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1.
欧阳波 《园艺学报》2006,33(2):322-325
由中国园艺学会主办，湖北省园艺学会、国家蔬菜改良中心华中分中心、华中农业大学园艺林学学院共同承办的“2006中国蔬菜产业可持续发展研讨会”于2006年4月13-15日在湖北武汉华中农业大学举行，来自全国17个省（市）和自治区47个单位的近120名代表出席这次全国性会议。会议开幕式由中国园艺学会蔬菜专业委员会主任、中国农业科学院蔬菜花卉研究所副所长孙日飞研究员主持。华中农业大学副校长李名家教授、武汉市张学忙副市长、科技部农村司魏勤芳处长、农业部科技司刘艳处长、武汉市科协黄和平主席和中国园艺学会理事长方智远院士先后致辞。  相似文献   

2.
AIM: To investigate the effects of internal change of serum insulin and plasma glucose levels on serum free fatty acid (FFA) concentrations after glucose loading. METHODS: Serum insulin, plasma glucose and FFA concentrations were measured simultaneously in 234 essential hypertension patients who were undergoing oral glucose tolerance test (OGTT)[including 20 cases with 2 type diabetes mellitus(DM),74 impaired glucose tolerance(IGT),140normal glucose tolerance(NGT);98 males,136 females]. RESULTS: Fasting serum FFA concentration (μmol/L) in DM (1 048.47±481.6) was higher than that in IGT (760.1±332.1) (P＜0.05) and in NGT (725.8±353.9) (P＜0.05). Compared with the NGT group, the glucose curve was elevated and the insulin releasing curve was characterized by a low response and a delayed peak in DM group. As for the FFA releasing curve, three groups showed a significantly decreasing trend, which was more evident in DM group. Serum FFA levels at 30 min, 60 min and 120 min after glucose ingestion were not significantly different between the three groups. CONCLUSIONS: Easting serum FFA levels were elevated in DM group. The absolute deficiency of insulin secretion decreased rather increased the difference of FFA level difference between DM group and IGT group, NGT group during OGTT. These results suggest the level of glucose utilization may have an important effect on serum FFA concentration.  相似文献   

3.
AIM: To investigate the effect of pioglitazone (Pio) on glucose metabolism and peroxisome proliferators-activated receptor (PPAR)-γ expression in free fatty acid (FFA) -induced insulin resistance in rats. METHODS: A hyperinsulinaemic-euglycaemic clamp and ［3-3H］-glucose tracing technique were used in awake rats. Glucose metabolism in vivo and PPAR-γ in adipose tissue expression were assessed with elevation FFA by lipid infusion over 4 h in rats pretreated with or without Pio.RESULTS: During steady-state of clamp, there was a significant increase in plasma FFA in two lipid-infused groups, compared to control rats (P<0.01). The glucose infusion rates (GIR) in Pio-treated rats (P/L group), compared with controls, were significantly reduced ［(20.6±0.4) mg·kg-1·min-1 vs (33.6±0.6)mg·kg-1· min-1, P<0.01］, whereas the GIR was lower in the lipid group (L group) than that in the P/L group［(12.6±0.8) mg·kg-1·min-1 vs (20.6±0.4) mg·kg-1·min-1, P<0.01］. The hepatic glucose production (HGP) was significantly suppressed (85%) ［(18.3±2.1)mg· kg-1·min-1 (basal) vs (2.7±2.4)mg· kg-1·min-1, and (17.5±2.6) mg· kg-1·min-1 vs (2.6±1.0)mg· kg-1·min-1］, all P<0.01 during clamp in control and P/L groups. The suppressive effect of insulin on HGP was significantly blunted in L group［(17.3±2.1)mg· kg-1·min-1 vs (15.8±1.5)mg· kg-1·min-1］. The rate of glucose disappearance (GRd) was significantly reduced in two lipid-infused rats compared with controls［(26.6±1.6)mg· kg-1·min-1 and (23.2±0.9)mg· kg-1·min-1 vs (37.7±2.6)mg·kg-1·min-1,P<0.01］. The PPAR-γ expression of adipose tissue in P/L group was significantly upregulated. CONCLUSION: Lipid-infusion induces an acute insulin-resistance in vivo. Pio treatment upregulates the PPAR-γ of adipose tissue and suppresses HGP. Pio can protect partly against lipid-induced insulin resistance.  相似文献   

