Effect of phosphocreatine on transient outward potassium current in ischemic ventricular mid-myocardial cells of rats

AIM: To determine the effect of exogenous phosphocreatine (PCr) at different concentrations on transient outward potassium (I_to) current in rat ischemic ventricular mid-myocardial (M) cells and to explore the antiarrhythmia mechanism in the treatment of ischemic heart disease. METHODS: M cells were isolated enzymatically from left ventricular mid-myocardium of rats. Peak I_to current was recorded by patch-clamp technique in the whole-cell configuration when M cells were superfused with normal Tyrode solution, simple ischemic solution,and simulated ischemic solution containing PCr at concentrations of 5, 10, 20 and 30 mmol/L for 10 min. RESULTS: Peak I_to current density of M cells superfused with simple simulated ischemic solution was significantly reduced by (76.1?6.3)% (P<0.05) compared with M cells superfused with Tyrode solution. Ischemic solution containing 5, 10, 20 and 30 mmol/L PCr reduced peak I_to current density by (57.1?9.6)% (P<0.05), (40.3?10.3)% (P<0.05), (34.3?9.6)% (P<0.05) and (32.1?10.6)% (P<0.05),respectively. There was statistical difference among ischemic solution without PCr and containing PCr at concentrations of 5 and 10 mmol/L groups (P<0.05). No statistical difference among groups of 10, 20 and 30 mmol/L PCr was observed (P>0.05). CONCLUSION: PCr reverses the inhibition of I_to current under ischemic condition in M cells, which may be the mechanism responsible for arrhythmia prevention in ischemic heart disease. PCr at concentrations of 0~10 mmol/L exerts significant dose-effect relationship.     

Alteration of transient outward potassium current in ventricular myocytes from 1-week and 2-month infarcted rabbit hearts

AIM: To study the current density of transient outward potassium current (I_to) in cells from the epicardial zone of the 1-week and 2-month infarcted rabbit heart. METHODS: Rabbits were infarcted by ligation of the left anterior descending coronary artery, 1 week as well as 2 months later, the single ventricular myocytes were isolated enzymatically from the infracted area of 1-week infracted rabbit heart (PMI-1 week) and 2-month infracted heart (PMI-2 months), region remote from the infracted zone of 2-month infracted heart (REM-2 months) and free wall of left ventricule from noninfarcted heart (CON). I_to was recorded using whole cell patch-clamp techniques. RESULTS: Membrane capacitance of myocytes in REM-2 months group was signifitantly larger than that in CON. I_tocurrent density (at +60 mV) was significantly reduced in PMI-1 week and PMI-2 months compared with CON , P＜0.01. Nevertheless, there was an significant increase in PMI-2M compared with PMI-1W, P＜0.05. I_to current density was also significantly decreased in REM-2 months compared with CON (P＜0.05), while there was an significant increase in REM-2 months compared with PMI-2 months, P＜0.05. CONCLUSION: The results indicated that the reduction and change of I_to in infarcted rabbit heart were heterogenous. These changes may underlie the abnormally long transmembrane action potentials of these arrhymogenic surviving ventricular fibers of the infarcted heart, thus contributing to reentrant arrhythmias in the infarcted heart. By 2 months after myocardial infarction, the depressed I_to of infracted area had returned to nearly normal, suggesting the presence of reverse remodeling.     

Effects of stretch on transient outward potassium and inward rectifier potassium current in cultured neonatal rat atrial myocytes

AIM：To investigate the effects of mechanical stretch on transient outward potassium current (Ito), inward rectifier potassium current (IK1) and action potential duration(APD) of cultured neonatal rat atrial myocytes. METHODS：Neonatal rat atrial myocytes were isolated and cultured on silicone sheeting with or without stretch for 24 h. The silicone membrane area was increased by 12% in stretched group. The cells without stretch served as control. Ito, IK1 and APD were recorded by the technique of whole-cell patch clamp. RESULTS：Compared with control group, Ito density in stretched myocytes was significantly reduced ［(16±04) pA/pF vs (121±29) pA/pF, P<001］, whereas IK1 density was increased ［(-108±08) pA/pF vs (-88±09) pA/pF, P<001］. The APDs at 50% and 90% levels of repolarization (APD50 and APD90) in the stretched cells were obviously decreased than those in non-stretched cells ［(105±14) ms vs (155±24) ms, (300±28) ms vs (563±36) ms, P<001］. CONCLUSION：Stretch stimulation leads to the reduction of Ito density, the increase in IK1 density and the shortness of APD in cultured rat atrial neonatal myocytes, which may contribute to atrial electrical remodeling induced by pressure overload.     

