Ulaş Nergis, Üstündağ Hilal, Özkanlar Seçkin, Erbaş Elif, Kara Adem, Özkanlar Yunusemre
Department of Internal Medicine, Faculty of Veterinary Medicine, Ataturk University, Erzurum, Turkey.
Department of Physiology, Faculty of Medicine, Erzincan Binali Yıldırım University, Erzincan, Turkey.
Naunyn Schmiedebergs Arch Pharmacol. 2025 Mar 21. doi: 10.1007/s00210-025-04024-y.
Acute lung injury (ALI) is a severe respiratory disorder associated with high morbidity and mortality. Lipopolysaccharide (LPS) is widely used to induce ALI in animal models. D-carvone, a natural monoterpene, has been reported to possess anti-inflammatory and antioxidant properties. This study aimed to investigate the protective effects of D-carvone on LPS-induced ALI in rats. Thirty-six male rats were randomly divided into six groups (n = 6): control, D-carvone (10 mg/kg and 20 mg/kg p.o.), LPS (10 mg/kg E. coli lipopolysaccharide i.p.), and LPS + D-carvone (LPS with either 10 or 20 mg/kg D-carvone). D-carvone was administered orally once daily for 10 days. On day 10, sepsis was induced with LPS administration, and samples were collected after 6 h under deep anesthesia. LPS administration caused significant lung injury, as evidenced by increased histopathological scores, upregulation of pro-inflammatory markers (TLR4, IL-1β, TNF-α), and oxidative stress (increased MDA, decreased GSH and SOD). Treatment with D-carvone at both doses significantly attenuated these changes. D-carvone downregulated pro-inflammatory markers, upregulated anti-inflammatory (NRF2) and anti-apoptotic (Bcl-2) proteins, and reduced the levels of pro-inflammatory cytokines (IL-1β, TNF-α, IL-8) in lung tissues. In conclusion, D-carvone protects against LPS-induced ALI in rats, possibly through its anti-inflammatory and antioxidant properties. These findings suggest that D-carvone could be a potential therapeutic candidate for preventing and treating ALI.
急性肺损伤（ALI）是一种严重的呼吸系统疾病，发病率和死亡率都很高。脂多糖（LPS）被广泛用于在动物模型中诱导ALI。D-香芹酮是一种天然单萜，据报道具有抗炎和抗氧化特性。本研究旨在探讨D-香芹酮对LPS诱导的大鼠ALI的保护作用。36只雄性大鼠被随机分为六组（n = 6）：对照组、D-香芹酮组（10毫克/千克和20毫克/千克，口服）、LPS组（10毫克/千克大肠杆菌脂多糖，腹腔注射）以及LPS + D-香芹酮组（LPS与10或20毫克/千克D-香芹酮联合使用）。D-香芹酮每天口服一次，持续10天。在第10天，通过给予LPS诱导脓毒症，并在深度麻醉6小时后采集样本。给予LPS导致了显著的肺损伤，组织病理学评分增加、促炎标志物（TLR4、IL-1β、TNF-α）上调以及氧化应激（MDA增加、GSH和SOD减少）均证明了这一点。两种剂量的D-香芹酮治疗均显著减轻了这些变化。D-香芹酮下调了促炎标志物，上调了抗炎（NRF2）和抗凋亡（Bcl-2）蛋白，并降低了肺组织中促炎细胞因子（IL-1β、TNF-α、IL-8）的水平。总之，D-香芹酮可能通过其抗炎和抗氧化特性保护大鼠免受LPS诱导的ALI。这些发现表明，D-香芹酮可能是预防和治疗ALI的潜在治疗候选药物。