4.
SONG Chun-yu  BI Hui-min 《园艺学报》2004,20(10):1866-1870
AIM: To explore the change of the amount of GLUT4 protein at the plasma membrane of the rat skeletal muscle after high-fat feeding. METHODS: The animals were divided into three groups (ten for each): group I: control; group II: high-fat feeding; group III: high-fat feeding + dietary treatment. The rat model of insulin resistance (IR) was made by feeding high-fat diet for eight weeks. And then insulin-resistant rats were fed with chow diet for 4 weeks. Fasting plasma glucose and fasting serum insulin levels were measured before and after dietary treatment, respectively. Insulin treatment was achieved by intraperitoneal injection of insulin (10 unit insulin per kg body weight) 15 minutes before killing the animals. The right hindlimb skeletal muscle was rapidly dissected. Then the expression of GLUT4 protein at the plasma membrane in all the animals was assessed with Western bloting. RESULTS: The GLUT4 content at the plasma membrane in high-fat-fed rat skeletal muscle was significantly lower (about 31%) than that in controls (P<0.01). Dietary treatment partly corrected fasting blood glucose [from(6.20±0.39)mmol/L to(5.78±0.74)mmol/L]and fasting serum insulin levels [from(17.19±1.93)mU/L to(11.68±1.28)mU/L] and increased the GLUT4 content at the plasma membrane by 1.14-fold in insulin-resistant rat skeletal muscle. CONCLUSION: High-fat feeding induces IR in Sprague-Dawley rats. The mechanism may be involved in decreased cell-surface level of GLUT4 through affecting intracellular insulin signaling and then decreasing GLUT4 trafficking.  相似文献   

5.
《园艺学报》2013,29(7):1313-1317
AIM：To investigate the effects of asiatic acid, one of triterpenoids from Psidium guajava leaves, on the proliferation and differentiation of 3T3-L1 preadipocytes, and glucose and lipid metabolism of insulin-resistant adipocytes. METHODS：The proliferation of 3T3-L1 preadipocytes was tested by MTT assay, and the accumulation of lipid droplets in differentiated preadipocytes was measured by oil red O staining. The insulin-resistant cell model was established by exposure of the cells to dexamethasone. The cellular glucose uptake was determined by glucose oxidase-peroxidase assay. The free fat acid (FFA) concentration was detected by colorimetric method. Secreted adiponectin were measured by ELISA. The protein levels of peroxisome proliferator-activated receptor γ (PPARγ) and protein tyrosine phosphatase 1B (PTP1B) in insulin-resistant adipocytes were analyzed by Western blotting. RESULTS：Compared with medium group, asiatic acid increased the proliferation of 3T3-L1 preadipocytes and inhibited their differentiation at a concentration range of 10~100 μmol/L (P<0.05 or P<0.01). At concentrations of 30 μmol/L and 100 μmol/L, asiatic acid enhanced cellular glucose uptake in the insulin-resistant adipocytes both in basic and insulin-stimulation states. Asiatic acid decreased FFA production (P<0.05), and down-regulated the protein expression of PTP1B (P<0.05, or P<0.01). However, no effect on the secretion of adiponectin and the protein expression of PPARγ was observed (P>0.05). CONCLUSION：Asiatic acid enhances glucose uptake and inhibits FFA production in insulin-resistant adipocytes via down-regulating the protein expression of PTP1B, all of which play the roles of increasing insulin signaling sensitivity to improve insulin resistance.  相似文献   

