Intravenous Xuebijing (XBJ) therapy suppresses paraquat (PQ)-induced pulmonary fibrosis. However, the mechanism underlying this suppression remains unknown. This work aimed to analyze the miR-140-5p-induced effects of XBJ injection on PQ-induced pulmonary fibrosis in mice. The mice were arbitrarily assigned to four groups. The model group was administered with PQ only. The PQ treatment group was administered with PQ and XBJ. The control group was administered with saline only. The control treatment group was administered with XBJ only. The miR-140-5p and miR-140-5p knockout animal models were overexpressed. The gene expression levels of miR-140-5p, transglutaminase-2 (TG2), β-catenin, Wnt-1, connective tissue growth factor (CTGF), mothers against decapentaplegic homolog (Smad), and transforming growth factor-β1 (TGF-β1) in the lungs were assayed with quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot analysis. The levels of TGF-β1, CTGF, and matrix metalloproteinase-9 (MMP-9) in the bronchoalveolar lavage fluid were assessed by enzyme-linked immunosorbent assay (ELISA). Hydroxyproline (Hyp) levels and pulmonary fibrosis were also scored. After 14 days of PQ induction of pulmonary fibrosis, AdCMV-miR-140-5p, and XBJ upregulated miR-140-5p expression; blocked the expressions of TG2, Wnt-1, and β-catenin; and decreased p-Smad2, p-Smad3, CTGF, MMP-9, and TGF-β1 expressions. In addition, Hyp and pulmonary fibrosis scores in XBJ-treated mice decreased. Histological results confirmed that PQ-induced pulmonary fibrosis in XBJ-treated lungs was attenuated. TG2 expression and the Wnt-1/β-catenin signaling pathway were suppressed by the elevated levels of miR-140-5p expression. This inhibition was pivotal in the protective effect of XBJ against PQ-induced pulmonary fibrosis. Thus, XBJ efficiently alleviated PQ-induced pulmonary fibrosis in mice.

静脉注射血必净 (XBJ) 疗法可抑制百草枯 (PQ) 诱导的肺纤维化。然而，这种抑制的机制仍然未知。本工作旨在分析XBJ注射液对miR-140-5p诱导的PQ诱导的小鼠肺纤维化的影响。这些小鼠被任意分配到四组。模型组仅给予PQ。 PQ治疗组给予PQ和XBJ。对照组仅施用生理盐水。对照组仅给予XBJ。 miR-140-5p和miR-140-5p敲除动物模型过表达。 miR-140-5p、转谷氨酰胺酶-2 (TG2)、β-连环蛋白、Wnt-1、结缔组织生长因子 (CTGF)、母亲抗十五瘫同源物 (Smad) 和转化生长因子-β1 (TGF) 的基因表达水平通过定量逆转录聚合酶链反应 (qRT-PCR) 和蛋白质印迹分析来检测肺部中的β1)。通过酶联免疫吸附测定（ELISA）评估支气管肺泡灌洗液中TGF-β1、CTGF和基质金属蛋白酶-9（MMP-9）的水平。还对羟脯氨酸（Hyp）水平和肺纤维化进行了评分。 PQ 诱导肺纤维化 14 天后，AdCMV-miR-140-5p 和 XBJ 上调 miR-140-5p 表达；阻断 TG2、Wnt-1 和 β-catenin 的表达；并降低 p-Smad2、p-Smad3、CTGF、MMP-9 和 TGF-β1 表达。此外，XBJ 治疗小鼠的 Hyp 和肺纤维化评分均有所下降。组织学结果证实，XBJ 治疗的肺中 PQ 诱导的肺纤维化得到减轻。 miR-140-5p 表达水平升高抑制了 TG2 表达和 Wnt-1/β-catenin 信号通路。 这种抑制作用对于 XBJ 对 PQ 诱导的肺纤维化的保护作用至关重要。因此，XBJ 有效减轻 PQ 诱导的小鼠肺纤维化。