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1.
AIM: To observe the therapeutic effect of stachydrine hydrochloride on experimental acute cerebral infarction in rats and to explore the underlying mechanisms. METHODS: SD rats (n=75) were randomly divided into 5 groups: sham group, cerebral infarction model group, and stachydrine hydrochloride (10 mg/kg, 20 mg/kg and 40 mg/kg) treatment groups. After the establishment of cerebral infarction model, the rats were given stachydrine hydrochloride at dose of 10 mg/kg, 20 mg/kg or 40 mg/kg by gavage daily for 14 d. The impairment of neurological function in each group was scored. The cerebral infarction volume and brain water content were measured. Moreover, the protein levels of β-catenin, cyclin D1, glycogen synthase kinase 3β (GSK-3β) and p-GSK-3β in the brain tissues were detected by Western blot. RESULTS: Compared with cerebral infarction group, the score of neurological function impairment, cerebral infarction volume and brain water content were significantly decreased in stachydrine hydrochloride treatment groups. In addition, the protein levels of β-catenin, cyclin D1 and p-GSK-3β were markedly increased after stachydrine hydrochloride treatment. CONCLUSION: Stachydrine hydrochloride protects against experimental acute cerebral infarction through activation of Wnt/β-catenin signaling pathway.  相似文献   

2.
AIM:To study the relationship between ApoE polymorphism and lipid metabolism of patients with cerebral infarction. METHODS:ApoE phenotype was determined in 110 patients with cerebral infarction and 60 normal controls by isoelectric focusing and immunoblotting. The TC, TG and HDL-C levels in serum of these subjects were measured with enzymes methods, ApoA I and ApoB levels with rocket immunoelectrophoresis methods, ApoE and Lp(a) levels with ELISA methods. RESULTS:The differences of the ApoE polymorphism distribution and ApoE allele frequencies (P＜0.05) occurred between two groups. The frequence of ApoE ε4 allele in patients with cerebral infarction was significantly higher than those in the normal controls (P＜0.05). However, ApoE 3/3 phenotypes was significantly lower (P＜0.05). Comparison of values of serum lipid with various ApoE phenotyoe among patients with cerebral infarction revealed that there was correlation between ApoE polymorphism and TC(P＜0.05), TG(P＜0.05), HDL-C(P＜0.05), LDL-C(P＜0.05), ApoA I(P＜0.05), ApoB(P＜0.05), ApoE(P＜0.05)and Lp(a)(P＜0.05). Patients carrying ε4 were associated with increased TC, LDL-C, ApoB and Lp(a), while those with ε2 were assiociated with decreased TC, LDL-C, and ApoB. Patients carrying ε2 were associated with increased TG, HDL-C, ApoAⅠ, and ApoE.CONCLUSIONS:ApoEε4 allele was associated with the development of cerebral infarction. ApoE polyphorphism affects lipid metabolism of cerebral infarction patients.  相似文献   

3.
AIM: To explore the changes in serum TGF β1 in type 2 diabetes mellitus. METHODS: Forty-five cases type 2 diabetes mellitus patients were divided into three groups according to urine albumim excretion rate(UAER): normoalbuminuria(NA)group and microalbuminuria(MA) group and macroalbuminuria group (Overt DN). Serum TGF β1, fasting blood glucose(FBG), HbA1c,BUN,Cr,Ccr,lipidemia were detected in all cases. RESULTS: Serum TGF β1 in NA, MA and ODN groups was higher than that in control. Serum TGF β1 was positive correlation with Cr(r=0.390,P＜0.05), LDL(r=0.503,P＜0.01), HbA1c (r=0.676,P＜0.01), and UARE(r=0.777,P＜0.01). CONCLUSION: Type 2 diabetes mellitus have a higher serum TGF β1 than controls, serum TGF β1 was positive correlation with HbA1c and injury of renal function.  相似文献   

