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1.
AIM: To investigate the effects of pioglitazone,a PPARγ agonist,on endothelial cell (EC) dysfunction in hypercholesterolemic rats.METHODS: 36 healthy male Wistar rats were assigned to one of the following groups randomly (six rats in each group): control,hypercholesterolemia (HC),and HC treated with pioglitazone 1.5 mg·kg-1·d-1,3 mg·kg-1·d-1,10 mg·kg-1·d-1 and 20 mg·kg-1·d-1 (HC＋PIO),respectively.EC function was determined by comparing vasorelaxation to ACh,an EC dependent vasodilator,and acidified NaNO2,an EC-independent vasodilator.Maximal positive and negative values of the instantaneous first derivative of LVP (+dp/dtmax and dp/dtmax) were determined by MS2000 system.RESULTS: (1) Hypercholesterolemia caused a significant endothelial diastolic dysfunction (maximal relaxation to ACh: 50.51%±2.45% vs 99.78%±3.01% in control,P<0.01).(2) Treatment with pioglitazone relieved EC-dependent vasodilatation in a dose dependent manner,and 10 mg·kg-1·d-1 is the best dose.(3) Pioglitazone not only improved EC function,but also reduced cardiac functional injury induced by hypercholesterolemia.CONCLUSION: EC dysfunction induced by hypercholesterolemia can be directly extenuated by pioglitazone,which may effectively prevent from subsequent atherosclerosis and ischemic heart disease.  相似文献   

2.
AIM：To observe the effects of different doses of L-dopa on the rotational behavior and amounts of cells expressing D2 receptors in striatum in hemiparkinsonian rats.METHODS：A hemiparkinsonian model was established in rats by pretreatment with 6-hydroxydopamine.The D2 receptor expression were detected by immunohistochemical staining.The numbers of rotations induced by apomorphine was counted within 30 min before and after L-dopa (10 mg·kg-1·d-1,50 mg·kg-1·d--1 or 100 mg·kg-1·d-1,ip) was introduced to Parkinson’s disease (PD) model rats for 15 days.RESULTS：In successful PD model rats,the increased percentage of D2 receptor in lesioned side compared with intact side was associated linearly with the numbers of rotations within 30 min (r=0.927,P<0.01).After high dose of L-dopa intervention to PD model,the numbers of rotations decreased significantly (P<0.05),the amounts of cells expressing D2 receptor at the lesioned side striatum decreased significantly (P<0.01).CONCLUSION：After high dose of L-dopa intervention,rotation behavior of PD rats improves,and D2 receptor is down-regulated significantly.  相似文献   

3.
AIM: To study the effects and mechanism of recombinant human defensin α1 on cell proliferation in cultured rat glomerular mesangial cells.METHODS: The influences of defensin α1 at various concentrations on rat 1097 mesangial cell line cultured in vitro were evaluated with MTT assay.The different concentrations of U0126,signal-regulated protein kinase (MEK) inhibitor,were added into the culture mediums of mesangial cells to do blocking test.Incubated with a final concentration of 3 mg/L defensin α1,the phosphorylation of extracellular signal regulated kinase (ERK)1/2 and type IV collagen of mesangial cells in different times were evaluated by Western blotting.RESULTS: Defensin α1 at 3-20 mg/L enhanced proliferation of rat glomerular mesangial cells.The incubation times for the maximum effect on proliferation was 12 h (P<0.01),whereas defensin α1 concentration >20 mg/L decreased cell proliferation.The cell proliferation induced by defensin α1 was inhibited by U0126.Stimulation of the cells with defensin α1 at concentration of 3 mg/L for 5 minutes induced a maximum effect on a ratio of phosphorylation of ERK1/2 to total ERK.After 12 h incubation with defensin α1,an increase in type IV collagen was observed by Western blotting and continued to increase at 24 h and 48 h (P<0.01).CONCLUSION: Defensin α1 enhances rat glomerular mesangial cell proliferation and induces type IV collagen production by MAPK signaling pathway.  相似文献   

