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	Figure 1. Effects of 18α-GA and 18β-GA on INa,P mediated by the WT Nav1.5 channel. (A) and (C) Representative current traces elicited by 500-ms test pulses from -70 mV to 30 mV with 10 mV increments at 0.1 Hz in typical oocytes perfused before and after in 100 μmol/L 18α-GA (A) or 30 μmol/L 18β-GA (C). The membrane potential was held at -120 mV. (B) and (D) Averaged current-voltage relationships of INa,P before and after perfusion with 100 μmol/L 18α-GA (B) or 30 μmol/L 18β-GA (D); n=6 per group; bP<0.05.
	Figure 2. Effects of 18α-GA and 18β-GA on ΔKPQ Nav1.5 channels. (A) and (C) Original current recordings in the absence and presence of 100 μmol/L 18α-GA (A) or 18β-GA (C). Current was elicited by a depolarizing pulse from a holding potential of -120 mV to -30 mV for 500 ms. Insets show magnified current traces for comparison of the late component. (B) and (D) Averaged current-voltage relationships of INa,P before and after perfusion with 100 μmol/L 18α-GA (B) or 18β-GA (D); n=6 per group; bP<0.05.
	Figure 3. Concentration-dependent block by 18β-GA of WT INa,P (A), ΔKPQ INa,P (B), and INa,L (C). INa was elicited by a depolarizing pulse from a holding potential of -120 mV to -30 mV for 500 ms at 0.1 Hz. Representative traces (upper panels) were superimposed before (control) and during perfusion of 18β-GA (1–100 μmol/L). (B, C) are traces from the same oocyte on an expanded scale. Summarized dose-response data (lower panels) fitted with the Hill equation. IC50 values and the Hill coefficient are provided in the figure. n=6–27 oocytes/point.
	Figure 4. Rate-dependent blockade of WT and ΔKPQ Nav1.5 channels. INa was elicited by a series of 30 depolarizing pulses of -120 mV to -20 mV at different stimulation frequencies. The relative current amplitude elicited by each pulse was normalized to the respective amplitudes the currents elicited by the first pulse and plotted against each pulse number: for WT INa,P, 30 μmol/L 18β-GA at 4 Hz (A) (n=6) and 100 μmol/L lidocaine at 1, 2, and 4 Hz (B) (n=5); for ΔKPQ, 100 μmol/L 18β-GA of INa,P (C) and INa,L (D) at 4 Hz (n=6). bP<0.05, cP<0.01.
	Figure 5. Effects of 18β-GA on HERG (A) and Kv1.5 potassium channels expressed in Xenopus oocytes. The voltage protocols are shown in the upper panels. 18β-GA at 100 μmol/L had no significant effects on HERG (n=6) or Kv1.5 channels (n=7).
	Figure 6. Effects of 18β-GA on INa,P and INa,L induced by ATX-II in isolated human atrial myocytes. (A) Original INa,P recoding in control oocytes and in the presence of 30 μmol/L 18β-GA. Current was elicited by a depolarizing pulse from a holding potential of -80 mV to -30 mV for 100 ms. (B) Representative INa,L induced by ATX-II (30 nmol/L) in the absence and in the presence of 30 μmol/L 18β-GA. Current was elicited by a depolarizing pulse from a holding potential of -80 mV to -30 mV for 500 ms. (C) The bar graph shows the percentage of inhibition of INa,P and INa,L induced by ATX-II mediated by 30 μmol/L 18β-GA. The numbers of cells are indicated in parentheses. bP<0.05.

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