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Integrating Transcriptomics, Proteomics, and Metabolomics Profiling with System Pharmacology for the Delineation of Long-Term Therapeutic Mechanisms of Bufei Jianpi Formula in Treating COPD

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ABSTRACT

In previous work, we identified 145 active compounds from Bufei Jianpi formula (BJF) by system pharmacology and found that BJF showed short-term effect on chronic obstructive pulmonary disease (COPD) rats. Here, we applied the transcriptomic, proteomic, and metabolomics approaches to illustrate the long-term anti-COPD action and its system mechanism of BJF. BJF has obvious anti-COPD effect through decreasing inflammatory cytokines level, preventing protease-antiprotease imbalance and collagen deposition on week 32 by continuous oral administration to rats from weeks 9 to 20. Subsequently, applying the transcriptomic, proteomic, and metabolomics techniques, we detected a number of regulated genes, proteins, and metabolites, mainly related to antioxidant activity, focal adhesion, or lipid metabolism, in lung tissues of COPD and BJF-treated rats. Afterwards, we integrated system pharmacology target, transcript, protein, and metabolite data sets and found that many genes, proteins, and metabolites in rats BJF-treated group and the target proteins of BJF were mainly attributed to lipid metabolism, inflammatory response, oxidative stress, and focal adhesion. Taken together, BJF displays long-term anti-COPD effect probably by system regulation of the lipid metabolism, inflammatory response pathways oxidative stress, and focal adhesion.

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Effect of BJF on MMP-2, MMP-9, and TIMP-1 expression in the COPD rat lung tissue. Immunohistochemical analysis for MMP-2, MMP-9, and TIMP-1 expression in the lung tissues was performed on week 32 (magnification, ×100) (a). Quantitative analysis expression level of MMP-2, MMP-9, and TIMP-1 was quantified based on the immunohistochemical testing (b). Values represent means ± SEM and n = 10. ∗p < 0.05 and ∗∗p < 0.01 versus model.
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fig5: Effect of BJF on MMP-2, MMP-9, and TIMP-1 expression in the COPD rat lung tissue. Immunohistochemical analysis for MMP-2, MMP-9, and TIMP-1 expression in the lung tissues was performed on week 32 (magnification, ×100) (a). Quantitative analysis expression level of MMP-2, MMP-9, and TIMP-1 was quantified based on the immunohistochemical testing (b). Values represent means ± SEM and n = 10. ∗p < 0.05 and ∗∗p < 0.01 versus model.

Mentions: The protease-antiprotease imbalance and collagen degradation play significant role in the extensive remodeling of lung tissue structure, which is important pathogenesis of COPD [20–22]. Thus, we tested the long-term effect of BJF on MMP-2, MMP-9, TIMP-1, and collagens I, III, and IV expression. In Figure 5, on week 32, the protein levels of MMP-2/-9 were markedly suppressed by BJF treatment, and the expression of TIMP-1, endogenous inhibitor of MMP, was significantly increased by BJF. The expression of collagens I, III, IV was significantly decreased by BJF treatment (Figure 6).


Integrating Transcriptomics, Proteomics, and Metabolomics Profiling with System Pharmacology for the Delineation of Long-Term Therapeutic Mechanisms of Bufei Jianpi Formula in Treating COPD
Effect of BJF on MMP-2, MMP-9, and TIMP-1 expression in the COPD rat lung tissue. Immunohistochemical analysis for MMP-2, MMP-9, and TIMP-1 expression in the lung tissues was performed on week 32 (magnification, ×100) (a). Quantitative analysis expression level of MMP-2, MMP-9, and TIMP-1 was quantified based on the immunohistochemical testing (b). Values represent means ± SEM and n = 10. ∗p < 0.05 and ∗∗p < 0.01 versus model.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5382313&req=5

fig5: Effect of BJF on MMP-2, MMP-9, and TIMP-1 expression in the COPD rat lung tissue. Immunohistochemical analysis for MMP-2, MMP-9, and TIMP-1 expression in the lung tissues was performed on week 32 (magnification, ×100) (a). Quantitative analysis expression level of MMP-2, MMP-9, and TIMP-1 was quantified based on the immunohistochemical testing (b). Values represent means ± SEM and n = 10. ∗p < 0.05 and ∗∗p < 0.01 versus model.
Mentions: The protease-antiprotease imbalance and collagen degradation play significant role in the extensive remodeling of lung tissue structure, which is important pathogenesis of COPD [20–22]. Thus, we tested the long-term effect of BJF on MMP-2, MMP-9, TIMP-1, and collagens I, III, and IV expression. In Figure 5, on week 32, the protein levels of MMP-2/-9 were markedly suppressed by BJF treatment, and the expression of TIMP-1, endogenous inhibitor of MMP, was significantly increased by BJF. The expression of collagens I, III, IV was significantly decreased by BJF treatment (Figure 6).

View Article: PubMed Central - PubMed

ABSTRACT

In previous work, we identified 145 active compounds from Bufei Jianpi formula (BJF) by system pharmacology and found that BJF showed short-term effect on chronic obstructive pulmonary disease (COPD) rats. Here, we applied the transcriptomic, proteomic, and metabolomics approaches to illustrate the long-term anti-COPD action and its system mechanism of BJF. BJF has obvious anti-COPD effect through decreasing inflammatory cytokines level, preventing protease-antiprotease imbalance and collagen deposition on week 32 by continuous oral administration to rats from weeks 9 to 20. Subsequently, applying the transcriptomic, proteomic, and metabolomics techniques, we detected a number of regulated genes, proteins, and metabolites, mainly related to antioxidant activity, focal adhesion, or lipid metabolism, in lung tissues of COPD and BJF-treated rats. Afterwards, we integrated system pharmacology target, transcript, protein, and metabolite data sets and found that many genes, proteins, and metabolites in rats BJF-treated group and the target proteins of BJF were mainly attributed to lipid metabolism, inflammatory response, oxidative stress, and focal adhesion. Taken together, BJF displays long-term anti-COPD effect probably by system regulation of the lipid metabolism, inflammatory response pathways oxidative stress, and focal adhesion.

No MeSH data available.


Related in: MedlinePlus