Characteristics of ventricular electrophysiology in a right ventricular rapid pacing-induced canine heart failure model

AIM: To research the characteristics of ventricular electrophysiology in right ventricular rapid pacing-induced congestive heart failure (CHF) dogs.METHODS: Dogs (n=16) were randomly divided into 2 groups: the control (n=7) and the CHF group (n=9) induced by rapid right ventricular pacing at 240 pulse·min-1 for 4 to 5 weeks.The electrophysiologic parameters were evaluated by the technique of standard electric stimulation and monophasic action potential (MAP) recording.RESULTS: (1) Ventricular effective refractory period (VERP),ventricular MAP duration (MAPD90),ventricular late repolarization duration (VLRD) and intra-ventricular conduction time (IVCT) were prolonged by 26% (P<0.01),43% (P<0.01),318% (P<0.05),and 19% (P<0.01),respectively in CHF group.(2)The ratio of VERP to MAPD₉₀ (VERP/MAPD₉₀) was decreased by 13% (P<0.05) in CHF group.(3) The dispersion of ventricular recovery time (VRT-D) was increased by 185% (P<0.01) in CHF group.(4) The ventricular fibrillation threshold (VFT) was decreased by 48% (P<0.01) in CHF group.CONCLUSION: The abnormal electrophysiological changes in the CHF condition may be contributing factors of lethal ventricular arrhythmias and sudden cardiac deaths in CHF.     

Effects of simvastatin on transient outward potassium current in ventricular myocytes of normocholesterolemic rabbits suffering from ischemia and reperfusion

AIM: To investigate the effects of simvastatin on transient outward potassium current (Ito) in left ventricular myocytes of rabbit heart undergoing ischemia-reperfusion, so as to explore the cellular (ionic) mechanism of statin treatment for antiarrhythmia. METHODS: Forty-five rabbits were randomly divided into three groups: ischemic-reperfusion group (I-R), simvastatin intervention group (statin) and sham-operation control group (sham). Anesthetized rabbits were subjected to 30 min ischemia by ligation of the left anterior descending coronary artery and 60 min reperfusion after oral administration of simvastatin at dose of 5 mg·kg-1·d-1(statin group) or placebo (I-R group) for 3 d. Single ventricular myocytes were isolated enzymatically from the epicardial zone of the infracted region derived from the hearts in I-R, statin group and the same anatomy region in sham. Whole cell patch clamp technique was used to record Ito. Simultaneously, the level of serum cholesterol was examined. RESULTS: No significant difference in serum cholesterol concentration among three groups was observed. The Ito current density (at +60 mV) was significantly decreased in I-R ［(9.49 ±1.91) pA/pF, n=11］ compared with sham ［(17.41± 3.13) pA/pF, n=15, P＜0.01］ and statin ［(15.24 ± 2.41) pA/pF, n=11, P＜0.01］, although there was slight reduction in statin group compared with sham (P＜0.05). CONCLUSION: Ischemia-reperfusion induces significant down-regulation of Ito, which may underlie the altered electrical activity and prolong abnormal transmembrane action potential duration of the surviving ventricular myocytes. Pretreatment with simvastatin attenuates these changes without lowering the serum cholesterol level, suggesting that simvastatin may reverse this electrical remodeling, thus contributing to the ionic mechanism of statin treatment for antiarrhythmia.     

The changes of intrarenal endothelin system in the course of congestive heart failure induced by rapid right ventricular pacing in dogs

AIM: To investigate the changes of intrarenal endothelin system in the course of congestive heart failure. METHODS: A canine congestive heart failure model induced by rapid right ventricular pacing was used in the present study. Twenty-one mongrel dogs divided randomly into 3 groups: control, congestive heart failure 2 weeks (CHF2) and congestive heart failure 4 weeks (CHF4). The severity of heart failure was evaluated by means of hemodynamic measurement. The concentration of plasma endothelin was detected via RIA, and the expression of endothelin was detected by RT-PCR. RESULTS: The concentration of plasma endothelin in both of CHF2 and CHF4 elevated significantly. In CHF2, the expression of endothelin receptor B(ETB) in renal medulla increased significantly. And in CHF4, the expression of preproendothelin, endothelin receptor A (ETA) and ETB increased both in renal cortex and medulla. Furthermore, in cortex, the expression of ETA increased more significantly than ETB, while in medulla, ETB expressed much more than ETA. CONCLUSION: The changes of renal endothelin system expression plays a role in the regulation of water and electrolyte balance during the progress of congestive heart failure.     