4.
AIM and METHODS:To detect the changes of amyloid protein (β-AP) and polypeptide growth factor levels and study their role in the possible pathogenesis of Alzheimers disease (AD) and vascular dementia (VD). We detected serum β-AP, transforming growth factor- α(TGF-α) and insulin-like growth factor (IGF-Ⅱ) levels by radio immunoassay in 8 patients with AD,15 patients with VD and 63 patients with ischemic cerebrovascular disease(ICVD) and 38 cases healthy volunteers. RESULTS:In AD and VD groups, serum β-AP, TGF-α and IGF-Ⅱ were significantly higher than that in ICVD and control group; Serum β- AP,TGF-α and IGF-Ⅱ contents in ICVD group were obviously higher than that in normal control, the highest increase occurred in sequel of cerebral infarction(SCI) and vertebrobasislar ischemia(VBI) groups. There are positive correlation among β- AP, TGF-α and IGF-Ⅱ in AD and VD groups.CONCLUSION:①β- AP is a risk factor in the pathogenesis of AD and VD. ② TGF- α and IGF-Ⅱ play roles in the neurotoxin effect that lead to dementia. ③ β-AP plays a important role in formation of senile plaque.  相似文献   

5.
AIM:To investigate the effects of IL-13 on expression of IL-1β in acute renal ischemia/reperfusion injury.METHODS:Fifty-seven male Wistar rats were randomly divided into 8 group: normal group, sham operation group, ischemia group, ischemia/reperfusion injury group(I/R), normal saline(NS)-treated group 1(C-1), NS-treated group 2(C-2), IL-13-treated group1(T-1)and IL-13-treated group 2(T-2).Rats were subjected to 45 min bilateral renal ischemia followed by reperfusion. rmIL-13 (1.5 μg/50 g body weight )was injected into the renal arteries through the abdominal aorta before ischemia(T-1) or immediately afterischemia(T-2).The serum level of IL-1β and the renal expression of IL-1β were determined in each group at 24 h post-ischemia. In addition, BUN, Cr and renal histology were also measured.RESULTS:(1)The serum level of IL-1β, gene expression and protein production of IL-1β in kidney decreased markedly in IL-13-treated groups.(2)Renal function and histology were significantly improved in IL-13-treated groups, renal injury scores decreased significantly.(3)A positive correlation were found between the serum level of IL-1β and BUN, SCr(r=0.708, P＜0.01;r=0.770, P＜0.01).CONCLUSION:These data suggest that IL-13 inhibit the expression of IL-1βand improve func-tion and histology of kidney in acute renal ischemia/reperfusion injury.  相似文献   

6.
AIM:To study the effect of intestinal endotoxemia(IETM) on hepatic energy metabolism in acute liver failure. METHODS:Intoxication by thioacetamide (TAA) was used to establish rat model of acute liver injury.Ketone body(acetoacetate and β-hydroxybutyrate) in arterial blood and ATP content of hepatocellular mitochondria were determined by using enzymatic fluorimetric micromethod.Colectomy was adopted in observing the changes in plasma endotoxin content and serum alanine aminotransferase (ALT) activity. RESULTS:In the TAA group,plasma endotoxin content and serum ALT activity were all significantly higher than those in the control group(P＜0.01),arterial ketone body ratio of acetoacetate to β-hydroxybutyrate (AKBR) decreased below 0.4,total ketone body in arterial blood was significantly lower than that in the control group(P＜0.01).In the TAA+colectomy group,there was no endotoxemia to be found,ATP content of hepatocellular mitochondria was significantly higher than that in the TAA group(P＜0.01), though serum ALT activity was higher than that in the control group(P＜0.05),but significantly lower than that in the TAA group(P＜0.01). CONCLUSION:IETM played a key role in the occurrence of acute liver failure,hepatic dysfunction might be caused by IETM through damaging hepatic energy metabolism.  相似文献   

