Effects of Lizhong Tang on cultured mouse small intestine interstitial cells of Cajal

Figure 1 Effects of Lizhong Tang on pacemaker potentials in cultured interstitial cells of Cajal from murine small intestines. A-E: Pacemaker potentials in interstitial cells of Cajal exposed to Lizhong Tang (0-50 mg/mL) in current-clamp mode (I = 0); F: The responses to Lizhong Tang are summarized. Bars represent mean ± SE. ^bP < 0.01 vs control group. CTRL: Control.

Figure 2 Effects of flufenamic acid (a nonselective cation channel blocker) or niflumic acid (a Cl^- channel blocker) on Lizhong Tang-induced pacemaker potentials in cultured interstitial cells of Cajal from murine small intestines. A: The application of flufenamic acid (5 μmol/L) abolished the generation of pacemaker potentials, and in the presence of flufenamic acid, Lizhong Tang (30 mg/mL) did not cause membrane depolarization; B: In contrast, although niflumic acid (5 μmol/L) abolished the generation of pacemaker potentials, it did not block Lizhong Tang-induced (30 mg/mL) membrane depolarization; C: The responses to Lizhong Tang in the presence of flufenamic acid or niflumic acid are summarized. Bars represent mean ± SE. ^bP < 0.01 vs control group. CTRL: Control.

Figure 3 Effects of an external Ca²⁺-free solution, thapsigargin (an inhibitor of Ca ²⁺-ATPase in the endoplasmic reticulum), or U-73122 (an active phospholipase C inhibitor) on Lizhong Tang-induced pacemaker potentials in cultured interstitial cells of Cajal. A: External Ca²⁺-free solution abolished the generation of pacemaker potentials, but failed to block Lizhong Tang-induced (30 mg/mL) membrane depolarization; B: Thapsigargin (5 μmol/L) abolished the generation of pacemaker potentials, and blocked Lizhong Tang-induced (30 mg/mL) membrane depolarization; C: The responses to Lizhong Tang in external Ca²⁺-free solution in the presence of thapsigargin are summarized. Bars represent mean ± SE. ^bP < 0.01 vs control group. CTRL: Control.

Figure 4 Effects of GDP-β-S in the pipette on Lizhong Tang-induced pacemaker potentials in cultured murine small intestine interstitial cells of Cajal. A: Pacemaker potentials in interstitial cells of Cajal exposed to Lizhong Tang (30 mg/mL) in the presence of GDP-β-S (1 mmol/L) in the pipette. Under these conditions, Lizhong Tang (30 mg/mL) caused membrane depolarization; B: The responses to Lizhong Tang in the presence of GDP-β-S in the pipette are summarized. Bars represent mean ± SE. CTRL: Control.

Figure 5 Effects of phospholipase C inhibitors on Lizhong Tang-induced potentials in cultured interstitial cells of Cajal. A: U-73122 (5 μmol/L; a phospholipase C inhibitor) abolished the generation of pacemaker potentials, and blocked Lizhong Tang-induced (30 mg/mL) membrane depolarization; B: The application of U-73343 (5 μmol/L) did not influence the generation of pacemaker currents or block Lizhong Tang-induced (30 mg/mL) membrane depolarization; C: The responses to Lizhong Tang in the presence of phospholipase C inhibitors are summarized. Bars represent mean ± SE. ^bP < 0.01 vs control group. CTRL: Control.

Figure 6 Effects of chelerythrine or calphostin C (inhibitors of protein kinase C) on Lizhong Tang-induced pacemaker potentials in cultured interstitial cells of Cajal. A, B: Pacemaker potentials in interstitial cells of Cajal exposed to Lizhong Tang (30 mg/mL) in the presence of chelerythrine (1 μmol/L) or calphostin C (10 μmol/L). Lizhong Tang caused membrane depolarization in the presence of both inhibitors; C: The responses to Lizhong Tang in the presence of chelerythrine or calphostin C are summarized. Bars represent mean ± SE. CTRL: Control.