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1.
AIM: We sought to evaluate the expression of apoptosis related genes, p53 and bcl-2 , in cultured vascular smooth muscle cells (VSMCs) in which apoptosis was induced by the ligands of PPARγ-ox-LDL,ciglitazone and 15-deoxy-△12,14-PGJ2,and then influenced by PGF2α,an antagonist of PPARγ. To clarify whether PPARγ is involved in the regulations of p53 and bcl-2 .METHODS: Rat aorta smooth muscle cells were isolated and cultured in DMEM containing 10%FBS. ox-LDL,ciglitazone and 15 d-PGJ2 were added into the medium for 24 h, respectively. Using PGF2α to inhibit PPARγ activation via activation of MAP kinase. We employed the flow cytometry analysis to quantitatively analyze the apoptosis of VSMCs. Also, we measured and analyzed the discrepancies of the expression of p53 and bcl-2 between every groups. RESULTS: During the process of apoptosis induced by PPARγ,the expression of P53 protein increased (P＜0.05)and the Bcl-2 diminished. Inhibition of PPARγ through PGF2α attenuated such influences. CONCLUSION: In the apoptosis of VSMCs, the activation of PPARγ changes the expression of p53 and bcl-2. We suppose that the apoptosis of VSMCs is partly due to changes of expression of apoptotic genes regulated by PPARγ.  相似文献   

2.
AIM: To study the relationship between prostaglandins and acute pulpitis. METHODS: Rat traumatic pulpitis model was established by pulp exposure. The kinetic pathological changes in dental pulpal tissues and changes of PGE2,6-Keto-PGF1α and TXB2 concentration in dental pulp were observed. RESULTS: After pulpal trauma, the dental pulp showed inflammatory changes and the concentrations of PGE2,6-Keto-PGF1α and TXB2 were increased, which peaked at 6 hour post-trauma. CONCLUSION: Prostaglandins play a significant role in the pathogenesis of pulpitis.  相似文献   

3.
AIM: To explore the effects of chlorogenic acid (CGA) on endothelial dysfunction in db/db mice and the possible mechanism. METHODS: Male db/db mice (n=12) were divided into control group and CGA group, with 6 mice in each group. The mice in CGA group were treated with diet containing 0.02% CGA, while the mice in control group were given normal diet only. The observation period was 12 weeks. Fasting blood glucose level, tail blood pressure and the body weight were analyzed each week. At the end of the 12th week, the mice were anesthetized and blood was taken from carotid artery. The plasma levels of heme oxygenase-1 (HO-1), catalase (CAT), NAD(P)H dehydrogenase quinone 1 (NQO1) and glutathione peroxidase-1 (GPx-1) were measured by ELISA. The mouse aortas were isolated, and the superoxide anion and nitric oxide (NO) levels were measured by DHE and DAF-2 DA staining, respectively. Wire Myograph System was used to detect the vasorelaxation of db/db mouse aorta. The protein levels of peroxisome proliferator-activated receptor α (PPARα), nuclear factor E2-related factor 2 (Nrf2), phosphorylated AMP-activated protein kinase (p-AMPK), phosphorylated endothelial NO synthase (p-eNOS), P22phox and P47phox were determined by Western blot. RESULTS: Dietary CGA decreased fasting blood glucose and body weight in db/db mice as compared with control group (P<0.01 or P<0.05). The plasma levels of HO-1, CAT, NQO1 and GPx-1 in CGA group were higher than those in control group (P<0.01 or P<0.05). Administration of CGA for 12 weeks attenuated superoxide anion level, increased NO level in the mouse endothelium and improved endothelium-dependent relaxation of the db/db mouse aorta. CGA also increased the protein levels of PPARα, Nrf2, p-AMPK and p-eNOS, and decreased P22phox and P47phox levels (P<0.01). CONCLUSION: Dietary CGA improves db/db mouse endothelium-dependent relaxation. This effect may be related to the increases in the levels of antioxidant molecules PPARα, Nrf2 and p-AMPK, and the up-regulation of antioxidant capacity, thus decreasing the oxidative stress, promoting eNOS phosphorylation, and increasing NO level.  相似文献   