6.
AIM: To observe the potential effects of icariin on high glucose-induced insulin resistance in C2C12 myotubes and to investigate its underlying mechanisms. METHODS: The insulin resistance model was induced by high glucose (25 mmol/L) in the C2C12 myotubes. The effects of icariin on Akt phosphorylation at T308, glucose transporter 4 (GLUT4) membrane translocation, and glucose uptake were investigated in high glucose-treated C2C12 myotubes. The protein levels of phosphorylated proteins were determined by Western blot. The glucose uptake was measured by colorimetric method. The small interfering RNA (siRNA) was used to knockdown the expression of p38 MAPK. RESULTS: Icariin significantly increased insulin-stimulated Akt T308 phosphorylation in C2C12 myotubes treated with high glucose. Treatment with icariin at 25, 50 and 75 μmol/L for 24 h increased Akt T308 phosphorylation in a dose-dependent manner (P<0.05 or P<0.01). Treatment with icariin at 50 μmol/L for 12, 24 and 36 h increased Akt T308 phosphorylation in a time-dependent manner (P<0.05 or P<0.01). In addition, treatment with icariin at 50 μmol/L for 24 h significantly enhanced the expression of GLUT4 on plasma membrane (P<0.01) and 2-deoxyglucose (2-DG) uptake (P<0.01). Treatment with icariin recovered high glucose-reduced p38 MAPK phosphorylation (P<0.01). Pharmacological or genetic inhibition of p38 MAPK abolished the protective impacts of icariin on insulin-stimulated Akt T308 phosphorylation (P<0.01), GLUT4 plasma membrane translocation (P<0.01), and 2-DG uptake under high glucose condition (P<0.05). CONCLUSION: Icariin attenuates high glucose-induced insulin resistance in C2C12 myotubes by activating p38 MAPK.  相似文献   

7.
AIM: The study was undertaken to explore the dynamic changes of the concentration of nitric oxide(NO) in ischemic myocardium and its mechanism.METHODS: In vivo myocardial ischemia of mice and in vitro perfused isolated heart of rat were used in the experiment. The effects of severity and time of ischemia on NO production, NOS activity and mRNA were examined, respectively. RESULTS: There was a considerable difference (P<0.01) in the concentration of NO between ischemia group [(9.12±1.40) μmol/L] and control group [(20.16±1.67) μmol/L] after Pit(30 U/kg) administration, and the concentration of NO of ischemic group significantly decreased [(9.17±1.33) μmol/L] compared with control group [(19.90±1.95) μmol/L] after 30 minutes of ischemia. Also, the concentration of NO after Pit(20 U/L) administration in K-H and 15 min of ischemia was (15.41±2.00) μmol/L and (15.09±2.00) μmol/L respectively in vitro, significantly lower than control group [(23.83±2.33) μmol/L and (23.63±2.52) μmol/L]. In addition, compared with control group, the number of NOS positive cells, NOS activity as well as mRNA expression in atrial muscle and ventricular muscle of ischemic group were markedly reduced, respectively. CONCLUSION: Myocardial ischemia could reduced the NO level in myocardium, down-regulation of NOS mRNA could be the possible mechanism.  相似文献   

8.
AIM:To investigate the role of expression of peroxisome proliferator-activated receptor α(PPAR α) in pathogenesis of rat fatty liver.METHODS:The rats were treated with a low dose of carbon terachloride (CCl4) and fed a high fat diet to produce fatty liver. We determined the concentrations of triglyceride (TG), total cholesterol (TC), free fatty acid (FFA) in liver and the alanine aminotransferase (ALT) activity, tumor necrosis factor-α (TNF-α), FFA in serum and the degree of hepatocytic steatosis. Total RNA of liver was extracted, and the expression of PPAR α were analyzed by semi-quantitative RT-PCR method.RESULTS:In model group, the hepatocytic PPAR α mRNA expression decreased to 0.41±0.28, compared to 1.41±0.29 in the control group (P＜0.01). The contents of TG, TC, FFA in model rat liver were (1.88±0.20) mmol·L-1, (11.03±1.12) mmol·L-1 and (1 260.38±151.27) μmol·L-1, respectively, compared to (0.53±0.10) mmol·L-1, (1.25±0.25) mmol·L-1 and (334.30±27.09) μmol·L-1 in the control group (P＜0.01). The activity of ALT, concentrations of TNF-α and FFA in serum were also increased remarkably in model group.CONCLUSION:Oxidation of fatty acid and utilization of lipids in liver are affected by reducing the expression of PPAR α, which result lipid accumulation in liver.  相似文献   

