Atasever Aslıhan, Tekin Samet, Bolat İsmail, Bolat Merve, Dağ Yusuf, ÇınaR Burak, Şengül Emin, Yıldırım Serkan, Warda Mohamad, Çelebi Fikret
Department of Veterinary Medicine, Çayırlı Vocational High School, Erzincan University, Erzincan, Turkey.
Department of Physiology, Faculty of Veterinary Medicine, Atatürk University, Erzurum, Turkey.
Naunyn Schmiedebergs Arch Pharmacol. 2025 May 22. doi: 10.1007/s00210-025-04292-8.
This study is to investigate the effects of melatonin on lung inflammation, oxidative stress, apoptosis, tissue damage, and MT1 and MT2 receptors in acrylamide-induced lung toxicity. Fifty male rats were randomly divided into five groups. The control group received distilled water orally for 11 days, while the acrylamide group received acrylamide (50 mg/kg, i.g.) for 11 days. The MEL10 + ACR and MEL20 + ACR groups received intraperitoneal injections of melatonin at doses of 10 mg/kg and 20 mg/kg, respectively, followed by acrylamide (50 mg/kg, i.g.) administered 1 h after melatonin injection. The MEL20 group received melatonin injections (20 mg/kg) for 11 days. Lung tissues collected at the end of the study underwent biochemical, histopathological, immunohistochemical, immunofluorescence, and in silico analyses. Acrylamide caused oxidative stress, inflammation, apoptosis, and tissue damage in the lungs. Melatonin treatment alleviated acrylamide-induced lung damage by exhibiting antioxidant, anti-inflammatory, and anti-apoptotic effects. Melatonin significantly improved the histopathological changes caused by acrylamide in lung tissue. Melatonin may have protective effects on health by regulating cellular processes such as oxidative stress, antioxidant enzyme activity, inflammation, and apoptosis through MT1 and MT2 receptors. Melatonin mitigates oxidative stress, inflammation, apoptosis, and tissue damage in acrylamide-induced lung injury in rats.
本研究旨在探讨褪黑素对丙烯酰胺诱导的肺毒性中肺部炎症、氧化应激、细胞凋亡、组织损伤以及MT1和MT2受体的影响。将50只雄性大鼠随机分为五组。对照组口服蒸馏水11天，而丙烯酰胺组给予丙烯酰胺（50 mg/kg，腹腔注射）11天。MEL10+ACR组和MEL20+ACR组分别腹腔注射剂量为10 mg/kg和20 mg/kg的褪黑素，随后在注射褪黑素1小时后给予丙烯酰胺（50 mg/kg，腹腔注射）。MEL20组注射褪黑素（20 mg/kg）11天。在研究结束时收集肺组织进行生化、组织病理学、免疫组织化学、免疫荧光和计算机分析。丙烯酰胺可导致肺部氧化应激、炎症、细胞凋亡和组织损伤。褪黑素治疗通过表现出抗氧化、抗炎和抗凋亡作用减轻了丙烯酰胺诱导的肺损伤。褪黑素显著改善了丙烯酰胺引起的肺组织病理变化。褪黑素可能通过MT1和MT2受体调节氧化应激、抗氧化酶活性、炎症和细胞凋亡等细胞过程对健康产生保护作用。褪黑素可减轻丙烯酰胺诱导的大鼠肺损伤中的氧化应激、炎症、细胞凋亡和组织损伤。
