Turkey.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 2024 Dec 24. doi: 10.1007/s00210-024-03733-0.


DOI:10.1007/s00210-024-03733-0
PMID:39718611
Abstract

This study evaluates the protective effects of sinapic acid (SA), a polyphenolic compound with diverse biological activities, against ethanol-induced gastric ulcers in rats. A gastric ulcer model was established using ethanol (ETH), and the experimental groups received either omeprazole (OMEP, 20 mg/kg) or SA at doses of 20 mg/kg and 40 mg/kg via oral gavage for 14 days. Biochemical markers, including total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), malondialdehyde (MDA), and myeloperoxidase (MPO) activity, were assessed alongside proinflammatory cytokines (tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and IL-6) using ELISA. Histopathological and immunohistochemical analyses were conducted to evaluate tissue integrity and apoptosis. Statistical analysis was performed using one-way ANOVA, followed by Tukey's HSD test for post hoc comparisons. For non-parametric data, the Kruskal-Wallis test and Mann-Whitney U test were used. A p-value < 0.05 was considered statistically significant. Results revealed that SA significantly enhanced antioxidant defenses, as evidenced by elevated TAS levels and reductions in TOS, OSI, MPO activity, and MDA levels (p < 0.05). Additionally, SA treatment mitigated inflammation and apoptosis by decreasing TNF-α, IL-1β, IL-6, and Bax expression (p < 0.05). These effects were comparable to those observed with OMEP, a widely used clinical agent. Notably, the findings underscore SA's potential as a novel therapeutic agent for managing ethanol-induced gastric ulcers. By targeting oxidative stress and inflammatory pathways, SA could complement or serve as an alternative to current treatment strategies. Future research should focus on exploring SA's molecular mechanisms, dose optimization, and long-term efficacy in clinical settings, paving the way for its integration into therapeutic regimens for gastric mucosal injuries.

摘要

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[1]
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Int J Biol Macromol. 2024-10

[2]
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Reprod Toxicol. 2024-10

[3]
Hepatoprotective effects of resveratrol on α-amanitin-induced liver toxicity in rats.

Toxicon. 2024-8-28

[4]
Histological Alterations in the Internal Organs of Wistar Han Rats () Euthanized by Five Different Methods.

J Am Assoc Lab Anim Sci. 2024-1-1

[5]
Mechanisms of anti-ulcer actions of (L.) in ethanol-induced gastric ulcer in rats.

Saudi Pharm J. 2023-12

[6]
Integrated network pharmacology and metabolomics to investigate the effects and possible mechanisms of Dehydroevodiamine against ethanol-induced gastric ulcers.

J Ethnopharmacol. 2024-1-30

[7]
Treatment of infection and gastric ulcer: Need for novel Pharmaceutical formulation.

Heliyon. 2023-9-24

[8]
mucin attenuates indomethacins-induced gastric ulcers in mice via alleviating oxidative stress and inflammation.

Heliyon. 2023-4-22

[9]
Sinapic acid-loaded gel accelerates diabetic wound healing process by promoting re-epithelialization and attenuating oxidative stress in rats.

Biomed Pharmacother. 2023-7

[10]
Gastroprotective effect of dapagliflozin in ethanol-induced gastric lesions in rats: Crosstalk between HMGB1/RAGE/PTX3 and TLR4/MyD88/VEGF/PDGF signaling pathways.

Int Immunopharmacol. 2023-2

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