Lipidomics reveals the potential mechanism of honokiol against adenine-induced chronic kidney disease

Figures

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  FIGURE 1. Effects of HKL on adenine-induced CKD rats. (A) Body weight. (B) Kidney weight to body weight ratio. (C) Serum creatinine. (D) Blood urea nitrogen. (E) PAS and Masson staining. All images are shown at identical magnification, ×200, scale bar = 50 μm. (F) Renal tubular injury score. (G) Quantification of tubulointerstitial fibrosis. Data are expressed as mean ± SEM, n = 4-6 rats per group, * p < 0.05, ** p < 0.01, *** p < 0.001.

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  FIGURE 2. Effects of HKL on liver function indexes. (A) Alanine transaminase levels. (B) Aspartate transaminase levels. Data are expressed as mean ± SEM, n = 6 rats per group, ns = no significance.

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  FIGURE 3. Score scatter plots of PCA models. (A) PCA score plot of the control and the CKD group in negative ion mode. (B) PCA score plot of the control and the CKD group in positive ion mode. (C) PCA score plot of the CKD and the CKD + HKL group in negative ion mode. (D) PCA score plot of the CKD and the CKD + HKL group in positive ion mode. The red dots represent the control group, the blue squares represent the CKD group, and the purple diamonds represent the CKD + HKL group.

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  FIGURE 4. Score scatter plots of OPLS-DA model. (A) OPLS-DA score plot of the control and the CKD group in negative ion mode. (B) OPLS-DA score plot of the control and the CKD group in positive ion mode. (C) OPLS-DA score plot of the CKD and the CKD + HKL group in negative ion mode. (D) OPLS-DA score plot of the CKD and the CKD + HKL group in positive ion mode. The red dots represent the control group, the blue squares represent the CKD group, and the purple diamonds represent the CKD + HKL group.

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  FIGURE 5. Permutation test of OPLS-DA. Permutation plots of OPLS-DA models for group CKD vs. control and group CKD + HKL vs. CKD in negative and positive ion modes.

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  FIGURE 6. Volcano plots of lipid differences between groups. (A) Differential lipid profiles in CKD versus control in negative ion mode. (B) Differential lipid profiles in CKD versus control in positive ion mode. (C) Differential lipid profiles in CKD + HKL versus CKD in negative ion mode. (D) Differential lipid profiles in CKD + HKL versus CKD in positive ion mode. The red dots represent significant upregulation, the green dots represent significant downregulation, and the grey dots represent insignificant.

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  FIGURE 7. Screening of lipids that could be reversed by HKL treatment in CKD rats. (A) The amount and classification of lipids that could be reversed by HKL treatment in negative ion mode. (B) The amount and classification of lipids that could be reversed by HKL treatment in positive ion mode.

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  FIGURE 8. Heatmap analysis of the lipids reversed by HKL treatment in CKD rats. (A) Relative expression of 47 lipids in the control, CKD, and CKD + HKL group in negative ion mode. (B) Relative expression of 66 lipids in the control, CKD, and CKD + HKL group in positive ion mode.

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  FIGURE 9. Effects of HKL on fatty acid oxidation in the kidney of CKD rats. (A) Representative Western blot bands of CPT1A, ACOX1, and ACADL expression in the kidneys of rats. (B–D) Densitometric analysis of CPT1A, ACOX1, and ACADL normalized to GAPDH content. Data are expressed as mean ± SEM, n = 5. (E–H) The activity of mitochondrial respiratory complex I, II, III, and IV in the kidney of rats. Data are expressed as min to max, n = 4. * p < 0.05, ** p < 0.01, *** p < 0.001, ns = no significance.