4.
AIM: To investigate the effects of lipopolysaccharide, hypoxia/reoxygenation,isoproterenol and high concentration of glucose on glycine receptor α1 subunit mRNA expression in the neonatal rat cardiomyocytes. METHODS: Isolation of cardiomyocytes from Sprague-Dawley rats aging 1～3 d were performed. Cardiomyocytes （1×105～5×105 cells·L-1）were cultured in DMEM medium containing 15% fetal bovine serum at 37 ℃ in 5%CO2 atmosphere for 72 h. Then, cultured rat cardiomyocytes were treated with lipopolysaccharide, isoproterenol or high concentration of glucose for 24 h, respectively, or were exposed to hypoxia for 3 h followed by reoxygenation for 3 h. Subsequently, the cell survival rate was measured using CCK-8 reactant and RT-PCR was applied to monitor the expression of glycine receptor α1 subunit mRNA. RESULTS: Compared with the control group, no significant difference in the cell survival rate was observed （P＞0.05）. The expression of glycine receptor α1 subunit mRNA was increased （P＜0.01） in lipopolysaccharide（5,10,20,40,80 mg/L）,isoproterenol（20,100,500 μmol/L） or hypoxia/reoxygenation, hypoxia groups, but decreased（P＜0.01）in the group treated with high concentration of glucose（25, 50 mmol/L）. CONCLUSION: Lipopolysaccharide, isoproterenol, hypoxia/reoxygenation or hypoxia upregulates the expression of glycine receptor α1 subunit mRNA,but high concentration of glucose down-regulates the expression of glycine receptor α1 subunit mRNA in cultured neonatal rat cardiomyocytes.  相似文献   

5.
AIM:To investigate the cellular mechanisms by which PGF2α promotes glucose-stimulated insulin secretion in NIT-1 beta cells. METHODS:Using the radioimmunoassay (RIA), the amount of the PGF2α augmentation of glucose stimulated insulin secession was determined in different conditions, and the confocal laser scanning methods by Fluo-3AM as a fluorescent probe were used to analyze the changes of intracellular calcium in NIT-1β cells. RESULTS:At the lower glucose (0, 5.5 mmol/L), PGF2α (5 μmol/L) failed to potentiate insulin secretion (P>0.05). However, in the presence of 16.5 mmol/L glucose, PGF2α increased significantly in insulin secretion (P<0.05). Neither the AC inhibitor ddA nor the GC inhibitor Ly-83583 altered PGF2α-potentiated insulin secretion in the presence of 16.5 mmol/L (P<0.05 or P<0.01). Otherwise, the PLC inhibitor U-73122 and the PKC blocker calphostin C both counteracted the insulinotropic of PGF2α (P<0.01 or P<0.05). Moreover, exposure of the NIT-1β cells to 5 μmol/L PGF2α induced a rapid increase of intracellular calcium (P<0.01). The inhibitor, ddA or Ly-83583 had no impact on PGF2α-induced elevation of the intracellular calcium (P<0.01). Pretreatment of the cells with U-73122 completely prevented the calcium response induced by PGF2α (P<0.01). CONCLUSION:Efects of PGF2α was independent of cAMP or cGMP, potentiated glucose (16.5 mmol/L)-induced insulin secretion in NIT-1β cells through stimulation of phospholipase C, which subsequently mediated the elevation of intracellular calcium and activation of protein kinase C.  相似文献   

6.
AIM:To study the apoptosis induction of cyclooxygenase-2 (COX-2) inhibitor，celecoxib and adriamycin (ADM) on tumor apoptosis of gastric carcinoma MGC-803 cells, and to explore their possible molecular mechanism(s) and interactions.METHODS:The number of MGC-803 cells was observed by MTT assay. Tumor apoptosis was studied by fluorescence microscopy, flow cytometry (FCM), and DNA ladder. RESULTS:MGC-803 cell number was significantly decreased with increasing dose of ADM. Cells were accumulated in G0/G1 phase and the number of cells in S phase was decreased. ADM (5 mg/L) combined with celecoxib (25 μmol/L) markably inhibited the growth of MGC-803 cells. Significant morphological changes of typical apoptosis were observed after treatment with combined use of celecoxib and ADM. Compared with ADM or celecoxib alone, ADM plus celecoxib obviously enhanced the DNA ladder fragment revealed by agarose gel electrophoresis of DNA. After exposure to combined celecoxib and ADM treatment for 48 h, MGC-803 cells were accumulated in G0/G1 phase. There was a decrease in the number of cells in S phase as compared to celecoxib or ADM alone. CONCLUSION:Celecoxib and ADM appear to have synergistic effects for the apoptosis induction. This may be an important prospect for applying COX-2 inhibitors to assist chemical therapy of ADM in clinical use.  相似文献   

