Department of Geriatric Medicine, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Department of Dermatology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
BMC Pharmacol Toxicol. 2024 Feb 14;25(1):18. doi: 10.1186/s40360-024-00737-7.
Pulmonary fibrosis is a chronic progressive disease with complex pathogenesis, short median survival time, and high mortality. There are few effective drugs approved for pulmonary fibrosis treatment. This study aimed to evaluate the effect of praziquantel (PZQ) on bleomycin (BLM)-induced pulmonary fibrosis.
In this study, we investigated the role and mechanisms of PZQ in pulmonary fibrosis in a murine model induced by BLM. Parameters investigated included survival rate, lung histopathology, pulmonary collagen deposition, mRNA expression of key genes involved in pulmonary fibrosis pathogenesis, the activity of fibroblast, and M2/M1 macrophage ratio.
We found that PZQ improved the survival rate of mice and reduced the body weight loss induced by BLM. Histological examination showed that PZQ significantly inhibited the infiltration of inflammatory cells, collagen deposition, and hydroxyproline content in BLM-induced mice. Besides, PZQ reduced the expression of TGF-β and MMP-12 in vivo and inhibited the proliferation of fibroblast induced by TGF-β in vitro. Furthermore, PZQ affected the balance of M2/M1 macrophages.
Our study demonstrated that PZQ could ameliorate BLM-induced pulmonary fibrosis in mice by affecting the balance of M2/M1 macrophages and suppressing the expression of TGF-β and MMP-12. These findings suggest that PZQ may act as an effective anti-fibrotic agent for preventing the progression of pulmonary fibrosis.
肺纤维化是一种慢性进行性疾病，发病机制复杂，中位生存时间短，死亡率高。目前批准用于肺纤维化治疗的有效药物很少。本研究旨在评估吡喹酮（PZQ）对博来霉素（BLM）诱导的肺纤维化的作用。
在这项研究中，我们研究了 PZQ 在 BLM 诱导的小鼠肺纤维化模型中的作用和机制。研究的参数包括存活率、肺组织病理学、肺胶原沉积、参与肺纤维化发病机制的关键基因的 mRNA 表达、成纤维细胞活性以及 M2/M1 巨噬细胞比例。
我们发现 PZQ 提高了小鼠的存活率并减轻了 BLM 引起的体重减轻。组织学检查显示，PZQ 显著抑制了 BLM 诱导的小鼠炎症细胞浸润、胶原沉积和羟脯氨酸含量。此外，PZQ 降低了体内 TGF-β和 MMP-12 的表达，并抑制了 TGF-β体外诱导的成纤维细胞增殖。此外，PZQ 影响了 M2/M1 巨噬细胞的平衡。
我们的研究表明，PZQ 可通过影响 M2/M1 巨噬细胞的平衡并抑制 TGF-β和 MMP-12 的表达来改善 BLM 诱导的小鼠肺纤维化。这些发现表明 PZQ 可能作为一种有效的抗纤维化药物，用于预防肺纤维化的进展。