4.
AIM:To investigate the influence of exogenous somatostatin (stilamin) on pancreatic blood flow in normal rats or rats with acute necrotizing pancreatitis (ANP).METHODS:Pancreatic blood flow (PBF) was detected with computerized tissue blood flowmeter and rats with ANP were triggered with sodium taurocholate. Metabolites of eicosanoids in plasma were determined with radioimmunoassay. Other laboratory tests including histopathologic observation under optical or electron microscope were used. RESULTS:There was a significant decrease in PBF in normal rats after stilamin administration in comparison with that before use of the drug. There was significant decrease in PBF after onset of ANP, but, compared with that in ANP group, significant increase was shown in SS(stilamin)+ANP group. Plasma thromboxin-B2(TXB2) in ANP group at 6 hours after ANP was significantly higher, with increase of 4.5 times, than that in Sham(sham operated) group while TXB2, detected each time during the course of ANP, significantly decreased in SS+ANP group. 6-Keto-prostagland in F1α(6-Keto-PGF1α) at 6 h after ANP was significantly higher, and the ratio of TXB 2／6-Keto-PGF1α, significantly lower in SS+ANP group than that in ANP group. Lessened necrosis of acinar cells, along with much fewer microthrombi in microvessels in SS+ANP group, was shown by pathologic scoring or electron microscope than that in ANP group.CONCLUSION:Administration of exogenous somatostatin leads to the decrease in PBF in physiological setting but it attenuates pancreatic ischemia in SS+ANP group, which may be attributed to correction of abnormal metabolism of eicosanoids, improvement of pancreatic microcirculation and cytoprotection of acinar cells as well.  相似文献   

5.
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   

6.
AIM: To investigate the role of α1 and β2 adrenoceptors(α1AR and β2AR) in the proliferation of hypoxic pulmonary artery smooth muscle cells (PASMCs).METHODS: PASMCs were isolated by an explant method from neonatal bovine pulmonary arteries. The cultured PASMCs were exposed to 6.6% O2 for 6 h, 12 h and 24 h. The method of -TdR incorporation was used to measure the proliferation of PASMCs. i was assayed with Fura-2/AM. The mRNA expression of α1AR, β2AR, c-fos and c-myc was determined by Northern blotting. The effects of activation of α1AR and β2AR, and inhibition of α1AR on the above indexes were observed by treating PASMCs with different AR agonists and antagonists under hypoxic condition.RESULTS: Significant increase in TdR incorporation in hypoxic PASMCs with α1AR activation was observed, and marked decrease in that was induced by α1AR inhibition. However, no significant change was found after β2AR activation. i , the mRNA expression of c-fos, c-myc, α1AR and β2AR in PASMCs were increased after hypoxia.CONCLUSION: Hypoxia induces the increase in i and mRNA expression of c-fos and c-myc, leading to the proliferation of PASMCs. The hypoxic proliferation of PASMCs is intervened by α1AR, but not β2AR. The remodeling of pulmonary arteriole and pulmonary hypertension may be involved in the processes of pulmonary arteriole constriction and proliferation induced by hypoxia through up-regulation of α1AR.  相似文献   

7.
AIM: To investigate the effect of human amniotic fluid on the release of thromboxane A2 (TXA2), prostaglandin I2 (PGI2) and Leukotriene C4 (LTC4) from blood cells. METHODS: 1 mL human amnioticfluid and 10 mL oneself blood collected from 38-41 weeks with cesarean section were cultured at 37 ℃ for 30 min, and then centrifuged. The supernatants were taken and stored at -70 ℃. TXB2 and 6-Keto-PGF1α of the superntants were determined by radioimmunoassay and LTC4 by enzyme immunoassay. RESULTS: It was found that the levels of TXB2 and LTC4 in blood were elevated from (63.5±52.0)ng/L and (40.1±39.2) ng/L to (189.1±102.0) ng/L and (293.5±206.1) ng/L, respectively (P<0.01), after cultivation of oneself amniotic fluid with blood, the concentrations of TXB2 and LTC4 were higher in meconium-stained group than those in clear amniotic fluid group, but the concentration of PGI2 only elevated slightly from (27.4±11.6) ng/L to (33.9±10.6) ng/L (P>0.05). CONCLUSION: Amniotic fluid might stimulate the release of TXA2 and LTC4 from blood, it might affect the balance of TXA2 and PGI2 in blood, which might play an important role in the pathogenesis of amniotic fluid embolism.  相似文献   