7.
AIM:To investigate the effects of phytoestrogen α-zearalanol (ZAL) on hypoxia/reoxygenation (H/R) injury and mechanism involved in human umbilical vein endothelial cells (HUVECs). METHODS:HUVECs were exposed to hypoxia for 3 hours and then reoxygenation 1 hour. ZAL or 17β-estradiol (E2) at concentrations of 10-9-10-6 mol/L were pretreated before hypoxia. The survival rate of HUVECs was detected by MTT. Either the activities of LDH and SOD or the level of MDA in supernatant was detected by spectrophotometry. RESULTS:The survival rate of HUVECs and the activity of SOD were significantly decreased (P<0.01), while the activity of LDH and the level of MDA were significantly increased (P<0.01) after H/R. These changes were reversed by pretreatment with ZAL or E2, and there was no significant difference between their effects in the same dose of ZAL and E2. CONCLUSION:These results suggest that phytoestrogen ZAL protects HUVECs from H/R injury by inhibiting the oxidative stress, which was similar to E2.  相似文献   

8.
AIM:To induce preconditioning and oxidativ e stress by H2O2 in HepG2 cells.METHODS:The different doses of H2O2 were used to induce apo ptosis in HepG2 cells,which was estimated by AO/EB staining,MTT assay and flow cytometry.RESULTS:The different group of HepG2 cells stained with AO/EB s howed different staining state.The high dose of H2O2 resulted in the increa se in apoptosis rate of HepG2 cells and made MTT activity decreased.However,af ter pretreated with low dose of H2O2,the apoptosis rate was decreased and M TT activity was increased.CONCLUSION:The high dose H2O2 induced apoptosis in HepG2 ce lls and the low dose H2O2 protected HepG2 cells against the oxidative stress .  相似文献   

9.
AIM: To observe the effect of endoxin antagonist,anti-digoxin antiserum,on endoxin level,ATPase activities,intramitochondrial total calcium concentration and gene expression of sodium pump isoforms in myocardium of rats with myocardial ischemia reperfusion (MIR).METHODS: Fifty-six male Sprauge Dawley rats were randomly divided into 7 groups.Sham operation group: silk suture threading the left anterior descending coronary artery without ligature;MIR group: left anterior descending coronary artery was subjected to 30 min ligation followed by 45 min reperfusion;normal saline group: MIR model was given 5 mL/kg normal saline;verapamil group: MIR model was given 5 mg/kg verapamil;low dose antidigoxin antiserum group: MIR model was given 8.6 mg/kg antidigoxin antiserum;middle dose antidigoxin antiserum group: MIR model was given 17.3 mg/kg antidigoxin antiserum;high dose antidigoxin antiserum group: MIR model was given 34.5 mg/kg antidigoxin antiserum.All drugs were injected into vessel via femoral vein within 5 min before reperfusion,respectively.After reperfusion,left ventricle myocardium samples were processed immediately in order to measure the activity of Na+ K+ATPase and Ca2+Mg2+ATPase,endoxin level,intramitochondrial total calcium concentration and the experssion of α1,α2,α3 and β1 isoforms of sodium pump on mRNA and protein levels by RT-PCR and Western blotting and immunohistochemical assay,respectively.RESULTS: After MIR,the level of endoxin in myocardium was obviously increased.The activities of Ca2+Mg2+ATPase and Ca2+ Mg2+ ATPase in myocardial membrane were significantly decreased while intramitochondrial total calcium concentration increased.The gene expression of the α1,α2,α3 and β1 isoforms of sodium pump at both mRNA and protein levels were reduced markedly.Only the effect of verapamil on reducing intramitochondrial total calcium concentration was observed.Antidigoxin antiserum significantly reduced the level of endoxin in myocardium,restored the activities of Na+ K+ATPase and Ca2+Mg2+ATPase,reduced intramitochondrial total calcium concentration,and up-regulated the expression of α1,α2,α3 and β1 isoforms of sodium pump at both mRNA and protein levels.CONCLUSION: MIR results in increase of endoxin secretion.The latter depresses the activity of Na+ K+ATPase by down-regulating the gene expression of α1,α2,α3 and β1 isoforms of sodium pump in myocardial membrane,and also induces intramitochondrial calcium overload,thereby mediates MIR injury.  相似文献   