9.
AIM: To reverse multidrug resistance (MDR) of A549/DDP cells with short hairpin RNA (shRNA) expression vectors. METHODS: Two multidrug resistance-associated protein 1( MRP1 ) gene-specific shRNA expression plasmids pSilencer 2.1-U6 neo-MRP1 were constructed and introduced into A549/DDP cells. MRP1 mRNA was assayed by real-time fluorescent quantitative PCR. The MRP1 function was determined by rhodamine 123(Rho123) retention and the protein expression of MRP1 was detected by immunofluorescent staining. The viability of A549/DDP cells was evaluated by MTT method. RESULTS: MRP1 shRNA expression plasmids were successfully constructed. The expression of MRP1 at mRNA and protein levels was significantly decreased after sh-MRP1-2.1-1 and sh-MRP1-2.1-2 were transfected into A549/DDP cells. The intracellular accumulation of Rho123 significantly increased from(16.93±0.58)% to (89.02±0.59)% and (82.56±1.37)%. IC50 of cisplatin were decreased from (101.45±0.64) μmol/L to (38.06±0.05) μmol/L and (53.72±0.36) μmol/L. IC50 of 5-fluorouracil were decreased from (263.20±2.00) μmol/L to (98.82±1.16) μmol/L and (141.81±0.49) μmol/L. CONCLUSION: The shRNA expression plasmid pSilencer 2.1-U6 neo-MRP1 can stably and permanently inhibit MRP1 gene. The sensitivity of A549/DDP cells to drug is reversed.  相似文献   

10.
AIM:To investigate the effects of magnolol (MAG) on blood pressure and aortic vasodilatation to insulin in juvenile spontaneous hypertensive rats (SHR). METHODS:Four-week-old male SHR and age-matched normotensive Wistar-Kyoto (WKY) control rats were used. SHR and WKY rats were randomized into 2 groups and treated daily by gavage with vehicle (distilled water) or MAG (100 mg·kg-1·d-1). After 3 weeks of treatment, blood pressure, aortic vasorelaxation, fasting glucose and plasma insulin levels, the expressions of PPARγ and TRB3, and insulin-stimulated Akt/endothelial nitric oxide synthase (eNOS) activation were measured. In vitro, human umbilical vein endothelial cells (HUVECs) were cultured in the medium containing glucose (25 mmol/L) and palmitate (500 μmol/L). RESULTS:Treatment of young SHR with MAG for 3 weeks decreased blood pressure, improved insulin-induced aortic vasodilation, and Akt and eNOS activation , increased PPARγ expression and decreased TRB3 expression. In cultured HUVECs, MAG incubation increased PPARγ exprssion, decreased TRB3 expression, and elevated insulin-induced phosphorylated Akt and eNOS levels and NO production, which were reversed by PPARγ antagonist. CONCLUSION: Treatment of young SHR with MAG at the prehypertensive stage decreases blood pressure via improving vascular insulin resistance that is at least partly attributable to up-regulation of PPARγ, down-regulation of TRB3 and consequently activation of Akt and eNOS in blood vessel .  相似文献   

