Effect of ghrelin in septal nucleus on gastric motility of diabetic gastroparesis rats and its potential mechanism regulated by hypothalamic arcuate nucleus

AIM：To study the effect of ghrelin in septal nucleus on the gastric motility of the rats with diabetes mellitus (DM) and to investigate the regulation of ghrelin pathway between arcuate and septal nucleus nuclei on gastric motility. METHODS：Streptozotocin was injected intraperitoneally to establish a DM rat model. Fluorescence immunohistochemistry and real-time PCR were used to detect the expression of ghrelin receptor GHS-R1a. The gastric motility was evaluated by implantation of a force transducer on the surface of rats stomachs and the motility index was also calculated. The neural connections between arcuate and septal nuclei were analyzed by the technique of fluorogold tracing. The neural control pathway of gastric motility was determined by central drug injection, nucleus lesion or nucleus electrical stimulation. RESULTS：The expression of GHS-R1a in the septal nucleus of DM rats was lower than that in normal rats (P<0.05). The amplitude and frequency of gastric motility in the DM rats were lower than those in the normal rats (P<0.05). The gastric motility of normal and DM rats were increased by injection of ghrelin into the septal nucleus in a dose-dependent manner. Seven days after injection of fluorogold into the septal nucleus, some neurons in arcuate nucleus were labeled by fluorogold and part of the labeled neurons were ghrelin immunopositive. No effect of nucleus lesion or nucleus electrical stimulation on the gastric motility in the normal rats was observed. In DM rats, the lesion of septal nucleus decreased the gastric motility (P<0.05). In the normal rats, the change of gastric motility caused by electrical stimulation in arcuate nucleus was not affected by the lesion of septal nucleus (P>0.05), while the change was attenuated in DM rats (P<0.05). The ghrelin receptor antagonist ［D-Lys-3］-GHRP-6 had no significant effect on the gastric motility induced by electrical stimulation in arcuate nucleus of the normal rats (P>0.05), but it reduced the change in the DM rats (P<0.05). CONCLUSION:Ghrelin in septal nucleus and the ghrelinergic pathway between arcuate and septal nuclei play an important role in the modulation of gastric motility in DM rats.     

Effect of altitude hypoxia on glutamate,aspartate and NOS in the rat hypothalamus

AIM: To investigate the effects of external counterpulsation (ECP) on nitric oxide (NO) and nitric oxide synthase (NOS) and the expression of NOS gene in myocardial infarction canines. METHODS: Nineteen healthy dogs were randomly divided into three groups ie. controls, ischemia group, ischemia and ECP group. Serum NO concentrations and myocardium NO levels and NOS specific activity were determined by modified nitrate reductase method. The protein synthesis of sub-type NOS including inducible NOS (iNOS) and endothelial NOS (eNOS) of myocardial tissue were also determined by immunohistochemical method. The constitutive NOS (cNOS) mRNA was measured via in situ hybridization. RESULTS: 120 and 180 minutes after the ligating of LAD, serum NO concentration in ECP groups were higher than those in ischemic groups (P＜0.05). The NO levels and NOS specific activity in myocardium of ischemic dogs were lower than those in controls and ECP group (P＜0.05). Protein synthesis of iNOS increased and that of eNOS decreased in ischemic myocardium. But ECP could control the protein synthesis of iNOS, and increase that of eNOS. Further studies showed that the expression of cNOS mRNA decreased in ischemic myocardial tissue, ECP might promote the expression of it and regulate NOS in the gene level. CONCLUSION: The results suggested that it was one of the most important mechanisms through raising the NO levels to protect ischemic myocardium in ECP.     

Effects of ghrelin on firing activity of gastric distension-sensitive neurons in hypothalamic arcuatus nucleus and gastric motility in diabetic rats

