Fig. 6

HIF-1α plays a key role in treatment with AsA A Experimental scheme comparing tumor progression and lung fibrosis among the AsA–, AsA + , and AsA + HIF-1α-ac groups. The injected cancer cells were LLC cells. OA, oropharyngeal administration, BLM bleomycin, AsA ascorbic acid, HIF-1α hypoxia-inducible factor 1α, HIF-1α-ac HIF-1α activator, HC Healthy control. B Hematoxylin and eosin staining of lung sections and macroscopic evaluation results from the AsA−, AsA + , and AsA + HIF-1α-ac groups on day 28. Scale bar: 300 μm. C–E Comparison of C tumor volume, D weight of mediastinal lymph nodes, and E number of metastatic foci among the AsA−, AsA + , and AsA + HIF-1α-ac groups on day 28 (n = 8/group). *P < 0.05, **P < 0.01, ****P < 0.001. F Comparison of hydroxyproline level among the AsA−, AsA + , and AsA + HIF-1α-ac groups on day 28 (n = 10/group). *P < 0.05. G–I Comparison of the concentrations of G HIF-1α, H TIMP-1, and (I) VEGFA proteins in the tumor tissue among the AsA−, AsA + , and AsA + HIF-1α-ac groups on day 28 (n = 8/group). TIMP-1, tissue inhibitor of metalloproteinase-1. VEGFA, vascular endothelial growth factor A. *P < 0.05, **P < 0.01. J Comparison of the concentrations of serum TGFβ-1 protein among the AsA−, AsA + , and AsA + HIF-1α-ac groups on day 28 (n = 8/group). *P < 0.05. K–P Comparison of K cancer cell fraction, L tumor-associated macrophages (TAM) fraction, M cancer-associated myofibroblasts (CAMF) fraction, N regulatory T cells (Treg) fraction, O cytotoxic T lymphocytes (CTL) fraction, and P CTL/Treg ratio among the AsA−, AsA + , and AsA + HIF-1α-ac groups on day 28 (n = 6/group). NS represents not significant. *P < 0.05, **P < 0.01