纤维母细胞衰老被报道为导致特发性肺纤维化（IPF）病理发展的原因之一，黄芩素被报道为减轻IPF的一种方法。该研究探讨了黄芩素通过调节肺纤维母细胞衰老来减轻肺纤维化的可能性。肿瘤研究所（ICR）小鼠被随机分配到对照组、博莱霉素（BLM）组、黄芩素组和BLM+黄芩素组。通过单次气管内给予BLM（3mg/kg）来建立肺纤维化模型。黄芩素组每天口服黄芩素（100mg/kg）。通过尾静脉注射Sirtuin 3（Sirt3）siRNA（50μg）用于探讨其对黄芩素抗肺纤维化的影响。BLM处理的小鼠表现出明显的肺纤维化和纤维母细胞衰老，表现为肺组织中胶原沉积（27.29％vs.4.14％）、羟脯氨酸（208.05 vs. 40.16 ng / mg）、胶原I（25.18 vs. 9.15 μg / mg）、p53、p21、p16、MCP-1、PAI-1、TNF-α、MMP-10 和MMP-12水平升高，而黄芩素减轻了这些现象。黄芩素还减轻了BLM介导的TGF-β1/Smad信号通路的激活。黄芩素还恢复了BLM诱导的肺Sirt3表达下调，并且Sirt3的沉默废除了黄芩素对BLM诱导的肺纤维化、纤维母细胞衰老以及TGF-β1/Smad信号通路激活的抑制作用。黄芩素保护了BLM诱导的肺Sirt3表达下调，从而抑制了TGF-β1/Smad信号通路和肺纤维化，可能为IPF的治疗提供了实验基础。

Fibroblast senescence was reported to contribute to the pathological development of idiopathic pulmonary fibrosis (IPF), and baicalein is reported to attenuate IPF.This study explores whether baicalein attenuates lung fibrosis by regulating lung fibroblast senescence.Institute of Cancer Research (ICR) mice were randomly assigned to control, bleomycin (BLM), baicalein and BLM + baicalein groups. Lung fibrosis was established by a single intratracheal dose of BLM (3 mg/kg). The baicalein group received baicalein orally (100 mg/kg/day). Sirtuin 3 (Sirt3) siRNA (50 μg) was injected through the tail vein once a week for 2 weeks to explore its effect on the anti-pulmonary fibrosis of baicalein.BLM-treated mice exhibited obvious lung fibrosis and fibroblast senescence by showing increased levels of collagen deposition (27.29% vs. 4.14%), hydroxyproline (208.05 vs. 40.16 ng/mg), collagen I (25.18 vs. 9.15 μg/mg), p53, p21, p16, MCP-1, PAI-1, TNF-α, MMP-10 and MMP-12 in lung tissues, which were attenuated by baicalein. Baicalein also mitigated BLM-mediated activation of TGF-β1/Smad signalling pathway. Baicalein restored the BLM-induced downregulation of Sirt3 expression in lung tissues and silencing of Sirt3 abolished the inhibitory role of baicalein against BLM-induced lung fibrosis, fibroblast senescence and activation of TGF-β1/Smad signalling pathway.Baicalein preserved the BLM-induced downregulation of lung Sirt3 expression, and thus the suppression of TGF-β1/Smad signalling pathway and lung fibrosis, which might provide an experimental basis for treatment of IPF.