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Journal: Drug Design, Development and Therapy
Article Title: Integrated Serum Pharmacochemistry, Network Pharmacology, and Transcriptomics Reveal the Mechanisms and Active Constituents of Qingfei Huoxue Decoction Against Bleomycin-Induced Pulmonary Fibrosis
doi: 10.2147/DDDT.S592770
Figure Lengend Snippet: Effects of QFHXD on histopathology and pro-fibrotic markers in BLM-induced PF mice. ( A ) Dynamic changes in body weight. ( B ) The Kaplan-Meier survival curve of each group. Compared with the model group, Treatment with different doses of QFHXD markedly boosted the survival rate of PF mice. ( C ) The representative images of lung sections stained with H&E, Masson’s trichrome, and immunohistochemical staining for α-SMA and FN proteins (×200 magnification, scale bar: 100 μm, n = 6). ( D ) Ashcroft score for grading PF severity (n = 6). Quantification of immunohistochemical results of α-SMA ( E ) and FN ( F ) expression (n = 6). The relative mRNA levels of Fn1 ( G ) and Col1a1 ( H ) in lung samples of each group (n = 5). QFHXD administration effectively mitigated fibrotic lesions, inhibited collagen deposition, and decreased the expression of pro-fibrotic markers. Serum levels of TGF-β1 ( I ), CCL2 ( J ), and KL-6 ( K ) were measured by ELISA (n = 8). Data are displayed as the mean ± SD. ## P < 0.01 versus the control group; * P < 0.05, and ** P < 0.01 versus the model group. Model, BLM-induced PF model; QFHXD-L, QFHXD low dose (4.78 g/kg); QFHXD-H, QFHXD high dose (9.56 g/kg).
Article Snippet:
Techniques: Histopathology, Staining, Immunohistochemical staining, Expressing, Enzyme-linked Immunosorbent Assay, Control
Journal: Drug Design, Development and Therapy
Article Title: Integrated Serum Pharmacochemistry, Network Pharmacology, and Transcriptomics Reveal the Mechanisms and Active Constituents of Qingfei Huoxue Decoction Against Bleomycin-Induced Pulmonary Fibrosis
doi: 10.2147/DDDT.S592770
Figure Lengend Snippet: Experimental validation of inflammatory targets regulated by QFHXD in BLM-induced PF. ( A and B ) The relative mRNA levels of key inflammatory targets obtained from network pharmacology and RNA-Seq analysis, including Tlr2, Tlr4, Rela, Nfkb1, Il1b, Il6, Tnf, Tgfb1, Ccl2, Spp1, Mmp9, Mmp13, and Mmp14 (n = 5). The concentrations of TLR2 ( C ), TLR4 ( D ), NF-κB ( E ), IL-1β ( F ), IL-6 ( G ), TNF-α ( H ), TGF-β1 ( I ), CCL2 ( J ), and SPP1 ( K ) proteins were investigated by ELISA (n = 6). ( L ) The typical images of immunohistochemical staining of MMP9 protein in each group (×200 magnification, scale bar: 100 μm, n = 6). Black arrows indicated MMP9-positive cells. ( M ) Quantification of MMP9-positive cells (n = 6). Compared with the untreated PF model group, QFHXD intervention significantly suppressed the mRNA and protein expression of pro-inflammatory mediators in fibrotic lung samples. RT-qPCR results are expressed as the mean ± SEM. Data of ELISA and immunohistochemical staining are displayed as the mean ± SD. ## P < 0.01 versus the control group; * P < 0.05, and ** P < 0.01 versus the model group. Model, BLM-induced PF model; QFHXD-L, QFHXD low dose (4.78 g/kg); QFHXD-H, QFHXD high dose (9.56 g/kg).
Article Snippet:
Techniques: Biomarker Discovery, RNA Sequencing, Enzyme-linked Immunosorbent Assay, Immunohistochemical staining, Staining, Expressing, Quantitative RT-PCR, Control