7.
AIM:To study the roles of isotropic diffusion weighted imaging(DWI)and apparent diffusion coeficient(ADC)mapping in diagnosing early cerebral infarction.METHODS:21 patients with cerebral in farction (8hyperacute,13 acute)were imaged with both convent ional MRI and single-shot echo-planar isotropic diffusion weighted imaging.Among them 12 pat ients had CT scanning simultaneously within 24 hours after onset.The positive rate of early in farction was comparted on CT,T2WI and DEI.The change of the infarct lesion in DWI and T2WI was also analysed.The av erage ADC,relat ive ADC(rADC)and the ADC from center to periphery of the lesion were calculated.RESULTS:8 hypera cute cerebral ischemic regions were revealed at DWI and ADC mapping,but CT and conventional MR were not.Hyperacute and acute infarcts appeared as areas of hyperintensity on DWI,and their average ADC was significantly depressed comparted with homologous contralateral tissue(0.698±0.104)×10-3mm2/s vs(0.990±0.161)×10-3mm2/s(P<0.01).ADC value in 21 hypera cute had gradient sign.CONCLUSION:Isotropic diffusion weighted imaging and ADC mapping have greater senstitivity for acute and hyperacute cerebral infarction than conventional MRI and CT,and may be used to defined the core and penumbra of ischemic lesion.  相似文献   

8.
AIM: To investigate the plasma neurotensin(NT) concentration in patients with coronary heart disease: acute myocardial infarction(AMI),unstable angina(UA),stable angina pectoris(SAP), old myocardial infarction (OMI), and to study the relationship between the plasma NT level and the myocardial ischemia . METHODS:The plasma NT concentration of 30 patients with AMI,32 pat ients with UA,35 patients with SAP,31 pat ients with OMI and 32 normal controls were determined by radioimmunoassay(RIA). RESULTS: The plasma NT level in patients with AMI(24 h),in patients with UA when angina attacked is significantly higher than that of healthy controls. The plasma NT level in patients with SAP, in patients with OMI is not significantly different from that of healthy controls. The NT level of patients with UA when angina attacked is significantly higher than that after 2 weeks treatment (P＜0.01). The NT level of AMI patients rose from early period and reached peak value at 24 h .It began to decline at 48h,and restored to normal level at 72h. CONCLUSION: When acute myocardial ischemia occured in patients with coronary heart disease, the plasma NT level was elevated. This suggests NT may have participated in the pathophysiological course of myocardial ischemia.  相似文献   

9.
XIE Jing  GAO Hui-chun  ZHENG Xi 《园艺学报》2016,32(10):1905-1908
AIM: To investigate the effect of astragaloside IV on neurological function and the protein expression of neuron-specific enolase (NSE), Notch1 and NF-κB in acute cerebral hemorrhage (ACH) rats.METHODS: ACH model in rats was established via injection of autologous blood, and the rats were divided into 4 groups:sham, ACH, ACH+astragaloside IV (100 mg/kg) and ACH+astragaloside IV (200 mg/kg) groups. The impairment of neurological function in each group was graded, and the brain coefficient and water content were calculated. The serum level of NSE was measured by ELISA. Additionally, the expression of Notch1 and NF-κB was determined by Western blot.RESULTS: Astragaloside IV improved the neurological function and decreased the brain coefficient and water content in ACH rats. Moreover, the ACH-induced increase in NSE was inhibited after astragaloside IV treatment. Similarly, astragaloside IV also significantly attenuated the expression of Notch1 and NF-κB in ACH rats.CONCLUSION: Astragaloside IV attenuates the impairment of neurological function in ACH rats, which may be through decreasing the NSE level and down-regulating the expression of Notch1 and NF-κB.  相似文献   

10.
AIM: To study the changes of serum autoantibodies against β1-adrenergic and M2-muscarinic receptors in obstructive sleep apnea syndrome (OSAS) patients with chronic obstructive pulmonary disease (COPD), that is, overlap syndrome (OS). METHOD: Serum autoantibodies against β1 and M2 receptors in 26 cases with OS, 32 with OSAS, 30 with COPD and 28 normal subjects were determined by using enzyme-linked immunosorbent assay(ELISA). RESULTS: The positive rates and titer of β1 and M2 receptor autoantibodies are significantly increased in OS group (92.2％,57.7% and 1:98, 1:67), compared to OSAS (71.9%, 40.6% and 1:83, 1:30) or COPD group (70.0%, 36.7% and 1:79, 1:28) (P＜0.05), and they are higher in these groups than in the control (25.0%, 14.3% and 1:20, 1:20) (P＜0.01). CONCLUSION: Serum β1-and M2 receptor autoantibodies are significantly increased in the patients with COPD, OSAS or OS, compared to the control, and the highest is in OS.  相似文献   