8.
AIM:To investigate the effect of salvianolic acid B (Sal B) on high glucose-induced phenotypic transition and extracellular matrix (ECM) secretion in human glomerular mesangial cells (HGMCs) and the underlying mechanisms. METHODS:HGMCs were randomly divided into control group, high glucose group and high glucose plus high dose, medium dose and low dose of Sal B groups. The HGMCs except those in control group were exposed to high glucose (33.3 mmol/L) for 72 h, while those in Sal B groups were co-incubated with indicated concentrations of Sal B. The protein levels of α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1) and phosphorylated Smad2 and p38 mitogen-activated protein kinase (MAPK) were determined by Western blot. The secretion levels of collagen type I (Col I), collagen type Ⅲ (Col Ⅲ), fibronectin (FN) and laminin (LN) were measured by ELISA. RESULTS:Exposure to high glucose markedly increased the protein expression of α-SMA, TGF-β1, Col I, Col Ⅲ, FN and LN in the HGMCs (P<0.01). The phosphorylation levels of Smad2 and p38 MAPK were also significantly increased (P<0.01). Co-incubation with Sal B evidently decreased the protein expression of α-SMA, TGF-β1, Col I, Col Ⅲ, FN and LN in the HGMCs induced by high glucose (P<0.05 or P<0.01). The phosphorylated levels of Smad2 and p38 MAPK were also reduced noticeably (P<0.05 or P<0.01). CONCLUSION:Sal B significantly suppresses high glucose-induced phenotypic transition and ECM secretion in the HGMCs, which might be attributed, at least partly, to inhibition of TGF-β1/Smad signaling pathway and p38 MAPK activation.  相似文献   

9.
AIM:To study the relationship between the activity of phospholipase A2 (PLA2) and chronic hypoxic pulmonary hypertension. METHODS:29 healthy SD rats were randomly divided into normal control group, chronic hypoxic group and hypoxia plus Polidatin (PD) group. The model of rat chronic hypoxic pulmonary hypertension was made by method of intermittent isobaric hypoxia for 21 days. The mean pulmonary arterial pressure (mPAP) was measured by inserting a microcatheter into the pulmonary artery. RESULTS:After exposing hypoxia for 21 days, the mPAP, R/L+S, the PLA2 activity, TXB2, MDA in plasma and lung homogenate increased significantly, while 6-k-PGF1α, SOD decreased significantly. Pretreatment with PD could relieve the changes mentioned above.CONCLUSION:PLA2 plays an important inducing role through its metabolic products and the interactional radicals in the formation of chronic hypoxic pulmonary hypertension.  相似文献   

10.
AIM: Using simvastatin and vitamine E (Vit-E) treatment to coronary artery disease (CAD) patients with low HDL, to investigate the relationship between Ox-LDL, platelet activation and HDL. METHODS: 40 CAD patients with low HDL were divided into two groups (A and B): A group oral simvastatin, B group oral simvastatin and Vit-E. The level of serum Ox-LDL, TXB2 and GMP-140 were measured before and after treatment. The relationship between Ox-LDL, TXB2, GMP-140 and HDL were analysed. RESULTS:The level of serum HDL was significantly increased in A and B group after treatment and attained normal level. The level of serum Ox-LDL, TXB2 and GMP-140 were decreased significantly after simvastatin and Vit-E treatment and neared normal. CONCLUSIONS:This study confirmed that HDL can effectively refrain LDL oxidation. It also revealed that Vit-E and simvastatin treatment were more effectively refrained platelet activation by increasement of HDL and decreasement of Ox-LDL.  相似文献   

