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AIM:To investigate the effect of resveratrol on the lipids ( CHOL, TG, LDL-C and HDL-C) , ni-tric oxide ( NO) , peroxynitrite anion ( ONOO-) and the expression of inducible nitric oxide synthase ( iNOS) in the artery of the mice with ovariotomy ( OVX) .METHODS:The lipid levels and NO level in the serum were measured .The chan-ges of atherosclerosis were evaluated with Oil Red O staining .The expression of iNOS was measured by DAB staining and Western blot .The ONOO-production was measured by DAB staining .RESULTS:Compared with sham group , the levels of the lipids and NO production in OVX +high fat (HF) group were increased (P<0.05).Compared with OVX+HF group, the levels of the lipids and NO production in resveratrol group were decreased (P<0.05).Fourteen weeks later, the atherosclerosis model was successfully established .Compared with OVX +HF group, the iNOS expression and the ONOO-production in resveratrol group were decreased ( P<0.05 ) , while those in sham group were increased ( P <0.05).CONCLUSION:Resveratrol prevents and treats atherosclerosis by inhibiting the iNOS expression in C 57BL/6J mice.
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【Objective】 The effect of pretreatment with Buyang Huanwu Decoction(BHD) on L-type calcium channels of cortical neurons in rats with global cerebral ischemia was observed,thus to explore the molecular therapeutic mechanism of BHD for cerebral ischemia as well as the pathogenic mechanism of Ca2+ message in ischemic injury of neurons.【Methods】SD rats were randomized into pseudo-operation group,model groups and BHD groups.And the model groups and BHD groups were divided into six groups according to the time points after reperfusion(2nd,12th,24th,48th and 72nd hour after reperfusion respectively).BHD groups received 0.64g/kg BHD by gastric infusion,bid,for 5 continuous days.Except the rats in pseudo-operation groups,the rats in other groups were induced global cerebral ischemia by modified Pulsinelli's four-vessel occlusion.Cerebral cortical neurons in rats were isolated promptly in 2nd,12th,24th,48th and 72nd hour after reperfusion.The recorded single-channel current was amplified by the EPC-9 patch-clamping amplifier,and then input into the computer by Pulse+Pulsefit.The analytical software TAC was used to detect the opening time and opening probability of the L-type Ca2+ channels in rats at different time points after reperfusion.【Results】In the model groups,the opening time of the L-type Ca2+ channels was prolonged after reperfusion as compared with that in the pseudo-operation group,and the opening probability of the L-type Ca2+ channels arrived at the peaks in 2nd and 24th hour after reperfusion.In BHD groups,the opening time in 72nd hour after reperfusion was decreased(P
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Objective To observe the effect of breviscapine on the open probability(Po)and the average open time(To) of L-type calcium channel in the hippocampal neurons of the whole brain ischemia-reperfusion rat model.Methods The whole brain ischemia rat model was established.At the reperfusion periods of 1.5 h,3.0 h,4.5 h and 6.0 h,the hippoeampal CA1 neurons were dissociated abruptly and the Ca~(2+)electricity of single channel on the neuron membrane were recorded with cell-attach model of patch clamp techniques.The Po and To of the L-type calcium channel were an- alyzed and the effect of the breviscapine was observed.Results Different concentrations of breviscapine can decrease the Po and To of the L-type calcium channel in hippoeampal neurons,particularly within 3 hours after ischemia-reperfu- sion.Conclusions Breviscapine has protective effect on the cerebral ischemia-reperfusion injury.
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Objective To observe the effect of Shenfu Injection (SI)on adriamycin(ADR)-induced calcium overload in myocardial cells of rats.Methods SD rats were randomized into normal group, saline group, ADR group, ADR+saline group, low-, middle-and high-dosage SI groups (treated with SI 0.3, 0.6 and 1.2gkg-1d-1). Except the normal and saline groups, the rats in other groups were given ADR injection. Meanwhile,SI groups received treatment of SI for two weeks. Three weeks after modeling, the single myocardial cells were isolated. The free Ca2+ concentration was detected by ionic imaging method, and the ionic current through L-type calcium channel in cellular membrane was observed by patch clamp technique.Results The free Ca2+ concentration, the mean open probability of L-type calcium channel in cellular membrane and the mean ionic current through L-type calcium channel were increased in ADR group (P0.05).Conclusion The mechanism of SI counteracting the ADR-induced calcium overload in myocardial cells may be related with preventing external calcium from entering the cells,and with inhibiting the release of internal calcium.
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AIM To study the mechanism of puerarin against arrhythmias. METHODS Standard microelectrode intracellular recording technique was used RESULTS ①Puerarin 0 005, 0 01,0 015 mmol?L -1 prolong the action potential duration at 50% and 90% of repolarization (APD 50 ,APD 90 ) respectively APD 50 was prolonged from (176 43?51 37) ms to (192 86?60 82) ms ( n=7, P