11.
AIM: To investigate the effects of selenium (Se) compounds on the generation of nitric oxide (NO) and reactive oxygen species (ROS), and the activity of nitric oxide synthase (NOS) in umbilical cord mesenchymal stem cells (MSCs). METHODS: MSCs were cultured in the medium of DMEM/F12 containing 10% FBS and exposed to the compounds of selenium , selenocysteine (Se-Cys) or nano-selenium (Nano-Se) at concentrations of 0.1 μmol/L to 0.5 μmol/L. The concentration of NO and the activity of NOS in treated MSCs were detected by the method of nitrate reductase assay. The fluorescent intensity of ROS was determined by DCFH-DA probe. RESULTS: The production of NO was (18.13±6.80) μmol/L in the control MSCs,(20.93±5.68) μmol/L in the MSCs treated with Se(Ⅳ) at concentration of 0.1 μmol/L and (16.73±5.03) μmol/L in the MSCs treated with Se(Ⅳ) at concentration of 0.5 μmol/L for 24 h. The production of NO was (17.20±9.11) μmol/L (P<0.05) in the MSCs treated with Se(IV) at concentration of 0.1 μmol/L and (9.98±4.35) μmol/L (P<0.01) in the MSCs treated with Se(IV) at concentration of 0.5 μmol/L for 48 h, which was significantly lower than that in the control MSCs . No inhibitory effect of Nano-Se and Se-Cys on the production of NO in MSCs was observed. Compared with the control MSCs, Se(Ⅳ) at concentrations of 0.1 μmol/L and 0.5 μmol/L significantly inhibited the generation of ROS and the activity of NOS in MSCs at 24 h and 48 h. CONCLUSION: Se(Ⅳ) inhibits NO/ROS production and NOS activity in a dose-dependent manner in MSCs.  相似文献   

12.
AIM: To investigate the effect of zacopride, an inward rectifier potassium channel agonist, on ouabain-induced arrhythmias in adult rats, and to explore the underlying electrophysiological mechanism.METHODS: Using ouabain to establish in vitro and in vivo arrhythmic rat models, the effects of zacopride on ouabain-induced arrhythmias were observed. The technique of whole-cell patch clamp was used to observe the effects of zacopride on inward rectifier potassium current (IK1), resting membrane potential (RMP) and delayed afterdepolarizations (DADs) in single rat ventricular myocyte. RESULTS: Zacopride at 1 μmol/L significantly reduced total number of premature ventricular beats, and the duration and incidence of ventricular tachycardia and ventricular fibrillation induced by ouabain in rat hearts in vitro (P<0.05). In anesthetized rats, zacopride at 15 μg/kg significantly reduced total number of premature ventricular beats, and the duration and incidence of ventricular tachycardia and ventricular fibrillation induced by ouabain (P<0.05). IK1 was significantly inhibited by ouabain (P<0.05), which was partially and even completely reversed by zacopride at 0.1~10 μmol/L. RMP value was significantly reduced by ouabain (P<0.05), and then increased to different levels after treatment with zacopride (0.1~10 μmol/L). Zacopride at 1 μmol/L showed its maximal effect and RMP was restored to normal level. Moreover, zacopride at 1 μmol/L markedly suppressed ouabain-induced DADs in single rat ventricular myocyte. The incidence of DADs decreased from 91.67% to 12.50% after zacopride was applied (P<0.05), and this effect was abolished by 1 μmol/L BaCl2. CONCLUSION: Inward rectifier potassium channel agonist zacopride significantly inhibits ouabain-induced ventricular arrhythmias in adult rats. The mechanism is related to increased RMP level and inhibition of DADs by activation of IK1 channel.  相似文献   

13.
AIM: To investigate the effects of total triterpenoids from Psidium guajava leaves (TTPGL) on blood glucose and lipids in type 2 diabetic rats. METHODS: The diabetic rats were induced by intraperitoneal injection of streptozotocin at dose of 35 mg/kg and feeding with high-fat diet. The animals were divided into 5 groups: diabetic model control group (model), TTPGL treatment groups (with the doses of 60, 120 and 240 mg/kg, respectively) and rosiglitazone treatment group (3 mg/kg). Another 12 normal SD rats were used as the normal controls. The rats received daily treatment for 6 weeks, and then the levels of fasting blood glucose (FBG), fasting insulin (FINS), triglyceride (TG), total cholesterol (TCH), free fatty acid (FFA), glycosylated hemoglobin (GHb) and glycosylated serum proteins (GSP) were measured. The protein expression of peroxisome proliferator-activated receptor γ (PPARγ) in adipose tissues was detected by Western blotting. RESULTS: Compared with normal control group, the levels of FBG, GHb and blood lipids were increased in type 2 diabetic rats. The FINS, insulin sensitivity index, and the protein expression of PPARγ in adipose tissues were decreased. Compared with model group, the levels of FBG and GSP were decreased,and the FINS, insulin sensitivity index, and the protein expression of PPARγ in adipose tissues significantly increased in TTPGL treatment groups (with the doses of 120 and 240 mg/kg). The levels of serum TG,TCH and FFA were significantly lower in TTPGL treatment groups (P<0.01 or P<0.05) as compared with the model controls. CONCLUSION: TTPGL decreases the levels of blood glucose and lipids in diabetic rats. TTPGL also increases serum insulin level and improves insulin sensitivity. The action mechanism of TTPGL may be related to the increase in the protein expression of PPARγ.  相似文献   