11.
AIM and METHODS: To study the changes of serum vascular endothelial growth factor (VEGF) levels in a rat model of acute myocardial infarction (MI) and its significance. Eighty-eight male Sprague-Dawley rats were used in this study. MI was produced by left coronary arterial ligation in 80 animals, and eight rats undergoing thoracotomy but not coronary ligation served as controls (sham).Blood samples were drawn from the right atrium before (sham animals) and 1, 3, 6, 12, 24 hours and 2, 3, 5, 7, 14 days after MI(n=8, respectively). Serum VEGF concentrations were measured by a sensitive enzyme-linked immunosorbent assay with a rabbit polyclonal antibody specific for VEGF. RESULTS: In 8 sham animals, the concentration of serum VEGF was (66.99±17.83) pg/mL. Six hours after MI, the level of serum VEGF significantly increased to (125.68±28.07)pg/mL (P＜0.01 vs sham control), and reached a peak (240.61±70.63 pg/mL, P＜0.01 vs sham control) at 24 hours after ligation and then decreased gradually over the remaining 2 weeks. But the level remained significantly elevated for 14 days (107.64±30.31 pg/mL, P＜0.01 vs sham control).CONCLUSION: Serum VEGF levels markedly and permanently increase in the rat model of acute MI may play an important role in the angiogenesis associated with MI  相似文献   

12.
AIM: To investigate the effects of aliskiren on the injury of SH-SY5Y cells induced by oxygen-glucose deprivation (OGD) and its possible mechanisms. METHODS: The SH-SY5Y cells were randomly divided into control group, OGD group and aliskiren (5.0, 10.0 and 20.0 μmol/L) groups. The cell viability was measured by CCK-8 assay. The levels of excitatory amino acid transporter 2 (EAAT2/GLT-1), EAAT3/EAAC1, EAAT4, endothelin-1 (ET-1) and S100 calcium-binding protein β subunit (S-100β) in the SH-SY5Y cells were detected by ELISA. The morphological changes of the cells were observed by Hoechst 33258 staining. Meanwhile, the content of lactic acid (LD) and activity of Na+-K+-ATPase were also analyzed. RESULTS: The viability of SH-SY5Y cells was not more than 60% after OGD injury for 4 h, so the appropriate time for OGD injury was 4 h. Compared with control group, the protein levels of GLT-1, EAAC1 and EAAT4 in the SH-SY5Y cells of OGD group were significantly decreased (P<0.05), but the protein levels of ET-1 and S-100β were significantly increased (P<0.05). Compared with OGD group, treatment with aliskiren dose-dependently increased the protein levels of GLT-1, EAAC1 and EAAT4 in the SH-SY5Y cells, but decreases in the levels of ET-1 and S-100β were observed (P<0.05). The results of Hochest 33258 staining showed that aliskiren significantly reduced the apoptosis of SH-SY5Y cells. Compared with control group, a significant increase in the content of LD (P<0.05) and a significant decrease in Na+-K+-ATPase activity (P<0.05) were found in the SH-SY5Y cells of OGD group. Compared with OGD group, aliskiren dose-dependently decreased the content of LD, but increased the Na+-K+-ATPase activity in the SH-SY5Y cells (P<0.05). CONCLUSION: Aliskiren has good neuroprotective effects on SH-SY5Y cells after OGD injury. The underlying mechanisms may be associated with the increases in the protein levels of GLT-1, EAAC1 and EAAT4, the enhancement of Na+-K+-ATPase activity, and the decreases in the levels of ET-1 and S-100β and the content of LD.  相似文献   

