ABSTRACT
OBJECTIVE To explore the effect of chloride channels on the neuronal injury following cerebral ischemia. METHODS Tweleve day in vitro (12dIV) neurons in rats were randomly divided into normal control, 3-morpholinosydnonimine (SIN-1, 1.0 mmol·L~(-1) for 18 h) group, SIN-1+4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid(SITS, 0.5 mmol·L~(-1)) group and SIN-1+4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS, 0.1 mmol·L~(-1)) group. Drugs were added with SIN-1 simultaneously and coincubated for 18 h. The neuronal apoptosis and morphological changes were detected with Hoechst 33258. Chloride channels(ClC)-2/ClC-3 were analyzed with immunofluorescence, the chloride channel currents were recorded with whole cell patch-clamp technique. RESULTS Hoechst 33258 staining showed that the apoptotic percentages were (18.61±0.59) %, (50.43±0.56)%, (23.37±0.52)% and (23.37±0.84)% in normal control group, SIN-1 group, SIN-1+SITS or SIN-1+DIDS groups, respectively. ClC-2/ClC-3 were positively expressed in normal neurons. The currents in neurons exposed to SIN-1 were increased about 55%-56%, SITS and DIDS, two kinds of chloride channel blockers could inhibited the currents about 50%-60% and 30%-40%, respectively. CONCLUSION Voltage-dependent chloride channel maybe participate in the neuronal apoptosis induced by NO, and the activities of chloride channels are perhaps involved in the cerebral ischemic injury.
ABSTRACT
AIM To elucidate the possible antiarrhythmic mechanism of matrine. METHODS Whole-cell patch-clamp technique was used to record ionic currents in ventricular myocytes. RESULTS In guinea pig ventricular myocytes, matrine 100 μmol·L-1 prolonged 90% action potential duration (APD90) by 40% at a stimulation of 0.1 Hz in a frequency-independent manner, inhibited IK1 by 47% at the test potential of -120 mV, reduced IKr,tail by 50% and had no effect on IKs,tail. CONCLUSION Matrine prolonged APD through blockade of multiple potassium currents, which may relate to its antiarrhythmic efficacy.