14.
AIM: To investigate the effects of human urotensin II (hUII) on ischemia/reperfusion (I/R) injury in isolated rat hearts. METHODS: In the ischemia/reperfusion (I/R) model of isolated perfused rat hearts, the effects of hUII pretreatment on cardiac function was monitored with cardiac function software of MFL Lab200. ATP, total calcium, and malondialdehyde (MDA) content in myocardium were detected. The coronary perfusion flow (CPF) and lactate dehydrogenase (LDH) activity in coronary effluent were measured during reperfusion. RESULTS: In the hUII pretreated group, the release of LDH from myocardium was lower [(78.3±18.1)U/L] than I/R group [(109.3±23.9) U/L, P< 0.05], with decreased contents of MDA and calcium in myocardium (decreased by 24% and 27%, respectively, P< 0.05) and an increased myocardial ATP content [(3.8±0.4)μmol/g dw vs (2.2±0.4)μmol/g dw, P< 0.05)]. At the same time, hUII pretreatment increased CPF [(5.4±0.7) mL/min vs (3.8±0.8) mL/min in I/R group, P< 0.05], reduced left ventricular end-diastolic pressure (LVEDP) by 20% ( P< 0.05) with increased±d p /d t max [(217±38) kPa/s and (119±18) kPa/s vs (173±29) kPa/s and (82±25) kPa/s in I/R groups, respectively, P< 0.05]. hUII pretreatment also increased natrite/natrate (NO2-/NO3-) content in coronary effluent [(52.2±12.0)μmol/L vs (32.1±10.2)μmol/L in I/R group, P< 0.05)]. CONCLUSION: hUII pretreatment attenuated I/R injury in isolated perfused rat hearts. The protective mechanism might be associated with NO-mediated coronary vasodilation.  相似文献   

15.
AIM: To observe the effects of methionine-induced hyperhomocysteinemia on protein C(PC), antithrombin-Ⅲ (AT-Ⅲ) and von willebrand factor (vWF).METHODS:The proliferat ion of HL-60 leukemia cell was observed by hemopoiet ic cell culture.Apoptosis was measured by the morphology of apoptosis cell, the quantitation of DNA fragmentation with the diphenylamine reaction.The change in drug sensitivity was measured by MTT.RESULTS:In group M, the levels of methionine(29.97±5.34 μmol/L) and homocysteine(13.30±2.19 μmol/L) in serum were signifficantly higher than those(14.48±1.97 μmol/L and 5.36±1.19 μmol/L, respectively, P＜0.01) of group C.The levels of AT-Ⅲ and PC of group M were signifficantly lower than those of group C (P＜0.01). The level of vWF in plasma of group M was higher than that of group C (P＜0.01). Immunohistochemistry showed that vWF expression in endothelial cells of aorta was decreased. CONCLUSION:Methionine-induced hyperhomocysteinemia had promotive effects on coagulation and inhibiting effects on antioagulation.  相似文献   