Effect of hypercholesterolemia on the ionic currents in cardiac ventricular myocytes of rats

AIM: To determine whether chronic hypercholesterolemia affects ionic currents on cardiac ventricular myocytes of rats. METHODS: Whole-cell patch-clamp technique was used to record the ionic currents in single cardiac myocytes isolated from normal cholesterolemia and hypercholesterolemia rats. RESULTS: In the hypercholesterol group (group Ⅱ), serum total-cholesterol level was significantly higher than that of normal group (group Ⅰ) ［(3.10±0.62)mmol·L-1 vs (1.18±0.37)mmol·L-1, P<0.01, n=20］. The serum triglyceride content of group II was remarkably higher than that of group Ⅰ ［(1.51±0.30)mmol·L-1 vs (0.43±0.15)mmol·L-1, P<0.01, n=20］. In ventricular myocytes of rats, 50% repolarization of action potential duration (APD50) prolonged from (70.86±8.12)ms (group Ⅰ) to (116.16±6.90)ms (group Ⅱ) (n=10 in each group, P<0.01); APD90 prolonged from (95.10±7.27)ms (group Ⅰ) to (144.04±7.39)ms (group Ⅱ) (n=10 in each group, P<0.01); at the test potential of -120 mV, Ik1 increased from (-16.98±4.54) pA/pF(group Ⅰ) to (-19.92±4.08) pA/pF (group Ⅱ) (n=12 in each group, P<0.05); at the test potential of 0 mV, ICa-L decreased from (-8.56±1.29) pA/pF (group Ⅰ) to (-5.24±0.90) pA/pF (group Ⅱ) (n=10 in each group, P<0.01); at the test potential of +60 mV, Ito decreased from (13.20±1.97) pA/pF (group Ⅰ) to (10.30±1.97) pA/pF (group Ⅱ) (n=8 in each group, P<0.05). CONCLUSION: Hypercholesterolemia affects the ionic currents on cardiomyocytes of rats greatly, which may be the ionic mechanism of cardiac toxicity induced by hypercholesterolemia.     

Effect of platelet activating factor on the action potential and potassium currents in guinea-pig ventricular myocytes

AIM: To investigate the effects of platelet activating factor (PAF) on the action potential and potassium currents in guinea-pig ventricular myocytes. METHODS: By using whole-cell patch clamp technique, the effects of PAF on APD₉₀, I_K1 and I_K were investigated in enzymatically dispersed single guinea-pig ventricular myocytes. RESULTS: With 5 mmol/L ATP in the pipette electrode, 1 μmol/L PAF increased APD₉₀ from (225.8±23.3) ms to (352.8±29.8) ms (n=5, P<0.05), decreased I_K1 and I_K tail currents from (-6.1±1.3) nA to (-5.6±1.1) nA (n=5, P<0.05) at -120 mV and from (173.5±16.7) pA to (152.1±11.5) pA (P<0.05, n=4) at +30 mV, respectively. In contract, without ATP in the pipette electrode, 1 μmol/L PAF shortened APD₉₀ from (153.0±24.6) ms to (88.2±19.4) ms (n=5, P<0.01). Incubation of myocytes with 1 μmol/L glibenclamide, a blocker of I_KATP restored prolongation of APD induced by PAF. CONCLUSION: In guinea-pig ventricular myocytes, with 5 mmol/L ATP in the pipette, PAF prolonged APD partly due to the inhibition of I_K and I_K1, while with 0 mmol/L ATP in the pipette, PAF induced an activation of I_KATP, hence a decrease in APD was observed. Therefore, PAF might amplify the heterogeneity between ischemia and normal cardiac myocytes during ischemic reperfusion, which might play a vital role in the pathogenesis of the arrhythmias induced by ischemia/reperfusion.     