AIM： To study the roles of ghrelin in the regulation of gastric distension (GD)-sensitive neurons in the hypothalamic arcuate nucleus (Arc) and gastric motility in diabetes mellitus (DM) rats. METHODS：DM rat model was made by intraperitoneal injection of streptozotocin. The effects of ghrelin and ［D-Lys3］-GHRP-6 on GD-sensitive neurons in the Arc of DM rats were observed by recording the extracellular potentials of single neurons, and the gastric motility was also monitored in vivo. The expression of ghrelin receptor,growth hormone secretagogue receptor (GHS-R), in Arc was studied by real-time PCR and immunofluorescene method. RESULTS：(1) Ninety-eight GD-sensitivity neurons were recorded in the Arc of normal rats, in which 64.3% were classified as GD-excitatory (GD-E) neurons and 35.7% were GD-inhibitory (GD-I) neurons. Microinjection of ghrelin excited 73.0% of the 63 GD-E neurons and the discharge frequency significantly increased as compared with the neurons treated with saline. Ghrelin inhibited 60.0% of the 35 GD-I neurons and the discharge frequency was significantly reduced (P<0.01). The effect of ghrelin was blocked by the antagonist of ghrelin ［D-Lys3］-GHRP-6. (2) Sixty-six GD-sensitive neurons were recorded in the Arc of diabetes rats, in which 64.3% were GD-E neurons, and 35.7% were GD-I neurons. Microinjection of ghrelin excited 35.1% of the GD-E neurons and the discharge frequency significantly increased as compared with the neurons treated with saline. Ghrelin inhibited 21 of the 29 GD-I neurons (72.4%) and the discharge frequency was significantly reduced. Compared with normal control group, the ratio of GD-E and GD-I neurons in diabetic rat Arc GD-sensitive neurons was not significantly changed. However, the ratio of GD-E neurons treated with ghrelin was significantly decreased, and the average increase rate of discharge frequency was significantly decreased. Ghrelin did not change GD-I neurons rejection ratio and discharge frequency average reduction rate. (3) Microinjection of ghrelin into the Arc significantly promoted gastric motility in normal and DM rats, and a significant dose-dependent manner was observed. However, the promotion effect of ghrelin on gastric motility in normal rats was stronger than that in DM rats, and the effect was completely blocked by ［D-Lys3］-GHRP-6. (4) The mRNA expression of GHS-R1a in the hypothalamic Arc of diabetic rats significantly reduced as compared with the normal control rats. The protein level of GHS-R1a in the hypothalamic Arc was also significantly reduced in DM rats. CONCLUSION：Ghrelin regulates the activity of GD-sensitive neurons in hippocampus Arc of diabetic rats by the action on ghrelin receptor.     

Effect of lipopolysaccharide on L-type voltage-gated calcium channel currents in primarily cultured rat caudate nucleus neurons and its modulation by 2-arachidonoylglycerol

AIM: To explore whether L-type voltage-gated calcium channel (L-VGCC) currents are involved in neurotoxicity of lipopolysaccharide (LPS) and the neuroprotective mechanism of 2-arachidonoylglycerol (2-AG) in caudate nucleus (CN) neurons. METHODS: On the 7th day, the primarily cultured CN neurons were treated with 2-AG, LPS, SR141716A (a CB1 receptor inverse agonist) and AM630 (a CB2 receptor inverse agonist) for 12 h. The L-VGCC currents in the CN neurons were recorded using the whole-cell patch-clamp technique. Hoechst staining was used to detect the effect of 2-AG on neurotoxicity of LPS. Caspase-3 assay kit was used to determine the activity of caspase-3 induced by LPS alone or with 2-AG. RESULTS: LPS enhanced the current density of L-VGCC, but did not influence the activation and deactivation of L-VGCC. 2-AG inhibited the enhancement of L-VGCC currents induced by LPS. The effect of 2-AG on the suppression of L-VGCC currents induced by LPS was not mediated through CB1 or CB2 receptor. 2-AG alone did not affect the L-VGCC currents, activation and deactivation in the CN neurons. 2-AG inhibited LPS-induced elevated activity of caspase-3 in the CN neurons. This effect was inhibited by SR141716A. 2-AG inhibited the cell apoptosis induced by LPS, and this effect was mediated via CB1 receptor. CONCLUSION: Endocannabinoid 2-AG may exert the anti-inflammatory and neuroprotective effects through the modulation of L-VGCC currents in primarily cultured rat CN neurons.     

Effect of Ba2+ concentration on L-type Ca2+ channel in hypothalamic neurons

AIM:To investigate the effect of Ba²⁺ concentration on L-type of Ca²⁺ channel in hypothalamic neurons.METHODS:The cell acute isolation technique and cell-attached patch-clamp technique were used.RESULTS:The slope conductance of L-type Ca²⁺ channel were 28.6 pS (110 mmol/L) and 19.1 pS (10 mmol/L), and the open probability (NP₀) obviously different with different Ba²⁺ concentration as carrier. CONCLUSION:Ba²⁺ concentration had the obvious effect on the L-type Ca²⁺ channel.     