16.
AIM: To investigate the regulatory effect of berberine on the endoplasmic reticulum stress-auto-phagy pathway in human ovarian cancer SKOV3 cells. METHODS: Human ovarian cancer SKOV3 cells were cultured in vitro, and berberine at doses of 12.5, 25, 50, 100, 200 and 400 μmol/L were added. After exposure for 12 h, 24 h and 48 h, the viability of the SKOV3 cells was measured by MTT assay. The cells were divided into control group, berberine (50 μmol/L) group, berberine (100 μmol/L) group, and berberine (200 μmol/L) group. After treatment with berberine for 24 h, the effects of berberine on the morphological changes of SKOV3 cells were observed under inverted phase-contrast microscope. The protein expression of microtubule-associated protein 1 light chain 3 (LC3) and ubiquitin-binding protein p62 was observed by indirect immunofluorescence method under laser confocal microscope. The protein expression of beclin-1,LC3,p62, CCAAT/lenhancer binding protein homologous protein (CHOP) and glucose-regulated protein 78 (GRP78) was determined by Western blot. RESULTS: Berberine at 12.5, 25, 50, 100, 200 and 400 μmol/L significantly decreased the viability of SKOV3 cells at 12 h, 24 h and 48 h, and the IC50 values of 12 h, 24 h and 48 h were (764.7±0.3) μmol/L, (231.6±0.1) μmol/L and (96.2±0.1) μmol/L, respectively. Laser confocal microscopy showed that the LC3 and p62 proteins were scattered and the fluorescence intensity was increased, while the point-like aggregation was also observed. Berberine at 200 μmol/L obviously enhanced the co-localization of LC3 and p62 proteins. Compared with control group, the expression of endoplasmic reticulum stress-related proteins GRP78 and CHOP, and autophagy-related proteins beclin-1, LC3 and p62 in berberine (200 μmol/L) group was increased significantly (P<0.05). CONCLUSION: Berberine may promote endoplasmic reticulum stress in SKOV3 cells by regulating autophagy.  相似文献   

17.
AIM: To investigate the effects of total triterpenoids from Psidium guajava leaf (TTPGL) on 3T3-L1 adipocyte insulin resistance (IR) and to explore the possible mechanism. METHODS: 3T3-L1 pre-adipocytes were cultured and induced to differentiate into 3T3-L1 adipocytes, then treated with TTPGL (0.3, 1, 3, 10 μg/L) for 48 h. The cells were divided into 0.1% DMSO group, positive drug sodium orthovanadate (Van, 10 μmol/L) group, model group and control group. The effect of TTPGL on the cell activity of pre-adipocytes was detected by MTT assay and its influence on the cellular differentiation was observed by oil red O staining. The IR model of the 3T3-L1 adipocytes was established successfully and then treated with different drugs for 48 h. The glucose consumption in the supernatant of IR adipocyte's culture medium was assayed by glucose oxidase-peroxidase (GOD-POD), free fatty acid (FFA) levels were measured by colorimetric method, and adipocytokines levels were assayed by ELISA. The mRNA expression of protein tyrosine phosphatase-1B (PTP1B) of IR adipocyte was detected by real-time PCR. The protein levels of phosphorylated insulin receptor substrate 1/insulin receptor substrate 1 (p-IRS-1/IRS-1) and phosphorylated protein kinase B/protein kinase B (p-Akt/Akt) were determined by Western blot. RESULTS: Compared with DMSO group, TTPGL treatment significantly promoted the cell activity of 3T3-L1 pre-adipocytes and inhibited its differentiation (P < 0.01). TTPGL (1~10 μg/L) improved glucose consumption of IR adipocytes significantly (P < 0.01), with or without insulin stimulation, and TTPGL (0.3~3 μg/L) restrained FFA production remarkably(P < 0.01). Compared with model group, TTPGL (0.3 and 3 μg/L) significantly increased the secretion of adiponectin in IR adipocytes (P < 0.05), and inhibited the secretion of tumor necrosis factor-α (TNF-α) (P < 0.01). TTPGL (3 μg/L) restrained the secretion of resistin significantly (P < 0.05), and showed no significant effect on secretion of leptin. It also down-regulated the mRNA expression of protein tyrosine phosphates 1B (PTP1B) in IR adipocytes significantly (P < 0.01), and increased the protein levels of p-IRS-1/IRS-1. TTPGL (0.3 and 3 μg/L) up-regulated the protein level of p-Akt/Akt in IR adipocytes significantly (P < 0.05).CONCLUSION: TTPGL reduces IR in 3T3-L1 adipocytes. The mechanism may be that TTPGL significantly down-regulated mRNA expression of PTP1B and increased the protein levels of p-IRS-1/IRS-1 and p-Akt/Akt in IR adipocytes.  相似文献   

