Ovatodiolide inhibits SARS-CoV-2 replication and ameliorates pulmonary fibrosis through suppression of the TGF-p/TpRs signaling pathway

• Published in: 中西整合醫學會會訊 p. 004
• Main Authors: Wei-Chung Chiou, Guan-Jhong Huang, Tein-Yao Chang, Tzu-Lan Hsia, Hao-You Yu, Jir-Mehng Lo, Pin-Kuei Fu, Cheng Huang
• Format: Journal Article
• Language: Chinese
• Published: 台灣 臺灣中西整合醫學會 01.07.2023

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection continues to pose threats to public health. The clinical manifestations of lung pathology in COVID-19 patients include sustained inflammation and pulmonary fibrosis. The macrocyclic diterpenoid ovatodiolide (OVA) has been reported to have anti-inflammatory, anti-cancer, anti-allergic, and analgesic activities. Here, we investigated the pharmacological mechanism of OVA in suppressing SARS-CoV-2 infection and pulmonary fibrosis in vitro and in vivo. Our results revealed that OVA was an effective SARS-CoV-2 3CLpro inhibitor and showed remarkable inhibitory activity against SARS-CoV-2 infection. On the other hand, OVA ameliorated pulmonary fibrosis in bleomycin (BLM)-induced mice, reducing inflammatory cell infiltration and collagen deposition in the lung. OVA decreased the levels of pulmonary hydroxyproline and myeloperoxidase, as well as lung and serum TNF-a，IL-ip，IL-6, and TGF-P in BLM-induced pulmonary fibrotic mice. Meanwhile, OVA reduced