10.
AIM: To observe the effects of arsenic trioxide (As2O3) on activities of matrix metalloproteinases (MMPs), expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) and transforming growth factor beta1 (TGF-β1) in human fibroblast (hFb), and to discuss weather As2O3 promotes the healing of chronic skin ulcer through regulating collagen metabolism. METHODS: Zymography was used for testing activity of MMP-9 deriving from rat polymorphonuclear neutrophils (PMNs) and activities of MMP-1, MMP-2 secreted by hFb. Immunocytochemical method was used to determine the expressions of TIMP-1 and TGF-β1. RESULTS: At the concentration of 50 mg/L, As2O3 elevated the activity of MMP-9 (P<0.01). At the concentration of 0.8 mg/L, As2O3 increased the activities of MMP-1 and MMP-2 (P<0.01, respectively). After hFb was cultured with As2O3 for 6 h, 12 h and 18 h, the expressions of TIMP-1 and TGF-β1 decreased continuously (P<0.01). CONCLUSION: As2O3 elevates the activities of MMP-1, MMP -2 and MMP-9, also inhibits the expressions of TIMP-1 and TGF-β1, suggesting that arsenic preparation may exert positive effect on healing chronic skin ulcer through regulating collagen metabolism.  相似文献   

11.
AIM: To provide the reference for optimizing the seed cells for tissue engineering,the relationship between apoptosis and differentiation in the process of induction on embryonic stem cells(ESCs) was investigated.METHODS: Day 2-3 embryoid bodys (EBs) were derived from ESCs,and then tissue growth factor-β1(TGF-β1) was added,and co-cultured with visceral endoderm like END-2 cell conditioned medium.The induced cells were evaluated by using immunofluoresence and transmission electron micrography.Cell apoptosis was analyzed using flow cytometry.RESULTS: The total percentage of beating EBs treated with TGF-β1 was 43%.All the beating cardiomyocytes derived from ESCs expressed cardiac-specific proteins for TnT,and were observed the cardiac-specific ultrastructure.Interestingly,the total percentage of beating EBs treated with TGF-β1 combined with END-2 cell conditioned medium was 88% (P＜0.01),and the beating areas were bigger.After 3 days of induction with different conditions,the apoptotic levels were (5.58%±0.65% and 9.60%±0.75%,P＜0.05),respectively.CONCLUSION: combination of TGF-β1 with co-cultured visceral endoderm like END-2 cell conditioned medium could get a higher induction efficiency on the differentiation of ESCs into the cardiomyocytes.The partly inducible effect mechanisms may induce EDCs differentiation toward a cardiac phenotype and enhance apoptosis in cells not committed to cardiac differentiation.  相似文献   