18.
AIM：To study the correlation of serum uric acid (UA) level with carotid plaques and arterial stiffness in the patients with essential hypertension (EH), and to explore the predictive value of serum UA for evaluating EH preclinically. METHODS：A total of 92 patients with EH and 30 healthy individuals were enrolled. The value of UA and other indicators were detected. B-mode ultrasound examination was performed to measure the common carotid artery intima-media thickness (IMT) and the sites of plaque in the internal carotid-artery, external carotid artery and carotid bifurcations. Carotid-femoral arterial pulse wave velocity (CFPWV) was assessed by Complior atherosclerosis measurement instrument. RESULTS：The serum level of UA in the patients with EH was higher than that in control group ［(361.51±83.81） μmol/L vs (317.03±62.22) μmol/L, P<0.05］. The mean value and abnormal rate of IMT between hypertension group and control group were significant difference ［(0.69±0.14) mm vs (0.60±0.12) mm, 42.39% vs 10.00%, P<0.05］. In 92 EH patients, 45 cases had carotid plaques. These 45 cases were divided into 3 groups according to the plaque severity, among which the serum UA level had statistically significant differences ［(285.25±78.41） μmol/L, （341.19±63.99） μmol/L and （401.33±88.49） μmol/L, P< 0.05］. Compared with rigid plaque group (n=34), the serum UA level in soft plaque group (n=11) was significantly higher ［(389.00±69.45) μmol/L vs （323.03±72.71） μmol/L, P<0.05］. A stepwise multiple linear regression analysis demonstrated that age (r=0.414), systolic blood pressure (r=0.224), pulse pressure (r=0.270) and uric acid (r=0.219) were predisposed factors for higher CFPWV (P<0.05). CONCLUSION：UA is one of the risk factors causing hypertension. Serum UA level may reflect the severity and stability of carotid plaques. The increased arterial stiffness is closely related to the increased serum UA level in EH.  相似文献   

19.
AIM and METHODS: The effects of hydrogen peroxide on Na+ currents were studied in freshly dissociated rat hippocampal CA1 neurons using the whole-cell patch-clamp techinique. RESULTS: ①H2O2 caused a dose-dependent and voltage-dependent increase in the voltage-activated Na+ currents. The amplitudes of Na+ currents were increased (48.0±4.2)% and (88. 2±5. 1)% (n=10) by H2O2 at 10 μmol/L and 100 μmol/L, respectively. ②H2O2 (10 μmol/L) did not affect the activation process, but changed the inactivation process significantly. Before and after application of 10 μmol/L of H2O2, the half-inactivation voltage was (-64.58±1.22)mV and (-53.55±0.94)mV (n=10, P<0.01), but the slope factor was not changed. CONCLUSION: As a product of oxidation metabolism, H2O2 is related to some diseases in the central nervous system.  相似文献   

20.
AIM: To investigate rat Urotensin-II(rat U-II)-induced vasoconstriction of rat main pulmonary arteries and the role of mitogen-activated protein kinase(MAPK). METHODS: The main pulmonary artery was dissected from the male Sprague-Dawley rats and artery ring width was 3-4 mm. Concentration-response curves were generated to rat U-II(0.03 nmol/L-30 nmol/L).Inhibitor of MAPK, PD 98059(0.1 μmol/L-10 μmol/L) were added into the medium after rat U-II(30 nmol/L)induced vasoconstriction had reached plateau to construct the relaxant concentration-response curves and their EC50 and Emax. RESULTS：Rat U-II was a potent vasoconstrictor of isolated rat main pulmonary arteries [EC50=7.95±0.40, Emax=(14.28±6.34)% of the response to 60 mmol/L KCl]; PD 98059 caused concentration-dependent relaxations of rat U-II precontracted arteries [EC50=5.91±0.45, Emax=(81.39±13.65)%]. CONCLUSION: Rat U-II was a potent vasoconstrictor of rat main pulmonary arteries and this response was mediated through MAPK.  相似文献   

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