Effect of hypothalamic PVN exogenous orexin-A on food intake in obese rats and regulation by NPY receptor signaling pathway

AIM:To investigate whether neuropeptide Y (NPY) receptor signaling pathway is involved in the regulation of orexin-A on food intake and glucose-sensitive (GS) neuronal excitability in the hypothalamic paraventricular nucleus (PVN) of diet-induced obese (DIO) rats. METHODS:Fluorescence immunohistochemistry experiment was used to observe the expression of orexin-A receptor (orexin receptor 1, OX1R) and NPY receptor Y5 (NPY-5R) in the PVN. The effect of orexin-A on the excitability of GS neurons in PVN was observed by single cell discharge recording. The cannula was implanted into the PVN of SD rats and DIO rats. The orexin-A, OX1R antagonist SB-334867 and NPY-5R antagonist CGP-71683 were injected through the cannula to observe the 0~2 h and 0~4 h food intake of the rats. RESULTS:The expression of OX1R and NPY-5R in the PVN of DIO rats was significantly higher than that in the SD rats. Orexin-A inhibited glucose-inhibited (GI) neurons and excited glucose-excited (GE) neurons in the PVN. However, the effects of orexin-A on GS neurons were partially blocked by the NPY-5R antagonist CGP-71683. Compared with the SD rats, orexin-A had more pronounced excitatory and inhibitory effects on PVN GS neurons in the DIO rats. Injection of orexin-A in the PVN increased food intake in the SD rats and DIO rats. However, the orexin-A-induced feeding was partially blocked by the NPY-5R antagonist CGP-71683. The effect of orexin-A on feeding was stronger in the DIO rats than that in the SD rats. CONCLUSION:The hypothalamic PVN orexin-A regulates food intake and GS neuronal excitability mainly through the OX1R signaling pathway, and NPY-5R signaling is also involved in this process, in which the regulatory effect on DIO rats is more sensitive.     

“信息园艺学论坛”在成都举行

由《园艺学报》编辑部和中国农业科学院蔬菜花卉研究所生物技术研究室共同发起和主办的“信息园艺学论坛”于2007年5月28～29日在成都举行。     

Establishment of autophagy model of rat gastric interstitial cells of Cajal induced by glutamic acid

AIM: To establish an autophagy model of glutamic acid-induced rat gastric interstitial cells of Cajal (ICCs) in vitro. METHODS: Glutamic acid was added to the medium of cultured ICCs in vitro at different concentrations (high, medium and low concentrations were 10 mmol/L, 5 mmol/L and 2.5 mmol/L, respectively) for different periods (3 h, 6 h and 24 h). The cell viability was measured by CCK-8 assay. The protein expression of microtubule-associated protein 1 light chain 3 (LC3) in the ICCs after cultured with glutamic acid at different concentrations for different periods was determined by Western blot. The ultrastructure and autophagic vacuoles of ICCs were observed under electron microscope, and immunofluorescence technique was used to measure the fluorescence intensity of autophagic protein LC3 after co-cultured with glutamic acid at medium concentration. RESULTS: Compared with control group, glutamic acid significantly inhibited the viability of ICCs (P<0.01). The ratios of LC3-Ⅱ/LC3-I in medium and high concentration groups at 3 h, 6 h and 24 h were significantly increased as compared with control group and low concentration group (P<0.01), and that in medium concentration group at 3 h was the best to increased the ratio of LC3-Ⅱ/LC3-I (P<0.01). Under electron microscope, the ICCs in glutamic acid group showed obvious autophagic vacuoles and cytoplasmic vacuoles. The fluorescence intensity of autophagic protein LC3 in the ICCs of glutamic acid group was significantly enhanced (P<0.01). CONCLUSION: Glutamic acid successfully induces autophagy in ICCs. The optimum condition of glutamic acid was 5 mmol/L for 3 h.     