11.
AIM: To study the expression of glycine receptor α1 subunit in neonatal rat myocardial cells and to investigate the effect of lipopolysaccharide (LPS), hypoxia/reoxygenation, isoproterenol (ISO) and high concentration of glucose (HG) on the expression of glycine receptor α1 subunit in the neonatal rat myocardial cells. METHODS: Neonatal rat myocardial cells were cultured in vitro. The expression of glycine receptor α1 subunit was detected by Western blotting. The neonatal rat myocardial cells were treated with LPS (20 mg/L), ISO (100μmol/L) or high concentration of glucose (25 mmol/L) for 24 h, or were exposed to hypoxia for 3 h followed by reoxygenation for 3 h. Subsequently, the cell viability was measured by CCK-8 assay, and the expression of glycine receptor α1 subunit was determined by Western blotting. RESULTS: The expression of glycine receptor α1 subunit in the neonatal rat myocardial cells was positively detectable by Western blotting. Compared with control group, no significant difference of the cell viability (P>0.05) in LPS group, ISO group, hypoxia/reoxygenation group and HG group was observed. The expression of glycine receptor α1 subunit was increased (P<0.01) in LPS group, ISO group and hypoxia/reoxygenatio group, but decreased (P<0.01) in HG group. CONCLUSION: Glycine receptor α1 subunit exists in the neonatal rat myocardial cells. A certain concentration of LPS or ISO, or hypoxia/reoxygenation for a certain period upregulate the expression of glycine receptor α1 subunit, but HG downregulates the expression of glycine receptor α1 subunit in cultured neonatal rat myocardial cells.  相似文献   

12.
AIM: To investigate the mechanism of protein phosphatase 2A (PP2A) activation in mesenteric arteries of angiotensinⅡ(AngⅡ)-induced hypertensive rats. METHODS: Adult male Sprague-Dawley (SD) rats were subjected to AngⅡinfusion (500 ng·kg-1·min-1) using osmotic minipump up to 14 d to established the hypertension model. The rats (n=40) were randomly divided into 4 groups:control group (n=10), AngⅡgroup (n=10), candesartan (CAN; AngⅡtype 1 receptor blocker)+AngⅡgroup (n=10) and CAN group (n=10). The rats in CAN+AngⅡgroup and CAN group were administered with candesartan ester at the dose of 10 mg·kg-1·d-1 by gavage on the first day after implantation of osmotic minipump. The rats were sacrificed on the 15th day after minipump implantation. Serum and mesenteric arteries were collected. Systolic blood pressure was measured by tail-cuff method. The serum levels of AngⅡ were measured by ELISA. The protein levels of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (Ser1177), PP2A catalytic subunit (PP2Ac), phosphorylated PP2Ac (Tyr307) and PP2A inhibitor 2 (I2PP2A) in the mesenteric arteries were determined by Western blot. The activity of PP2A in the arteries was detected using PP2A activity assay kit. RESULTS: Compared with control group, the systolic blood pressure in AngⅡgroup was significantly increased(P<0.05), while those in CAN+AngⅡgroup and CAN group were significantly decreased (P<0.05). The serum levels of AngⅡ in AngⅡ group and CAN+AngⅡ group were significantly higher than that in control group (P<0.05). Compared with control group, the phosphorylation levels of eNOS Ser1177 were decreased in AngⅡgroup (P<0.05), but the activity of PP2A was significantly increased (P<0.05), and Pearson correlation analyses showed a negative correlation between PP2A activity and eNOS S1177 phosphorylation (r=-0.842, P<0.05). Compared with AngⅡgroup, the phosphorylation levels of eNOS Ser1177 in CAN+AngⅡgroup were significantly increased (P<0.05), but the activity of PP2A was reduced (P<0.05). Compared with control group, the protein levels of phosphorylated PP2Ac (Tyr307) and I2PP2A in the mesenteric arteries were decreased in AngⅡgroup (P<0.05), but increased in CAN+AngⅡgroup (P<0.05). No significant difference in all above-mentioned measures between control group and CAN group, nor in the levels of total eNOS and PP2Ac protein expression among all the groups was observed. CONCLUSION: AngⅡmay reduce the protein levels of phosphorylated PP2Ac (Tyr307) and I2PP2A in the mesenteric arteries of AngⅡ-induced hypertensive rats through AngⅡ/AngⅡ type 1 receptor-mediated signaling pathway, resulting in the activation of PP2A, then leading to down-regulation of eNOS S1177 phosphorylation, which ultimately mediates the occurrence of vascular endothelial dysfunction.  相似文献   

