Inhibition of FABP4 attenuates hyperoxia-induced lung injury and fibrosis via inhibiting TGF-β signaling in neonatal rats.

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題名:	Inhibition of FABP4 attenuates hyperoxia-induced lung injury and fibrosis via inhibiting TGF-β signaling in neonatal rats.
作者:	黃亮迪 Liang-Ti Huang, Hsiu-Chu Chou, Chung-Ming Chen
貢獻者:	醫學系小兒學科
日期:	2022-02
上傳時間:	2025-03-31 14:47:03 (UTC+8)
摘要:	Abstract Bronchopulmonary dysplasia (BPD) is a chronic lung disease characterized by interrupted alveologenesis and alveolar simplification caused by oxygen therapy in premature infants. Metabolic dysfunction is involved in the pathogenesis of BPD. Fatty acid-binding protein 4 (FABP4) is significantly increased in specific lung tissues in patients with BPD. Therefore, we investigated whether BMS309403, an FABP4 inhibitor that can mitigate tissue fibrosis, can regulate pulmonary fibrotic processes in newborn rats exposed to hyperoxia. Newborn rat pups were exposed to room air (RA; 21% O2 ) or 85% O2 from 5 to 14 days of age and were then allowed to recover in RA until 29 days of age. They received intraperitoneal injection with placebo (phosphate-buffered saline [PBS]) or BMS 309403 (0.5 mg or 1.0 mg kg-1 d-1 ) every other day from 4 to 14 days of age then were divided into O2 plus PBS or low dose or high dose and RA plus PBS or low dose or high dose groups. We assessed lung histology and evaluated lung collagen I, FABP4 as well as TGF-β1 expression at 14 and 29 days of age. In the hyperoxia injury-recovery model, prophylactic BMS309403 treatment reduced mean linear intercept values and FABP4 expression (p < 0.001). Prophylactic BMS309403 treatment mitigated pulmonary fibrosis and TGF-β1 expression immediately after hyperoxia exposure (p < 0.05). The attenuation of hyperoxia-induced alveolar developmental impairment and pulmonary fibrosis by FABP4 inhibition indicated that such inhibition has potential clinical and therapeutic applications.
關聯:	J Cell Physiol. 2022 Feb; 237(2): 1509-1520
描述:	【110-2 升等】臺北醫學大學教師升等專門著作職別：專任送審等級：教授著作送審
資料類型:	article
顯示於類別:	[教師升等送審著作] 110

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