Effect of cimicifugoside H-1 on amino acid neurotransmitters in striatum of rats with cerebral ischemia

AIM: To study the neuroprotective effect of cimicifugoside H-1 and to explore the mechanism involved by determining the variation of amino acid neurotransmitters in extracellular fluid in the striatum of rats with cerebral ischemia. METHODS: The rats were randomly divided into sham-operated, cerebral ischemia, high-, middle- and low-dose cimicifugoside H-1, and ginkgo groups. Focal cerebral ischemia model was established by middle cerebral artery occlusion (MCAO) with sutures. Normal saline was intraperitoneally injected into the rats in sham-operated group and cerebral ischemia group, while ginkgo and different doses of cimicifugoside H-1 were injected into the rats in ginkgo group and high-, middle- and low-dose cimicifugoside H-1 groups, respectively, once a day for 7 d. The striatal fluids were gained in vivo by brain microdialysis. The contents of aspartic acid, glutamic acid, glycine and γ-aminobutyric acid were tested by high-performance liquid chromatography electrochemical detector system. RESULTS: Compared with sham-operated group, the contents of excitatory amino acids (aspartic acid and glutamic acid) were significantly increased 2 h after cerebral ischemia (P<0.05). Compared with cerebral ischemia group, the contents of aspartic acid and glutamic acid were significantly decreased 2 h after cerebral ischemia in high-dose cimicifugoside H-1 and ginkgo groups (P<0.05). Compared with cerebral ischemia group, the contents of aspartic acid and glutamic acid did not show significant decrease 2 h after cerebral ischemia in middle- and low-dose cimicifugoside H-1 groups. Compared with sham-operated group, the contents of inhibitory amino acid (γ-aminobutyric acid and glycine) were significantly decreased 3 h after cerebral ischemia in cerebral ischemia group (P<0.05). Compared with cerebral ischemia group, the contents of γ-aminobutyric acid and glycine were significantly increased 3 h after cerebral ischemia in high-dose cimicifugoside H-1 and ginkgo groups (P<0.05). Compared with cerebral ischemia group, the contents of γ-aminobutyric acid and glycine did not show significant decrease 3 h after cerebral ischemia in middle- and low-dose cimicifugoside H-1 groups. CONCLUSION: Cimicifugoside H-1 restrains the excessive releases of excitatory amino acids and increases the contents of inhibitory amino acids during cerebral ischemia. It doesn't only penetrate through the blood brain barrier, but also regulates the disorder of excitatory amino acid during cerebral ischemia, thus showing the protective function to cerebral neuron during cerebral ischemia.     

Effect of cyclophosphamide on proliferation and apoptosis of rat mesangial cells in vitro

AIM:To investigate the effect of cyclophosphamide(CTX) on proliferation and apoptosis of mesangial cells(GMC) of rat in vitro. METHODS:GMC proliferat ion was detected by MTT method,GMC apoptosis was examined by inverted microscopy for phase-contract and fluoroscopy and flow cytometry analysis.The levels of Fas and Bcl-2 were also detected by immunohistology. RESULTS:The proliferation of GMC were inhibited by CTX, methylprednisolone(MP), low molecular weight heparin(LMWH). Apoptosis of GMC was induced by CTX, the apoptosis rate of GMC was 8.2%, and the Fas level was increased. CONCLUSION:CTX could inhibit proliferation and induce apoptosis of GMC possibly by enhancing the Fas level.     

Activation of corticotrophin releasing hormone-containing neurons in hypothalamic paraventricular nucleus contributes to sympathoexcitation in rats with congestive heart failure