13.
AIM: To investigate the underlying mechanisms responsible for endothelial dysfunction of type 1 diabetes mellitus (DM) rats fed with high-salt diet. METHODS: Type 1 DM was induced by intraperitoneal injection of streptozotocin (70 mg/kg). Normal and diabetic rats were fed high-salt food (HS, 8% NaCl) and standard food for 6 weeks, respectively. Isometric tension of the mesenteric arteries were measured. The expression of Akt, endothelial nitric oxide synthase (eNOS) and caveolin-1 (Cav-1) was examined by Western blot. RESULTS: The rats in DM+HS group exhibited more pronounced impairment of vasorelaxation to acetylcholine and insulin compared with either DM group or HS group (P<0.01). Akt and eNOS phosphorylation levels, and nitric oxide (NO) concentration in DM+HS group were significantly lower than those in DM group (P<0.01). The level of Cav-1 in DM+HS group was significantly higher than that in DM group and HS group. CONCLUSION: Impaired endothelial Akt activation, increased Cav-1 expression and resultant decreased eNOS activation contribute to aggravate high-salt diet-induced endothelial dysfunction and hypertension in DM rats.  相似文献   

14.
AIM:To observe the dynamic changes of expression of PKCα, TGF-β1 and α-SMA in glomeruli of diabetic rats induced by the alloxon and to invesitigate their roles in the diabetic nephropathy(DN).METHODS:Rats were randomly divided into four groups: normal control group (group A), diabetic group of one week (group B), diabetic group of one month (group C), diabetic group of two months (group D). Immunohistochemistry and Western blotting were used to detect the expression of PKCα, TGF-β1 and α-SMA in renal tissue of all groups. Blood glucose, triglycerides, cholesterol, creatinine and urine protein were analysed by chemical methods. The morphological changes of renal tissue were checked through microscopy.RESULTS:The expression of PKCα and TGF-β1 in renal tissue of diabetic groups were increased comparing with those of nomal control group(P<0.05). The mesangial cells expressed α-SMA in two months group. Chronologically the expression of PKCα, TGF-β1 and α-SMA were positively correlative with each other and the impairment of kidney was also observed.CONCLUSIONS: During the DN process the expression of PKCα increased. PKCα raised GFR and the permeability of glomerular filtration membrane which enhanced urinary albumin excretion. PKCα also increased expression of TGF-β and therefore to induce the expression of α-SMA. The appearance of α-SMA was a marker of the phenotypic transform of renal cells.  相似文献   

15.
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   

16.
AIM: To investigate the effects of arginine vasopressin (AVP) on the expression and phosphorylation of γ-aminobutyric acid (GABA) subtype A receptor (GABAA receptor) subunits in the preoptic area (POA) of rats. METHODS: The rats were divided into AVP group (n=10), AVP+V1a receptor blocker group (n=10), V1a receptor blocker group (n=10) and control group (n=10). After intraperitoneal injection of AVP or V1a receptor antagonist for 0.5 h, the changes of the expression and phosphorylation of POA GABAA receptor subunits (α, β and γ2) were analyzed by RT-qPCR and Western blot. RESULTS: Compared with control group, no significant change of GABAA receptor subunit expression in the rats injected with AVP or V1a receptor antagonist was observed. AVP up-regulated the phosphorylation level of POA GABAA receptor γ2 subunit (P<0.05), and significantly increased the expression and phosphorylation of protein kinase C (PKC) and calcium/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ). CONCLUSION: Exogenous AVP has no effect on expression of POA GABAA receptor subunits (α, β and γ2) and is involved in modulation of GABAergic synaptic transmission in the POA by activation of PKC and CaMKⅡ and phosphorylation of γ2 subunit via V1a receptor.  相似文献   

17.
AIM: To study the effect of thyroid hormone on the expressional change of myosin heavy chain(MHC) gene in cardiomyocyte induced by angiotensinⅡ(AngⅡ) and its potential mechanism. METHODS: Cardiac myocyte was cultured according to the method of Simpson. 10-8 mol/L T3 and 10-7 mol/L AngⅡ were added to the culture medium, respectively or synchronously. After 48 h, the expression of α and β-MHC mRNA in myocytes were detected by RT-PCR. The protein kinase C activation were detected by PepTag non-radioactive PKC assay. The incorporation of -Leucine and [3H]-thymine to test the protein and DNA synthesis in myocytes were also performed. RESULTS: AngⅡalone increased the incorporation of [3H]-Leucine of myocytes while it had no effect on the incorporation of [3H]-thy mine. The expression of β-MHC mRNA was increased and the expression of α-MHC mRNA was decreased significantly at the condition of AngⅡ. The enhanced PKC activation was induced by AngⅡalso. When AngⅡand T3 were added to the culture medium synchronously, though the incorporation of [3H]-leucine and [3H]-thymine were not changed compared with AngⅡ treated alone. The α-MHC mRNA expression was increased and the β-MHC mRNA expression was decreased significantly. The PKC activation of the myocytes also was decreased. CONCLUSIONS: T3 inhibited the expressional change of myosin heavy chain gene in cardiac myocytes induced by AngⅡ. The effect of T3 on the change of PKC activation in cardiac myocytes may be one of its mechanisms.  相似文献   

