Efficacy of Poria cocos and Alismatis rhizoma against diet-induced hyperlipidemia in rats based on transcriptome sequencing analysis

Figures

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  Figure 1. Schematic diagram of strategies for clarifying the therapeutic mechanism of PC and AR used as a combined treatment for HLP. PC, Poria cocos; AR, Alismatis rhizoma; HLP, hyperlipidemia.

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  Figure 2. Changes in BW (a) in the control (n = 10), model (n = 10), 1.14 g/kg PC–AR (n = 10), 2.27 g/kg PC–AR (n = 10), and 4.54 g/kg PC–AR groups (n = 10) during the treatment period. After administration, liver coefficient (b) and Lee’s index (c), serum levels of TC (d), TG (e), LDL-C (f), and HDL-C (g) were determined. *P < 0.05, **P < 0.01, ***P < 0.001, compared with the control group; #P < 0.05, compared with the model group. BW, body weight; TC, total cholesterol; TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol.

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  Figure 3. HE staining of liver tissues of rats in each group. The liver histology of rats in the different groups was compared to demonstrate the efficacy of PC–AR against HLP (200\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\times$$\end{document}× magnification). The 4.54g/kg PC–AR group was selected as the PC–AR administration group. Compared with that in the control group, the degree of liver damage and hepatic steatosis was aggravated in the model group. In the PC–AR group, the pathological characteristics of the in liver cells were greatly alleviated, and a normal histology was recovered, compared to the model group. H&E, hematoxylin and eosin. Black arrows indicate the cytoplasmic vacuolation.

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  Figure 4. Volcano plots displaying DEGs based on the criteria of |log2(FC)|> 0.585 and FDR \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$<$$\end{document}< 0.05 in (a) model group versus control group (Model vs. Control)and (b) the PC–AR group versus model group (PC–AR vs. Model). Green spots indicate down-regulated genes, and red spots indicate up-regulated genes. FC, fold change; FDR, false discovery rate; DEG, differentially expressed gene.

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  Figure 5. (a) The 659 overlapping DEGs between the model group versus the control group (Model vs. Control) and the model group versus PC–AR group (Model vs. PC–AR). (b) A total of 580 up-regulated DEGs were shared. (c) A total of 42 down-regulated DEGs were shared. PC–AR treatment effectively regulated 622 of the 659 DEGs.

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  Figure 6. The top 10 ranked GO terms associated with the 622 regulated genes. (a) Top 10 BP terms; (b) top 10 MF terms; (c) top 10 CC terms. GO, gene ontology; BP, biological process; MF, molecular function; CC, cellular component, FDR or Q-value < 0.05.

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  Figure 7. GSEA of DEGs in the PC–AR group versus the model group. GSEA, gene set enrichment analysis; KEGG, Kyoto Encyclopedia of Genes and Genomes.

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  Figure 8. Relative expression of Cxcl10, Cxcl9, Ccl2, Ccl4, Cd40, Il-17rb and Il-1β mRNA (n = 4). *P < 0.05, **P < 0.01, ***P < 0.001, compared with the control group; #P < 0.05, ##P < 0.01, compared with the model group.

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  Figure 9. Schematic 3D representation of molecular docking models: (a) Trametenolic acid (Pubchem Cid: 125181708) to Cxcl10 (PDB ID: 1O7Y), (b) Alisol B 23-acetate (Pubchem Cid: 14036811) to Ccl2 (PDB id:1DOK), (c) Alisol B monoacetate (Pubchem Cid: 163083573) to Ccl4 (PDB ID: 2X6L), (d) Alisol C monoacetate (Pubchem Cid: 14036813) to Cd40 (PDB ID: 7P3I), (e) Ergosterol peroxide (Pubchem Cid: 5351516) to Il-1β (PDB ID: 5R8Q). The molecular docking results were visualized using PyMOL software (v 2.4.0 open source; https://github.com/schrodinger/pymol-open-source).