AIM:To observe the expression of corticotropin releasing hormone (CRH) within the paraventricular nucleus of hypothalamus (PVN) and to explore the relationship between the activated CRH-containing neurons and sympathetic activity in rats with heart failure (HF).METHODS:Healthy male Sprague-Dawley (SD) rats were subjected to coronary artery ligation to induce HF,and chronic intracerebroventricular (ICV) infusion was performed by osmotic pump for 4 weeks.The rats in sham group and HF group were given vehicle (VEH;artificial cerebrospinal fluid 0.25 μL/h).The rats in HF plus treatment group were treated with CRH competitive inhibitor αh-CRH (15 mg/h).Meanwhile,the Lewis rats and Fischer 344 rats for control study also underwent coronary ligation to induce HF or sham surgery.After 4 weeks,left ventricular end-diastolic pressure (LVEDP) and maximum positive/negative change in pressure over time (±dp/dt_max) were determined.The right ventricular-to-body weight (RV/BW) and lung-to-body weight (lung/BW) ratios were calculated.The renal sympathetic nerve activity (RSNA) was recorded and the plasma norepinephrine (NE) level was measured.The expression of CRH in the PVN combined with the plasma adrenocorticotrophic hormone (ACTH) levels were measured.RESULTS:Compared with the sham-SD rats,the HF-SD rats had a greater number of CRH positive neurons in the PVN (accordingly the plasma ACTH levels were increased),accompanied by decreased±dp/dt_max and increased RSNA,plasma NE,LVEDP,lung/BW and RV/BW.However,ICV treatment with αh-CRH attenuated these changes in the HF-SD rats (P<0.05).Compared with the sham-Fisher 344 rats,the HF-Fisher 344 rats also had a greater number of CRH positive neurons in the PVN (accordingly the plasma ACTH levels were increased).In addition,they had significantly increased RSNA and plasma NE level,higher LVEDP,RV/BW and lung/BW,and lower±dp/dt_max(P<0.05).Compared with the SHAM-Lewis rats,the HF-Lewis rats had not significantly changed in the above parameters.CONCLUSION:In CHF,the CRH-containing neurons in PVN are activated,thus aggravating cardiac function by increasing sympathoexcitation.     

Effects of glucose and Mg2+ in the neurons damaged by glutamate

AIM and METHODS: To observe the effects of glucose-free and Mg²⁺-free in the extracellular fluid on the changes of [Ca ²⁺]_i in the cerebro-cortical neurons damaged by 1mmol/L glutamate using laser confocal scanning microscope. RESULTS: Both frequency and amplitude of neuronal calcium oscillation induced by glutamate were lowered in glucose-free and Mg²⁺-free buffers. The basic [Ca²⁺]_i concentration was lowered in the former case , but it was elevated in the latter case. CONCLUSION: Mg²⁺-free aggravates [Ca²⁺]_i overload induced by 1mmol/L glutamate ,under certain conditions the glucose-free might resist damage role of glutamate and Mg²⁺-free.     

Effect of myocardial ischemia on expression of natriuretic peptide receptors in rat medulla oblongata

AIM:To evaluate the expression of natriuretic peptide receptor A (NPR-A) and C (NPR-C), choline acetyltransferase (ChAT) and tyrosine hydroxylase (TH) in the ventral medulla oblongata after myocardial ischemia in the rats. METHODS:All rats were randomly divided into blank control group, sham group and myocardial ischemia group. After the myocardial ischemia model was established, the rats were sacrificed, and the expression of NPR-A, NPR-C, ChAT and TH in the rostral ventral medulla oblongata and caudal ventral medulla oblongata was detected by Western blotting on day 3, day 7, day 14, day 18 and on day 28. RESULTS:On the above days after modeling, the expression of NPR-A in ventral medulla oblongata of the rats was significantly increased (P<0.05). The expression of NPR-C was also increased, but later than NPR-A. The expression of TH was significantly decreased (P<0.05). The expression of ChAT in the rostral ventral medulla oblongata was lower than that in blank control group (P<0.05), and had no significant difference as compared with blank control group in the caudal ventral medulla oblongata. CONCLUSION:In medulla oblongata, the expression of NPR-A and NPR-C in the central cardiovascular region significantly increases after myocardial ischemia, while the expression of ChAT and TH decreases markedly. The natriuretic peptide, ChAT and TH may participate in the autonomic nervous control of cardiovascular system after myocardial ischemia.     

Effect of arachidonylethanolamide in paraventricular nucleus on cardiac function and sympathetic nerve activity in rats with heart failure