Effect of hypoxia on persistent sodium current in ventricular myocytes from 3-week infarcted rat heart

AIM: To investigate the effect of hypoxia on persistent sodium current (INap) in single ventricular myocyte isolated from acute myocardial infarction (AMI) heart of rats and to study the mechanisms of cardiac arrhythmias that occur after AMI. METHODS: AMI model was induced by ligating the left anterior descending coronary artery in rats. The whole-cell patch clamp technique was used to record the current in epicardial myocytes in infarcted region from rats at 3 week after AMI. RESULTS: In normoxic conditions, the current density of INap in cardiomyocytes of fake operation (FO) and AMI hearts was 0.144±0.022 pA/pF (n=9), 0.121±0.013 pA/pF (n=9，P<0.01)， respectively, which was blocked by tetrodotoxin (TTX). The amplitude of INap was gradually increased with the prolongation of hypoxia time, but the increase in extent of INap in FO cells was significant bigger than that in AMI cells. The INap was blocked by 1 mmol/L glutathione. CONCLUSIONS: After AMI, the amplitude of INaP in infarcted and noninfarcted myocardium showed differences both in normoxic and hypoxic conditions, which increased dispersion of repolarization. This may be one of the reasons of reentrant ventricular arrhythmias that occur after AMI.     

Changes in action potential and the conduction time of ventricular cells in subendocardium and subepicardium during ischemia and early reperfusion

AIM:To investigate the electrophysiological characteristics of ventricular myocyte both in subendocardium and in subepicardium during ischemia. METHODS:Using modified Ferrier's method of ischemic and reperfusion injury in isolated guinea pig right ventricular wall. RESULTS: The transmembranal electric activities in subendocardium and in subepicardium were all significantly abnormal, and it was more significant in subendocardium. CONCLUSION: The alteration degree of ventricular myocyte in subendocardium and in subepicardium during ischemia and early reperfusion was different, and this might be the electrophysiological basis of the vulnerability of the subendocardium.     

Effect of cGMP on voltage-gated potassium channel in pulmonary artery smooth muscle cells from rats exposed to chronic hypoxia

AIM: To investigate the effect of cGMP on voltage-gated potassium channel in pulmonary artery smooth muscle cells (PASMCs) from rats exposed to chronic hypoxia. METHODS: (1) Wistar rats were randomly divided into control group (group A) and chronic hypoxia group (group B). Then group B received hypoxia 8 hours per day for 4 consecutive weeks. (2) Single PASMC was obtained via acute enzyme separation method. (3) Conventional whole-cell patch clamp technique was used to record resting membrane potential (Em) and ion currents of voltage-gated potassium channel. The changes of ion currents of voltage-gated potassium channel before and after applying cGMP (1 mmol/L), an agonist of protein kinase G (PKG), and cGMP plus H-8 (1 mmol/L), an inhibitor of PKG were compared between two groups. RESULTS: The Em of group B were significantly lower than that of group A. The ion currents of voltage-gated potassium channel in group A and group B were all significantly inhibited by cGMP [control group: from (118.0±5.0) pA/pF to (89.9±16.5) pA/pF, n=6, P＜0.05;chronic hypoxia group: from (81.0±5.0) pA/pF to (56.8±9.1) pA/pF, n=6, P＜0.05]and these effects were reversed by H-8 [control group: from (119.2±10.3) pA/pF to (117.8±9.1) pA/pF, n=6, P＞0.05;chronic hypoxia group: from (96.8±6.2)　pA/pF to (98.0±2.2)　pA/pF, n=6, P＞0.05]. CONCLUSIONS: The currents of voltage-gated potassium channel was inhibited by chronic hypoxic. The inhibitory effect of cGMP on currents of voltage-gated potassium channel in PASMCs from both normal and chronic hypoxic rats may be probably through the phosphorylation of voltage-gated potassium channel.     

Blunted response of L-type calcium current to simulated ischemia and reperfusion in ventricular myocytes from diabetic rabbits