18.
AIM:To observe the effects of cimetidine(Cim) on platelet function and thrombosis. METHODS:After incubated with Cimin vitro, rat platelets were activated with ADP or thrombin. The platelet aggregation, platelet malondialdehyde(MDA) formation, platelet intracellular free calcium( [Ca2+]i), and thromboxane B2 (TXB2) were measured. The effects of Cim on electric-induced thrombosis in rat carotid artery were examined. RESULTS:Cim potentiated ADP induced platelet aggregation, increased the thrombin induced [Ca2+]i and MDA formation, decreased TXB2. Also, Cim shortened the duration of electric-stimulated occlution time in rat carotid artery. CONCLUSION:Cim increased platelet function and accelerated thrombosis.  相似文献   

19.
AIM:To explore the effects of levcromakalim(Lev) on pulmonary arterial endothelial cells (PAEC) and smooth muscle cells (PASMC) exposed to hypoxia and the mechanisms involved.METHODS:The effects of Lev on [Ca2+]i, and expression of PKCα, eNOS, iNOS and PDGF-B mRNA and protein levels were observed. The nitrite (NO2-) and entothelin-1(ET-1) concentrations in supernatant in cultured PAEC and PASMC were measured. The proliferation and apoptosis of PASMC was also detected.RESULTS:When PASMC were exposed to hypoxia, Lev reduced concentration of ET-1 in cultured cell supernatant, lowed the expression of PKCα, iNOS and PDGF-B both at mRNA and protein levels, decreased [Ca2+]i concentration, increased proliferation and promoted the apoptosis in PASMC. However, in the presence of Lev, the [Ca2+]i concentration was not changed in the hypoxic PAEC. The NO2- concentration in cultured cell supernant and expression of eNOS at mRNA and protein levels in hypoxic PASMC and PAEC were also unchanged. The downregulated ET-1 activity in PASMC and PAEC and proliferation in PASMC involved in the inhibition of PKCα signaling pathway.CONCLUSIONS:Lev reduce some disadvatage effect of hypoxia on PASMC and PAEC. The mechanism of Lev action may partly involve in the downregulation of PKCα signaling functions.  相似文献   

20.
AIM: To investigate the effects of mollugin on the viability and collagen synthesis of rat hepatic stellate cell line CFSC-2G. METHODS: The activation of CFSC-2G cells was induced with low concentration (10 μmol/L) of hydrogen peroxide (H2O2) for 30 min in the experiment. The viability of the CFSC-2G cells after exposed to mollugin at different concentrations (0, 20, 40, 60 and 120 μmol/L) was detected by MTT assay. The mRNA and protein expression levels of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear factor-κB (NF-κB) p65, Bcl-2, Bcl-xL, Bax, and hepatic stellate cell activation markers α-smooth muscle actin (α-SMA) and collagen type I (Col Ⅰ) were detected by real-time PCR and Western blot. The phosphorylation level of p38 mitogen-activated protein kinase (p38 MAPK) was determined by Western blot. RESULTS: Mollugin significantly inhibited the viability and collagen synthesis of activated CSFC-2G cells induced by H2O2. The expression of Nrf2, HO-1 and Bax at mRNA and protein levels, and the phosphorylation level of p38 MAPK were promoted, while the levels of NF-κB p65, Bcl-2, Bcl-xL, α-SMA and ColⅠwere inhibited by mollugin (P<0.05). CONCLUSION: Mollugin may inhibit H2O2-induced viability and collagen synthesis of the CSFC-2G cells by activating Nrf2 and HO-1, and blocking the NF-κB p65 and Bcl-2 expression.  相似文献   

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