AIM:To determine the roles of the arachidonylethanolamide (AEA) in the paraventricular nucleus (PVN) in cardiac function and sympathetic activity in the rats with chronic heart failure (CHF). METHODS:Chronic heart failure was induced by left coronary ligation in Wistar rats and was confirmed using echocardiography. The rats with CHF and the sham-operated controls (sham group) were treated for 4 weeks with a continuous PVN infusion of AEA, cal-cium-calmodulin-dependent protein kinase Ⅱ (CaMKⅡ) selective inhibitor KN-93, transient receptor potential vanilloid type 1 (TRPV1) channel blocker capsazepine (CPZ), intracellular calcium chelator BAPTA-AM, small-conductance calcium-activated potassium channel (SK channel) blocker apamin and artificial cerebrospinal fluid (vehicle). Sympathetic drive indexes and cardiac function were detected. NG108 cells were incubated with AEA, and then the intracellular cal-cium concentration was measured by fluorometry. The protein expression levels of CaMKⅡ, SK₂ and phosphorylated TRPV1 were determined by Western blot. RESULTS:Compared with sham group, the left ventricular end-diastolic pressure (LVEDP) increased significantly, while peak rate of rise/decline of left ventricular pressure (±dp/dt_max) and ejection fraction (EF) decreased significantly in the CHF group. The concentrations of AEA and intracellular calcium, and the protein levels of CaMKⅡ, SK₂ and phosphorylated TRPV1 in PVN were significantly lower in CHF rats. Compared with the vehicle group, the mortality and sympathetic drive were decreased significantly and cardiac function was improved after treatment with AEA in CHF group. However, PVN perfusion of KN-93, CPZ, BAPTA-AM or apamin contributed to the sympathetic drive and deteriorated the cardiac function. AEA dose-dependently increased intracellular calcium ion concentration, and the protein levels of CaMKⅡ, SK₂ and phosphorylated TRPV1 in NG108 cells. CONCLUSION:AEA in the PVN may be involved in the improvement of cardiac function and sympathetic overdrive via CaMKⅡ/TRPV1/Ca²⁺/SK₂ pathway in rats with CHF.     

Effect of YIGU capsule on IGF-I mRNA and protein expression in rat osteoblasts in vitro

AIM: The effects of YIGU capsule on proliferation and IGF-I mRNA protein expressions in osteoblasts were studied. METHODS: (1) Forty 12-month old Sprague-Dawley female rats were divided randomly into four groups (YIGU capsule high dose group, medium dose group and low dose group; saline group), the drug-containing serum and control serum were prepared. (2) The new-born Sprague-Dawley rat osteoblasts were cultured with different YIGU capsule drug-containing serum at different concentrations and different exposure time. MTT method was used to observe proliferation of osteoblasts. (3) RT-PCR method was used to measure the relative IGF-I mRNA levels and ELISA method was used to measure IGF-I secretion at different exposure time. (4) ELISA method was used to measure IGF-I secretion at different exposure time. RESULTS: (1) Proliferation of osteoblasts was more than the control groups after 48, 72 and 96 h, respectively (P<0.01); (2) The relative IGF-I mRNA levels and IGF-I protein expression were higher than those in control group after 48, 72 and 96 h, respectively (P<0.01 or P<0.05). CONCLUSIONS: It was suggested that YIGU capsule drug-containing serum promoted proliferation, IGF-I mRNA and protein expression. These results may be parts of the mechanisms of YIGU capsule to prevent and treat osteoporosis.     

Protective effect of cardiomyopeptidin on cultured rat neonatal myocardial cells damaged by adriamycin

AIM:To investigate the protective effect of cardiomyopeptidin on cultured myocardial cells damaged by adriamycin in neonatal rats.METHODS:The activities of CPK, LDH and the dehydrogenase of mitochondria in the cells damaged by adriamycin were observed in the presence or absence of cardiomyopeptidin, _i was measured with fluorescent dye Fura-2-AM.RESULTS:Cardiomyopeptidin reduced the activities of CPK and LDH and increased the activities of dehydrogenase of mitochondria in a dose-dependent manner; CMP also dose-dependently decreased _i.CONCLUSION:Cardiomyopeptidin has a protective effect on cultured rat neonatal myocardial cells damaged by adriamycin.     

Effect of Fas ligand gene on reendothelialization in rat carotid artery with balloon withdrawal injury

AIM: To investigate the effect of Fas ligand on reendothelialization in the rat carotid artery with balloon withdrawl injury. METHODS: Balloon withdrawal injury was used to establish the denuded carotid artery rat model in twelve SD rats and then six SD rats were treated with β-gal virus supernatant (β-gal group), and the others were treated with FasL virus supernatant (FasL group). After fourteen days, Evans blue dying was conducted via injection through rat tail vein at 30 min before the animals were killed, then fixation perfusion in situ was performed with 10% formalin and specimens were obtained. Histologic observation and morphometric analysis were made. RESULTS: The reenothelialization area (RA) of arterial balloon injury and the ratio of the reenothelialization area to the total area (RA/TA) significantly increased in FasL group compared with those in β-gal group (P<0.05, respectively). CONCLUSION: FasL gene has an effect of accelerating reendothelialization on the injured vessels.