12.
AIM: To investigate the effects of rhTGF-β1 and TGF-β1 gene transfection on the proliferation of cultured rabbit corneal endothelial cells in vitro. METHODS: Cell growth induced by various concentrations of rhTGF-β1 was determined by MTT proliferation assay. Under the induction of liposomes, recombinant pSecTag2-TGF-β1MP vectors were transferred into the corneal endothelial cells. Morphological changes of transfected cells were observed by HE staining. The expression levels of TGF-β1 were assessed by ELISA. Cell cycle analysis was assessed by flow cytometry. DNA fragment analysis was used to confirm the presence of apoptosis. RESULTS: rhTGF-β1 in concentrations of 5-20 μg/L showed a significant suppressive effect on the proliferation of corneal endothelial cells, 0.5-1 μg/L had no effect, 0.05-0.1 μg/L facilitated cell growth, as compared with negative controls. The morphous of transfected corneal cells had no significant abnormality compared with normal cells. According to the result of ELISA, the concentration of TGF-β1 in the supernatant was calculated to be (98±3) ng/L. Flow cytometry assay showed that S and G2/M phase of transfected cells decreased significantly compared with that of control group, but the cell cycle recovered normally after adding 10 μg/L EGF into the culture medium. Agarose electrophoresis didn′t show marked ladders in transfected group. CONCLUSION: Effects of rhTGF-β1 on the proliferation of corneal endothelial cells are different with various concentrations. TGF-β1 gene transfection shows suppressive effect on the proliferation of cultured corneal endothelial cells, but does not induce cell apoptosis. EGF is the antagonist of this suppressive effect.  相似文献   

13.
AIM: To evaluate complement activation in patients with all forms of acute coronary syndromes (ACS) and to examine the relationship between the degree of complement activation and myocardial injury.METHODS: The subjects were divided into 2 groups: 110 ACS patients (group ACS) and 18 healthy persons (group control).One hundred and ten patients with ACS were divided into 3 sub-group: 51 patients with ST-segment elevated myocardial infarction (STEMI),28 patients with non-ST-segment elevated myocardial infarction (NSTEMI) and 31 patients with unstable angina (UA).Complement 3 (C3),complement 4 (C4),troponin T (TnT) as well as creatine kinase MB (CK-MB) were evaluated.RESULTS: Plasma C3 and C4 peak levels were significantly higher in patients with STEMI ［(1 525±302)mg/L and (423±123) mg/L］ and NSTEMI ［(1 516±289)mg/L and (396±68) mg/L］ than those in patients with UA ［(1 275±172)mg/L and (356±91) mg/L］ and the control subjects ［(1 072±196)mg/L and (182±73) mg/L］ (P<0.01 for all).Also,C3 and C4 serum levels in patients with UA were significantly higher than those in control subjects (P<0.01 for all).At one-week follow-up,plasma levels of C3 and C4 were significantly different among various days in patients with ACS (P<0.01).Plasma C3 and C4 levels in ACS showed a relationship with peak creatine kinase MB (CK-MB) and troponin T (TnT) levels (P<0.01).CONCLUSION: Plasma C3 and C4 levels are elevated in ACS in present study.The relationship between C3,C4 levels and ACS suggests that the complement activation is related to necrosis within the myocardium.  相似文献   

14.
AIM:To explore the role of extracellular signal-regulated kinases ERK1/2-STAT3 pathway in adaptive cytoprotection induced by H2O2 preconditioning in PC12 cells. METHODS:In PC12 cells, the experimental model of cytoprotection by H2O2 preconditioning against oxidative stress-induced injury was set up. The morphological changes in the apoptotic cells were observed by using of chromatin dye Hoechst 33258. The percent of apoptotic cells was determined by flow cytometry (FCM) with propidium iodide staining. The levels of p-ERK1/2 and p-STAT3 expression were detected by Western blotting assay. RESULTS:Preconditioning with H2O2 at concentration of 100 μmol/L for 90 min obviously inhibited apoptosis induced by 300 μmol/L H2O2, and both ERK1/2 and STAT3 were activated. UO126 (10 μmol/L, an inhibitor of ERK1/2) or AG-490 (10μmol/L, an inhibitor of JAK2) significantly blocked the cytoprotection effect of H2O2 preconditioning. Moreover, UO126 (10 μmol/L) also markedly inhibited the up-regulation of p-STAT3 expression by H2O2 preconditioning. CONCLUSION:H2O2 preconditioning activates ERK1/2-STAT3 signal pathway, which may be one of the mechanisms underlying H2O2 preconditioning-induced cytoprotection.  相似文献   