13.
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14.
AIM: To investigate whether activation of NLRP3 inflammasome-IL-1β axis is consistent with endothelial-mesenchymal transition (End-MT) during the process of myocardial fibrosis after acute myocardial infarction (AMI). METHODS: Adult male SD rats (n=30) were randomly divided into sham operation group (n=15) and AMI group (n=15). After 28 d, Masson staining was used to detect the level of myocardial fibrosis. The activation of NLRP3 inflammasome including NLRP3, ASC, pro-caspase-1 and caspase-1, the endothelial cell markers CD31 and VE-cadherin, and the mesenchymal cell markers α-SMA and FSP1 were analyzed by Western blot. The expression of IL-1β was measured by ELISA. RESULTS: The levels of myocardial fibrosis and End-MT, the activation of NLRP3 inflammasome, and the expression of caspase-1 and IL-1β were significantly increased in AMI group compared with sham operation group (P<0.05). CONCLUSION: The activation of NLRP3 inflammasome-IL-1β axis is significantly consistent with End-MT process, suggesting that NLRP3 inflammasome-IL-1β, as a potential target for the activation of End-MT, will provide a novel theoretical target for the treatment of myocardial fibrosis and heart failure after AMI.  相似文献   

15.
AIM: To investigate the effect of zinc finger protein 521 (Zfp521) on the differentiation of rat bone marrow mesenchymal stem cells (MSCs) into neurons. METHODS: Rat MSCs were cultured by conventional method in vitro and divided into non-transfection group, transfection group (transfected with Rn-Zfp521-siRNA) and negative control group (transfected with negative control siRNA). MSCs were induced by β-mercaptoethanol (β-ME) to differentiate into neurons. The fluorescence expressed by transfected MSCs was observed under inverted fluorescence microscope. The expression of Zfp521 was detected after transfection by RT-PCR. Immunohistochemistry, RT-PCR and Western blotting were used to detect the expression levels of neuron-specific enolase (NSE),microtubule-associated protein 2(MAP-2) and Zfp521 after induction. RESULTS: The fluorescence of MSCs was mostly displayed 72 h after transfection and the efficiency of transfection was up to 84.1%±2.3%. Meanwhile, the mRNA expression of Zfp521 was decreased (P<0.05). MSCs were induced by β-ME to differentiate into neurons. The differentiation efficiency of MSCs transfected with Rn-Zfp521-siRNA was the highest and the expression of NSE and MAP-2 was significantly increased compared with other groups (P<0.05). Zfp521 was detected in all groups, and the expression level of Zfp521 was significantly decreased after induction (P<0.01). CONCLUSION: Zfp521 may be down-regulated during the differentiation. The inhibition of Zfp521 promotes the neural differentiation of MSCs. Zfp521 may play an important role in regulating MSCs differentiation into neurons.  相似文献   

16.
AIM:To investigate the antipyretic effect of patchouli oil on lipopolysaccharide (LPS)-induced fever in rabbits. METHODS:Male rabbits (n=42) were randomly divided into 7 groups according to their body weight and basal body temperature, including control group, model group, western medical positive group, traditional Chinese medical positive group, and high, middle and low doses (2%, 1% and 0.5%) of patchouli oil groups. Subsequently, except the controls, the rabbits were injected with LPS at a dose of 1 mL/kg (2 mg/L) through marginal ear vein to establish rabbit fever model and the rabbits in control group received the same volume of NS. The rabbits in control group and model group were injected with 0.5% Tween-80 0.5 h late, and the rabbits in the other groups were treated with correspoonding drugs. The effect of patchouli oil on the body temperature was observed, and the levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the serum, and prostaglandin E2 (PGE2) and cyclic adenosine monophosphate (cAMP) in the hypothalamus were measured by radioimmunoassay. RESULTS:The body temperature and the levels of IL-1β, TNF-α, cAMP and PGE2 in model group were significant higher than those in control group. Patchouli oil notably inhibited the body temperature in the febrile rabbits. From 1.5 h to 5.5 h after administration, the body temperatures were increased by (1.06±1.55), (1.62±1.36), (1.38±1.22), (0.98±0.98) and (0.48±0.95) ℃ in high patchouli oil group, respectively. From 3.5 to 5.5 h after administration, the body temperatures were elevated by (1.47±0.73), (1.15±0.68) and (0.63±0.54) ℃ in middle patchouli oil group, respectively. A tendency of downregulation of the elevated body temperatures was observed at every time point after administration in low patchouli oil group. Patchouli oil significantly decreased the levels of TNF-α in the serum and cAMP content in the hypothalamus, and attenuated the elevated tendency of the IL-1β level in the serum and PGE2 level in the hypothalamus.CONCLUSION: Patchouli oil evidently has antipyretic effect on LPS-induced fever in the rabbits. The antipyretic mechanism might be related to the inhibition of TNF-α level in serum and cAMP content in the hypothalamus.  相似文献   