AIM: To evaluate the effects of simulated acute ischemia and reperfusion on L-type calcium current (I_{Ca, L}) in ventricular myocytes from diabetic and non-diabetic rabbits.METHODS: Using whole-cell patch clamp techniques, I_{Ca, L} was measured in left ventricular myocytes isolated from 6-week alloxan-induced diabetic rabbits and age-matched control ones at baseline, 5 min of simulated ischemia, and 5 min of reperfusion.RESULTS: There were no significant differences on baseline maximum I_{Ca, L} densities between diabetic and control ventricular myocytes. In control cells (n=11), maximal I_{Ca, L} densities of baseline, ischemia and reperfusion were (-8.36±1.63)pA/pF, (-5.90±1.75)pA/pF and (-4.22±1.02)pA/pF, respectively. The I_{Ca, L} of ischemia was less than that of baseline (P<0.01), while the I_{Ca, L} of reperfusion was less than those of baseline (P<0.01) and ischemia (P<0.05). In diabetic cells (n=9), the I_{Ca, L} of baseline, ischemia and reperfusion were (-7.55±1.62)pA/pF, (-6.05±1.58)pA/pF and (-5.12±1.13)pA/pF, respectively. Only I_{Ca, L} of reperfusion was less than that of baseline (P<0.01), while I_{Ca, L} of ischemia was not significantly different from that of baseline (P>0.05) or reperfusion (P>0.05).CONCLUSION: I_{Ca, L} in diabetic ventricular myocytes represents blunted response to acute ischemic injury, being decreased more slowly than that in control cells. Post-ischemic reperfusion is still a potent inhibitor against I_{Ca, L} in both diabetic and non-diabetic cells. This study may be indicative of the mechanism about ischemia-reperfusion injury to diabetic myocardium and the therapy for diabetic patients with ischemic heart disease.     

Characteristics of morphology and left ventricular function in the mouse with myocarditis

AIM:To determine the relationship between microhistology and cardiac contractility in myocarditis animal model. METHODS: Setting up myocarditis animal model by injecting Coxsackivevirus B₃ (CVB₃) into mice, then observed myocardial morphological changes and measured left ventricular function of mice at the time of first three days and two weeks after injecting CVB₃. RESULTS:Subcellular structure (mitochondria) changed at the first three days after injecting CVB₃. The left ventricular pressure (LVP) and the rate of intraventricular pressure development (dp/dt) which is the index of reflecting cardiac contractility depressed in this stage (14.2±0.8) kPa and (273.1±10.0)kPa/s, respectively. There were (17.1±0.7)kPa and (359.8±9.3)kPa/s in normal mice, respectively (P＜0.01). Myocardial lesions were more severe during immune response stage-two weeks after injecting CVB₃, including myocardial inflammation and necrosis. LVP was (11.8±0.2)kPa and dp/dt was (209.5±6.1)kPa/s in immune response stage. There was significant difference between mice with myocarditis at early stage and at immune response stage (P＜0.01).CONCLUSIONS:The factor of causing the depression of cardiac contractility in early stage (virus-induced damage) is mainly change of subcellular structure. Mitochondria cannot provide energy as normal. There were more severe myocardial lesions in later stage (cell-mediated autoimmune response)than in early stage. The depression of cardiac contractility is a consequence of multifactor.     

Chronic hypoxia altered the expression of ET-1 mRNA in response to acute hypoxia in pulmonary artery endothelial cells

AIM:To investigate the expression of ET-1 mRNA in porcine pulmonary artery endothelial cells cultured in normoxic and chronic hypoxic conditions, and their different responses to acute hypoxia were also evaluated.METHODS:Insituhybridization and image -analysis system were used. RESULTS:Acute hypoxia enhanced the expression of ET-1 mRNA in both normoxic and chronic hypoxic group. The increment was more significant in the latter group.CONCLUSION:Chronic hypoxia increased the expression of ET-1 mRNA in response to acute hypoxia in porcine pulmonary artery endothelial cells.     

Role of potassium channels in the regulation of intracellular free Ca2+ concentration of pulmonary artery smooth muscle cells in rats

AIM: To investigate the role of potassium channels in the regulation of intracellular free calcium concentration ( [Ca²⁺]_i) of pulmonary artery smooth muscle cells (PASMCs) in rats. METHODS: The fluorescence Ca²⁺ indicator Fura-2/AM was used to observe [Ca²⁺]_i of rat PASMCs in normal and chronic hypoxic condition. The influences of potassium channels on PASMCs proliferation were assessed by MTT assay. RESULTS: 1. In normoxic condition, [Ca²⁺]_i was (156.91±8.60) nmol/L, and in hypoxic condition, [Ca²⁺]_i was (294.01±16.81) nmol/L. 2. In normoxic condition, the voltage-dependent K⁺-channel antagonist 4-aminopyridine (4AP), but not the Ca²⁺-activated K⁺-channel antagonist tetraethylammonium (TEA) and the ATP-sensitive K⁺-channel antagonist glibenclamide (Glib) increased [Ca²⁺]_i. 3. In hypoxic condition, 4AP and TEA caused the rise in [Ca²⁺]_i , but Glib had no effect on [Ca²⁺]_i. 4. MTT assay showed that 4AP increased the value of absorbing light degree (A value) in normoxic and hypoxic condition (0.582±0.062,0.873±0.043,respectively, P＜0.01), TEA increased A value only in hypoxic condition, and Glib had no effect on the proliferation of PASMCs. CONCLUSIONS: K_V plays an important role in the regulation of [Ca²⁺]_i and proliferation of PASMCs. K_Ca serves as distinct responsive roles in the regulation of proliferation of PASMCs in hypoxic condition. K_ATP has no effect on [Ca²⁺]_i and proliferation of PASMCs in normoxic and hypoxic conditions.     

