Department of Pharmacology and Toxicology, College of Pharmacy, KSU, Riyadh, Saudi Arabia.
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.
J Biochem Mol Toxicol. 2022 Jan;36(1):e22932. doi: 10.1002/jbt.22932. Epub 2021 Oct 19.
5-Fluorouracil (5-FU) is a front-line cytotoxic therapy. However, intestinal mucositis is a well-known adverse event of 5-FU, which limits its therapeutic use. Indeed, thymol, which is a monoterpene component of the essential oil derived from thymus, has a potential anti-inflammatory and immunomodulatory activity. Therefore, this study aimed to investigate the potential chemoprotective effect of thymol against 5-FU-induced intestinal mucositis. Rats were either exposed to two doses of 5-FU (150 mg/kg, ip) and/or treated with thymol (60 or 120 mg/kg). Oxidative stress and inflammatory markers, as well as pathological changes, were assessed. 5-FU-induced severe intestinal damages as were evidenced by histopathological changes as well as oxidative and inflammatory responses. Thymol pretreatment inhibited 5-FU-induced oxidative stress by reducing lipid peroxidation and increasing intestinal levels of antioxidant systems. Moreover, inflammatory response markers, such as interleukin-6, prostaglandin E2, and COX-2 were also improved. The immunoblotting analysis also showed that thymol significantly inhibited the 5-FU-induced expression of nuclear factor-κB, tumor necrosis factor-α, and transforming growth factor β-1 (TGF-β1), in addition to the suppression of p38 and phosphorylated c-Jun N-terminal kinases (p-JNK) mitogen-activated protein kinase proteins' expressions. Our study is the first to demonstrate the promising protective effect of thymol against 5-FU-induced intestinal mucositis through inhibition of oxidative, inflammatory pathways, and suppression of TGF-β/p38/p-JNK signaling.
5-氟尿嘧啶(5-FU)是一种一线细胞毒性疗法。然而,5-FU 引起的肠道黏膜炎是一种众所周知的不良反应,限制了其治疗用途。事实上,百里香酚是从百里香油中提取的单萜成分,具有潜在的抗炎和免疫调节活性。因此,本研究旨在探讨百里香酚对 5-FU 诱导的肠道黏膜炎的潜在化学保护作用。大鼠分别暴露于两种剂量的 5-FU(150mg/kg,ip)和/或用百里香酚(60 或 120mg/kg)处理。评估了氧化应激和炎症标志物以及组织病理学变化。5-FU 诱导的严重肠道损伤表现为组织病理学变化以及氧化和炎症反应。百里香酚预处理通过减少脂质过氧化和增加肠道抗氧化系统水平来抑制 5-FU 诱导的氧化应激。此外,还改善了白细胞介素-6、前列腺素 E2 和 COX-2 等炎症反应标志物。免疫印迹分析还表明,百里香酚显著抑制了 5-FU 诱导的核因子-κB、肿瘤坏死因子-α和转化生长因子-β-1(TGF-β1)的表达,以及对 p38 和磷酸化 c-Jun N-末端激酶(p-JNK)丝裂原激活蛋白激酶蛋白表达的抑制。本研究首次证明了百里香酚通过抑制氧化、炎症途径和抑制 TGF-β/p38/p-JNK 信号通路对 5-FU 诱导的肠道黏膜炎具有有希望的保护作用。