芹菜素、橙皮苷及其联用对5-氟尿嘧啶致肺损伤不同生理病理通路的影响。

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2025-07-14 DOI:10.1080/13813455.2025.2531443

Hamit Uslu, Gözde Atila Uslu, Taha Abdulkadir Çoban, Mustafa Özkaraca, Nezahat Kurt, Ali Sefa Mendil

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引用次数: 0

摘要

背景：化疗药物的目标是癌细胞，但它们在健康组织中也有不可避免的毒性。目的：本研究探讨常用化疗药物5-氟尿嘧啶（5FU）对肺组织的影响，以及芹菜素（API）、橙皮苷（HES）及其联用可能的保护作用。方法：研究分为对照组、5FU组、API+ 5FU组、HES + 5FU组和API+HES + 5FU组。API 50 mg/kg, HES 200 mg/kg，连续7 d。第8天给药5FU 100 mg/kg。结果：分析显示API和HES通过抑制MAPK/NFκB和Caspase-3/Bax/Bcl-2通路，通过降低LC3B表达抑制自噬，调节Sigmar1表达，有效预防5FU诱导的肺组织氧化应激，减轻炎症和细胞凋亡。结论：这些结果表明，这两种黄酮类化合物单独或联合使用，可能有助于减少化疗期间经常发生的副作用。

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Effects of apigenin, hesperidin and their combinations on different physiopathological pathways in 5-fluorouracil-induced pulmonary damage.

Background: Chemotherapeutics target cancerous cells, but they also have unavoidable toxicities in healthy tissues.

Aim: In this study, the effects of the commonly used chemotherapeutic 5-fluorouracil (5FU) on lung tissue were investigated, along with the possible protective benefits of apigenin (API), hesperidin (HES), and their combination.

Methodology: The study consisted of control, 5FU, API + 5FU, HES + 5FU, and API+HES + 5FU groups. API 50 mg/kg and HES 200 mg/kg were administered for 7 days. On the 8th day, 5FU was administered a dose of 100 mg/kg.

Results: Analyses showed that API and HES were effective in preventing oxidative stress induced by 5FU in lung tissue, attenuating inflammation and apoptosis by suppressing MAPK/NFκB and Caspase-3/Bax/Bcl-2 pathways, suppressing autophagy by decreasing LC3B expression, and regulating Sigmar1 expression.

Conclusion: These results suggest that the two flavonoids, when administered separately or in combination, may be useful in reducing side effects that often occur during the use of chemotherapeutics.

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.