Wenxin Keli for the Treatment of Arrhythmia—Systems Pharmacology and In Vivo Pharmacological Assessment

Figures

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  FIGURE 1. Flowchart for the systems pharmacology approach used in this study.

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  FIGURE 2. UPLC-MS base peak intensity chromatograms of WK aqueous solution in negative and positive modes.

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  FIGURE 3. UPLC-MS base peak intensity chromatograms of serum after WK administration in negative and positive modes.

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  FIGURE 4. KEGG pathway analysis. The larger RichFactor is, the greater the degree of enrichment is; The range of p value is [0,1], and the closer it is to 0, the more significant the enrichment is.

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  FIGURE 5. The percentage of arrhythmias’ duration (%) (x¯±s, n = 8). VP: ventricular premature, VT: ventricular tachycardia, VF: ventricular fibrillation.

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  FIGURE 6. The levels of p-CaMKII protein. (x¯±s, n = 8) *p < 0.05, **p < 0.01, versus the control group. △ p < 0.05, △△ p < 0.01, versus the model group.

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  FIGURE 7. The level of CACNA1C. (x¯±s, n = 8) *p < 0.05, **p < 0.01, versus the control group. △ p < 0.05, △△ p < 0.01, versus the model group.

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  FIGURE 8. Effect of WK on cytoplasmic Ca2+ transient in cardiomyocytes. Black line: Ca2+ transient in the blank group; Red line: Ca2+ transient in the experimental group. n = 5 myocardial cells for each group. General Linear Model with Greenhouse-Geisser tests was applied for comparisons. The Ca2+ transient in the two groups was actually the same at baseline. However, after the infusion of high-dose WK, Ca2+ transient significantly reduced in the experimental group.

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  FIGURE 9. Mechanism of treating arrhythmia with WK.