نبذة مختصرة : Bleomycin (BLM) is a chemotherapy drug used to treat cancer, one of which side effects is that it can lead to pulmonary fibrosis (PF). Atractylenoide III (AtrIII), derived from the dried roots ofA BLM-induced pulmonary fibrosis model in SD rats was established. The respiratory dynamics were evaluated by using Wholebody flow-through plethysmography. Lung injury and pulmonary fibrosis were observed by Hematoxylin-eosin (HE) and Masson staining. Apoptosis was assay by Tunel assay. Inflammatory factors were detected with commercial kits. Expression of mRNAs and proteins were detected by RT-qPCR and Western blot, respectively.AtrIII (1.2, 2.4 mg/kg) improved the lung injury and lung function in the BLM-induced Sprague-Dawley (SD) rats. AtrIII reduced the apoptosis rate and protein expression of Caspase-3 and Caspase-9. AtrIII (1.2, 2.4 mg/kg) decrease the pulmonary fibrosis damage and protein expression transforming growth factor-β (TGF-β) and α-smooth muscle actin (α-SMA). AtrIII also down-regulated the levels of interleukin 6 (IL-6), inductible nitric oxide synthase (iNOS) and tumor necrosis factor-α (TNF-α), while up-regulated the level of IL-10 in peripheral blood serum. Moreover, AtrIII (1.2, 2.4 mg/kg) increased the activity of superoxide dismutase (SOD) and glutathione (GSH), while decreased the malondialdehyde (MDA) content and lactate dehydrogenase (LDH) activity. AtrIII (1.2, 2.4 mg/kg) increased the levels of Nrf2, NQO1 and HO-1. In addition, AtrIII reversed the effects of Nrf2 interference on pulmonary fibrosis damage, decreased SOD and GSH activity, and increased MDA content.AtrIII could attenuate the pulmonary fibrosis and reliev oxidative stress through the Nrf2/NQO1/ HO-1 pathway.
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