15.
AIM: To compare the effects of hypoxic preconditioning (HP) and mitochondrial ATP-sensitive potassium (KATP) channel opener pretreatment on the hyperpolarization-activated current (If) in sinoatrial node cells.METHODS: Sinoatrial node cells were randomized to five groups: ① Control;②Hypoxia/reoxygenation (H/R);③ HP;④ Diazoxide (mitochondrial KATP channel opener)+H/R;⑤ 5-HD (mitochondrial KATP channel blocker)+HP.At the end of the experiment, If was recorded by whole-cell patch clamp technology.RESULTS: ①H/R significantly enhanced the current densities of If, shifted the current activation curve to more positive value by changing the half-activation voltage from (-98.9±2.4)mV to (-85.2±2.5) mV (P＜0.01).② Both diazoxide pretreatment and HP remarkably reduced the augmented current density caused by H/R and shifted the current activation curve to more negative value by changing the half-activation voltage to (-90.7±5.0) mV (P＜0.01) and (-92.2±1.9) mV (P＜0.01).③ 5-HD pretreatment blocked the effects of HP and reversed the half-activation voltage to (-86.3±2.7) mV (P＜0.01).CONCLUSION: The study demonstrates that both mitochondrial KATP channel opener pretreatment and HP make current density and kinetics of If to approach normal level and to maintain electrophysiological stability of sinoatrial node cells during H/R.  相似文献   

16.
AIM: To study the effect of luteolin on endothelial cell injuries induced by H2O2. METHODS: Endothelial cells were cultured in vitro and divided into seven groups: control; solvent; H2O2; quercetin+H2O2; luteolin-L+H2O2; luteolin-M+H2O2; luteolin-H+H2O2 group, respectively. Endothelial cells were incubated with 750 μmol/L H2O2 for 18 h or 14 h in the absence or presence of various concentrations of luteolin and quercetin. The expression of caspase-3, the pro-apoptotic factors, was detected by immunohistochemical technique, and the apoptotic index was detected by flow cytometry. Meanwhile, the amount of malondialdehyde (MDA), nitric oxide (NO), lacate dehydrogenase (LDH) in serum, and cell viability were measured. RESULTS: Incubation of endothelial cells with H2O2 for 18 h elicited the increase in the extent of immunostaining for caspase-3, the rate of apoptosis, the release of LDH, and the number of dead cells accompanied by the decrease in the content of NO in the medium, which were inhibited by pretreatment of luteolin at concentrations of 0.5-50 μmol/L in a concentration-dependent manner (P<0.01). CONCLUSION: Luteolin possesses a protective effect against endothelial cell injuries induced by H2O2, which may be related with anti-oxidation, increasing the concentration of NO and inhibiting the activation of caspase-3.  相似文献   

17.
AIM:To investigate the neuroprotective effect of tubuloside B, one of the phenylethanoids isolated from the stems of Cistanche salsa, on H2O2-induced injury in PC12 cells.METHODS:PC12 cells were exposed to various doses of tubuloside B for 12 h, then treated with H2O2 at concentration of 100 μmol/L for 24 h. The cell viability was observed with MTT assay. Reactive oxygen species and the mitochondrial membrane potential were measured with laser scanning confocal microscopy (LSCM). The DNA content and percentage of apoptosis were assayed by DNA agarose gel electrophoresis and flow cytometry. The activation of caspase-3 was detected with the caspase-3 activity assay kit. RESULTS:Following treatment with H2O2 for 24 h, H2O2 induced a significant decrease in cell viability; DNA ladder was observed and apoptosis percentage was as high as 48.0%. Accumulation of intracellular ROS, increase in caspase-3 activity and the decrease in mitochondrial membrane potential as indicated with the decrease of red/green ratios (from 5.97 to 0.41) were detected. However, pretreatment with tubuloside B (1, 10 or 100 mg·L-1) for 12 h exhibited cytoprotective effects in a dose-dependent manner. Tubuloside B obviously enhanced the cell viability, reduced formation of the DNA ladder, and significantly reduced the number of cells labeled with Annexin-V. The percentage of apoptosis/necrosis neurons was significantly decreased to 30.9%, 18.3% and 6.2%, respectively. LSCM showed that the tubuloside B attenuated the accumulation of ROS and the H2O2-induced collapse of mitochondrial membrane potential in PC12 cells. The significant decrease in caspase-3 activity was detected, compared to the H2O2-treated cells at the same time point. CONCLUSION:Tubuloside B has the neuroprotective capacity to antagonize H2O2-induced apoptosis and injury in PC12 cells, indicating it may be useful for treating some neurodegenerative diseases.  相似文献   