新书推荐：《分子克隆实验指南》（第三版）

AIM: To study the effect of panax notoginseng sponins (PNS) on L-type Ca²⁺ current in isolated right ventricle myocytes from chronic hypoxic rats. METHODS: Using whole cell patch clamp recording technique,we measured I_Ca-L in isolated right ventricle myocytes which were divided into three group:control group, chronic hy-poxic group and chronic hypoxic group with PNS(100 mg·kg^-1·d^-1). RESULTS: The result showed I_Ca-L of cells from chronic hypoxic group were significantly larger than the other two groups(P＜0.05). CONCLUSION: PNS decreases L-type Ca²⁺ current of the right ventricle myocytes from chronic hypoxic rats.     

Role of nuclear factor κB on the expression of interleukin-6 in mouse mesangial cells induced by interleukin-1β

AIM:To investigate the regulatory role of nuclear factor κB (NF-κB) in the expression of interleukin-6 in mesangial cells (MC) induced by interleukin-1β.METHODS:Activation of NF-κB was measured by electrophoresis mobility shift assay (EMSA). RT/PCR and ELISA were used to detect IL-6 mRNA expression and IL-6 production, respectively.RESULTS:rhIL-1β could rapidly stimulate the activation of NF-κB in MC, and increase the expression of IL-6 mRNA and protein. PDTC, one of the inhibitor of NF-κB, could inhibit the expression of IL-6 in mRNA and protein in MC stimulated by rhIL-1β.CONCLUSION:IL-6 expression induced by IL-1β may be regulated by NF-κB in MC, NF-κB may modulate the immune-inflammatory reaction in glomerular disease.     

Effect of Ganoderma lucidum spores powder on the expression of IGF-1, NF-κB and apoptosis of nerve cells in the brain from epileptic rat

AIM: To investigate the effect of Ganoderma lucidum spores powder on the expression of insulin-like growth factor-1 (IGF-1), nuclear factor-κB (NF-κB) and apoptosis of nerve cells in rats with epilepsy established by pentetrazole. METHODS: The sub-eclampsia dosage of pentetrazole (PTZ) was used to make epilepsy model. Ganoderma lucidum spores powder group was given from stomach. The enduring time and latent period were recorded. The immune reactivity of IGF-1, NF-κB/P65 and apoptosis of nerve cells were measured with immunohistochemical staining and TUNEL method. RESULTS: In high power sight (×400), there were much more apoptosis cells in hippocampus and brain cortex of model group (18.80±2.13, 16.87±2.00) than those in control group (0.97±0.52, 0.58±0.25). The expressions of IGF-1, NF-κB in model group were higher than those in control group. Compared with model group, the latent period of Ganoderma lucidum spores powder group at the 17th, 21th, 25th days were longer (P<0.05, P<0.05, P<0.01, respectively).There were less apoptosis cells in hippocampus and brain cortex of Ganoderma lucidum spores powder group (12.30±2.46, 10.48±1.33) than those in model group. The expression of NF-κB/P65 in Ganoderma lucidum spores powder group was lower than that in model group, but the immune reactivity of IGF-1 increased more distinctly in Ganoderma lucidum spores powder group than that in model group. CONCLUSION: IGF-1, NF-κB and apoptosis of nerve cells may have play a role in occurrence and development of PTZ-induced epilepsy. Ganoderma lucidum spores powder can suppress expression of NF-κB strongly, and facilitate the immune reactivity of IGF-1, which may be one of the mechanisms by which Ganoderma lucidum spores powder restrains the apoptosis of nerve cells caused by epilepsy to prevent the damages of nerve cells.