17.
AIM:To observe the expression and tissue localization of matrix metalloproteinase 9 (MMP-9) and transforming growth factor beta 1 (TGF-β1) in the rat acute cerebral ischemia model. METHODS:Male Wistar rats were used to establish acute cerebral ischemia model by a suturing method. The rats were divided into normal control group, sham group and ischemia 6 h, 12 h, 1 d, 2 d, 6 d and 14 d groups. The rat cerebral cortex and hippocampus of the brain were collected at different time points.The mRNA and protein levels of MMP-9 and TGF-β1 in the brain tissues were detected by real-time PCR and in situhistochemistry staining, respectively. The levels of MMP-9 and TGF-β1 in the plasma were also measured by ELISA. RESULTS:The results of real-time PCR showed that the mRNA levels of MMP-9 began to increase 6 h after acute ischemia and reached to a peak 2 d after acute ischemia. Similarly, the mRNA level of TGF-β1began to rise 12 h after acute ischemia and reached to the highest level 6 d after acute ischemia. Compared with the sham rats, the mRNA levels of MMP-9 and TGF-β1 in the rat brains that collected at ischemic time of 12 h, 1 d, 2 d, 6 d and 14 d were significantly increased. Moreover, results of in situhistochemical staining showed that the expression of MMP-9 was detected at cerebral cortex and hippocampus 1 d after acute cerebral ischemia.Further studies showed that MMP-9 dyeing of the rat cerebral cortex was most obvious 2 d after the acute cerebral ischemia. Similarly, the rat cortex and hippocampus began to express TGF-β1 2 d after acute ischemia and TGF-β1 staining at rat cerebral cortex was most obvious 6 d after the acute cerebral ischemia. In addition, ELISA showed that the increase in MMP-9 and TGF-β1 was detected in the plasma 12 h after ischemia. Compared with the sham rats, the level of these 2 factors significantly upregulated since 1 d after ischemia. CONCLUSION: The brain tissue itself contributes to the upregulation of MMP-9 and TGF-β1 post acute cerebral ischemia, which shed light on the related research in the field.  相似文献   

18.
AIM:To explore the significance of platelet activation, fibrinolytic activity and the changes of vasoactive mediators in acute myocardial infarction in rabbits and the intervention of amiodarone and metoprolol.METHODS:Fifty New Zealand white rabbits were randomly assigned to five groups, ten for each. Group Ⅰ: sham group, group Ⅱ: acute myocardial infarction(AMI) group, group Ⅲ: AMI and lidocaine group, group Ⅳ: AMI and amiodarone group, group Ⅴ: AMI and metoprolol group.The middle point of left ventricular coronary artery was ligated (groupⅡ,Ⅲ, Ⅳ and Ⅴ ) or a sham ligation(group Ⅰ). Four hours later, blood was collected for measuring plasma concentration of TXB2, 6-Keto-PGF1α, ET, NO, plasma activity of t-Pa and PAI.After that, the heart was taken out to evaluate the infarction size(IS).RESULTS:Plasma concentration of TXB2, ET, NO and plasma activity of PAI were significantly higher in groupⅡ,Ⅲ, Ⅳ and Ⅴ than those in group Ⅰ(P＜0.01), but the plasma concentration of 6-Keto-PGF1α and plasma activity of t-Pa were remarkably lower in groupⅡ,Ⅲ, Ⅳ and Ⅴ than those in group Ⅰ(P＜0.01). There were no difference in plasma concentration of TXB2, 6-Keto-PGF1α, t-Pa activity and infarction size in group Ⅱ,Ⅲ and Ⅳ(P＞0.05).Compared to group Ⅱ, plasma concentration of ET, NO and PAI activity were significantly decresed (P＜0.01)in group Ⅳ. Plasma concentration of TXB2, ET, NO and plasma activity of PAI were significantly lower in groupⅤ than those in group Ⅱ(P＜0.01). Conversely, plasma concentration of 6-Keto-PGF1 and plasma activity of t-Pa were remarkably higher in group Ⅴ than those in group Ⅱ(P＜0.01). The infarction size was remarkly decrease(P＜0.01)in group Ⅴ.CONCLUSIONS:Amiodarone inhibited PAI avtivity, decreased release of ET and NO in AMI in rabbits. Metoprolol inhibited platelet activation, improved fibrinolytic, decreased release of ET and NO, and reduced myocardial infarction size in AMI in rabbits; Lidocaine had no effect above.  相似文献   