18.
AIM: To study the effect and mechanism of chlorophyllin (CHL) inhibiting HT29 cells. METHODS: IC50 value and growth curve of HT29 cells were detected with MTT method. Apoptosis was detected with Wright-Giemsa staining, FCM and DNA electrophoresis. Telomerase was detected by PCR-ELISA, and protein and mRNA expression of COX-2 gene were detected through RT-PCR and Western blot. RESULTS: CHL inhibited the growth of HT29 in a dose-dependent manner. CHL blocked HT29 cells in G1 phase but did not induce apoptosis. Different concentration of CHL inhibits the expression of telomerase and COX-2 in HT29 cells. CONCLUSION: CHL inhibited the growth of HT29 cells by inhibiting the expression of telomerase and COX-2 and blocking cells in G1 phase.  相似文献   

19.
AIM: To investigate the effect of isopsoralen(ISR) on the expression of estrogen receptor (ER) in human lens epithelial cells (HLECs). METHODS: HLECs were cultured and sub-cultured in vitro. The cultured HLECs pretreated with E2 or ISR were exposed to H2O2 at the concentration of 300 μmol/L. The expression of ERα and ERβ in HLECs was analyzed by flow cytometry. RESULTS: The expression of ERα and ERβ in H2O2 group was obviously decreased as compared to control group (P<0.01). The expression of ERα and ERβ in the cells treated with E2 and with ISR at the concentration of 10-5 mol/L, 10-6 mol/L or 10-7 mol/L plus H2O2 was obviously increased as compared to the cells treated with H2O2 only (P<0.01). A concentration-dependent effect of ISR was observed. CONCLUSION: H2O2 decreases the expression of ERα and ERβ in HLECs.E2 and ISR increase the expression of ERα and ERβ in HLECs treated with H2O2 in a concentration-dependent manner, which may account for their antioxidative effect.  相似文献   

20.
AIM: To observe the effects of Tongxinluo (TXL), a Chinese medicine, on hypoxic tolerance and expression of Bcl-associated X (Bax) and B-cell leukemia/lymphoma 2 (Bcl-2) in hypoxia-preconditioned mice. METHODS: The mice were randomly divided into groups of hypoxia preconditioning without (control group) or with TXL treatment (TXL group). The mice in TXL group were administered with TXL at dose of 1.52 g·kg-1·d-1 crude drug for 5 days. The mouse was exposed to normoxia (0 run, H0) and acute repetitive hypoxia for 1-5 runs (H1-H5) by placing the animal in an air-sealed jar. The hypoxic environment was established in the jar through consumption of the oxygen by the respiration of the mouse. A gasp breath was regarded as the hypoxic tolerant limit of the mouse and the animal was then transferred to another new jar. The mouse was exposed to hypoxia in this way for 5 times. In each run of hypoxic exposure, the time of hypoxic tolerance was measured. Western blotting was used to measure the protein levels of hypoxia inducible factor-1α (HIF-1α), Bax and Bcl-2 in the cerebral cortex. RESULTS: The hypoxic tolerance time in control and TXL groups was gradually increased run by run (P<0.01 or P<0.05). The protein levels of HIF-1α and Bcl-2 in the two groups were gradually increased (P<0.01 or P<0.05). Bax in control and TXL groups was significantly increased in H1. After H1, Bax was decreased run by run (P<0.01 or P<0.05). Compared with control group, the tolerance time, the expression of HIF-1α and Bcl-2 in the cerebral cortex in TXL group were increased in H1,H3 and H5. However, the expression of Bax was lower than that in control group in every run. CONCLUSION: Hypoxia preconditioning makes the organism produce a strong adaptive response. The increase in Bcl-2 and the decrease in Bax may be involved in the mechanism of adaptation. TXL obviously increases the adaptive ability of the mice to hypoxia.  相似文献   

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