19.
AIM: To study the influence of lithium chloride (LiCl) on the neuronal differentiation of rat bone marrow mesenchymal stem cells (MSCs), and to explore whether autophagy was involved in this process. METHODS: MSCs were isolated and cultured in vitro. The cells were divided into LiCl group and control group. MSCs were treated with β-mercaptoethanol as an inducer for triggering the cells to differentiate into neurons. The expression of neuronal markers-neuron specific enolase (NSE) and microtubule-associated protein-2 (MAP-2), and autophagic marker-microtubule-associated protein 1 light chain 3 (LC3) were measured by immunofluorescence method and Western blot. An autophagy activator rapamycin and autophagy inhibitor 3-methyladenine (3-MA) were applied to modulate the autophagy in the LiCl treated-cells. The protein expression of NSE and MAP-2 were determined by Western blot. RESULTS: After induction, the expression of NSE and MAP-2 were increased. The percentage of NSE-and MAP-2-positive cells and the expression of NSE and MAP-2 in the LiCl group were greater than those in control group (P<0.05). After induction, the number of LC3-positive dots and the expression of LC3-Ⅱ in LiCl group were greater than those in control group (P<0.05). The expression of NSE and MAP-2 increased when the autophagy was modulated by rapamycin in LiCl treated-cells, and on the contrary, the expression of NSE and MAP-2 were inhibited as autophagy was modulated by 3-MA. CONCLUSION: Lithium chloride may promote the neuronal differentiation of rat bone marrow mesenchymal stem cells by modulating autophagy.  相似文献   

20.
AIM：To investigate whether early endothelial progenitor cells (early-EPCs) express β2-adrenergic receptor (β2AR) in the chronic obstructive pulmonary disease (COPD) patients and the effect of β2AR expression on the migration of early-EPCs. METHODS：Venous blood samples (20 mL) were obtained from antecubital vein of COPD patients or healthy controls. Peripheral blood mononuclear cells were isolated by standard Ficoll gradient centrifugation, and purified by CD34 positive selection cocktail. The mRNA expression of β2AR in the early-EPCs was detected by RT-PCR. The protein levels of β2AR were assessed by Western blotting and flow cytometry. Chemotaxis was studied by Transwell assay. Cultured early-EPCs were treated with ICI118551, norpinephrine (NE) or monoclonal antibody of β2AR (mAb-β2AR) for 24 h. The number of migratory cells was counted under a light microscope. RESULTS：The level of β2AR expression in the COPD patients was higher than that in the controls. The number of migratory early-EPCs to stromal cell-derived factor 1α was significantly improved by ICI118551 compared with other COPD groups. When early-EPCs from the COPD patients or the controls were treated with different concentrations of mAb-β2AR for 24 h, the number of migratory early-EPCs from the COPD patients and the controls treated with NE at concentration of 100 nmol/L was significantly reduced. However, a marked decrease in the number of migratory early-EPCs from the COPD patients treated with NE was observed compared with control group. Before treated with ICI118551 or NE for 24 h, the early-EPCs were co-incubated with mAb-β2AR for 40 min, and the number of migratory early-EPCs was not significantly different between COPD group and control group. Genetic down-regulation of β2AR promoted the migration of early-EPCs in COPD group. CONCLUSION：The level of β2AR expression in the COPD patients is increased compared with the controls. The down-regulation of β2AR improves the migration of early-EPCs.  相似文献   

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