共查询到20条相似文献,搜索用时 15 毫秒
1.
AIM: In order to investigate the mechanisms involved in the vascular hyporeactivity after hemorrhagic shock, the changes of Ca2+ release from calcium store in vascular smooth muscle cells (VSMCs) with hypoxia were observed and the role of Ca2+ release from calcium store in the occurrence of vascular hyporeactivity to norepinephrine (NE) after hemorrhagic shock in rats was further explored.METHODS: A hemorrhagic shock model (40 mmHg for 2 h) in rats and a VSMCs hypoxic model were established. The changes of intracellular Ca2+ concentration in VSMCs were evaluated by fura3-AM and the role of IP3R and RyR mediated Ca2+ release from calcium store was further observed. The role of IP3R and RyR mediated Ca2+ release from Ca2+ store in the development of vascular hyporeactivity was measured with an isolated organ perfusion system. RESULTS: In the absence of extracellular Ca2+, NE upregulated by mobilizing Ca2+ release through calcium store. Compared to the normal control, the VSMCs had a slight increase when treated with hypoxia and NE-induced intracellular down-regulated, both without significant difference. Compared to the normal control cells, there was a significant change of Ca2+ release from calcium store in hypoxia-treated VSMCs, characterized by the significant increase in triggered by RyR-sensitive Ca2+ releasing activator caffeine. However, the increase in triggered by IP3R-mediated Ca2+ release agonist adenophostin A (10-5 mol/L) and ATP-Na2 (10-4 mol/L) had no significant difference in hypoxic VSMCs. Furthermore, the vascular reactivity to NE decreased in abdominal aorta in hemorrhagic shock (40 mmHg, 2 h) rats. The activation of IP3R mediated Ca2+ release with ATP-Na2 (10-4 mol/L) did not improve the vascular reactivity to NE, while inhibition of IP3R mediated Ca2+ release with heparin (104 U/L) significantly antagonized the vascular reactivity to NE in hemorrhagic shock rats. In addition, in normal K-H solution (with about 2.2 mmol/L) and Ca2+-free K-H solution, RyR antagonist ryanodine (10-5 mol/L) partly restored the vascular reactivity to NE in hemorrhagic shock rats, while RyR agonist caffeine(10-3 mol/L) further decreased the vascular reactivity. CONCLUSION: The over-activation of RyR-mediated Ca2+ release from calcium store is partly involved in the development of vascular hyporeactivity after hemorrhagic shock in rats. 相似文献
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AIM: To investigate the role of intracellular free Ca2+ concentration ([Ca2+]i) in the regulation of calcium-activated chloride (ClCa) channels in pulmonary artery smooth muscle cells (PASMCs) of rats under normoxic, acute and chronic hypoxic conditions. METHODS: Acute hypoxia-induced contraction was observed in rat pulmonary artery by using routine blood vascular perfusion in vitro. The fluorescence Ca2+ indicator Fura-2/AM was used to observe [Ca2+]i of rat PASMCs in normal and chronic hypoxic condition. The influences of ClCa channels on PASMCs proliferation were assessed by MTT assay. RESULTS: (1) The ClCa channel blockers niflumic acid (NFA) and indaryloxyacetic acid (IAA-94) produced inhibitory effects on acute hypoxia-evoked contractions in pulmonary artery. (2) Under chronic hypoxic condition, [Ca2+]i was increased. In normoxic condition, [Ca2+]i was (123.63±18.98) nmol/L, and in hypoxic condition, [Ca2+]i was (281.75±16.48)nmol/L (P<0.01). (3) In normoxic condition, [Ca2+]i had no significant change and no effect on ClCa channels was observed (P>0.05). (4) Chronic hypoxic increased [Ca2+]i which opened ClCa channels. The NFA and IAA-94 blocked them and decreased [Ca2+]i from (281.75±16.48)nmol/L to (117.66±15.36)nmol/L (P<0.01). (5) MTT assay showed that in chronic hypoxic condition NFA and IAA-94 decreased the value of absorbing light degree (A value) from 0.459±0.058 to 0.224±0.025 (P<0.01). CONCLUSION: Hypoxia increased [Ca2+]i which opened ClCa channels and had a positive-feedback to [Ca2+]i. This may play an important role in hypoxic pulmonary hypertension. In chronic hypoxic condition, ClCa channel may play a role in the regulation of PASMCs proliferation. 相似文献
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JIANG Qing-song HUANG Xie-nan ZHOU Qi-xin YANG Gui-zhong DAI Zhi-kai WU Qin SHI Jing-shan 《园艺学报》2007,23(7):1272-1276
AIM: To study the role of prostaglandin F2α (PGF2α) in cardiac hypertrophy and its relation with calcineurin (CaN) signal transduction pathway in vitro. METHODS: The cultured neonatal rat cardiomyocyte was used to observe the hypertrophic effect of PGF2α, and the hypertrophic response was assayed by measuring the cell diameter, protein content and atrial natriuretic factor (ANF) mRNA expression. For mechanism studies, the intracellular free calcium concentration ([Ca2+]i) in cultured cardiomyocytes was measured by using Fura-2/AM as a fluorescent indicator. ANF and CaN mRNA expressions, and the expressions of CaN and its downstream effectors, NFAT3 and GATA4 proteins were assayed by RT-PCR and Western blotting, respectively.RESULTS: In cultured cardiomyocytes, PGF2α induced profound hypertrophic morphology change, the significant increase in cell diameter and protein content in a concentration-dependent manner compared with those in vehicle control (P<0.01). The same result was found in measuring the [Ca2+]i in cardiomyocytes (P<0.01). PGF2α at concentration of 10-7 mol/L significantly promoted ANF and CaN mRNA expressions and the protein expressions of CaN/NFAT3/GATA4 compared with those in the vehicle control (P<0.05). Cyclosporin A, a CaN inhibitor, markedly inhibited the myocyte hypertrophy (P<0.01), reduced the increased [Ca2+]i(P<0.01) and decreased the expressions of CaN mRNA and CaN/NFAT3/GATA4 proteins (P<0.05) compared with those of only PGF2α 10-7 mol/L treatment. CONCLUSION: Cardiomyocyte hypertrophy induced by PGF2α may be, at least in part, mediated by CaN signal transduction pathway activated by increasing [Ca2+]i. 相似文献
4.
AIM:To study the effect of chronic hypoxia (CH) on the intracellular calcium ([2+]i) in pulmonary artery smooth muscle cells (PASMCs) and the role of L-type calcium channel and calcium store. METHODS:The rat chronic hypoxia model was set up and intervene the PASMCs with normal PSS, calcium-free PSS, nifedipine, and heparine respectively. The resting [Ca2+]i was determined with the Fura-2/AM calcium imaging technique. RESULTS:(1) The [Ca2+]i in CH group in normal PSS was higher than that in control group in normal PSS (P<0.05). The [Ca2+]i in CH group in normal PSS was higher than that in calcium-free PSS (P<0.05). (2) No obvious change of [Ca2+]i before and after application of nifedipine in PASMCs of CH groups was observed. (3) No difference of [Ca2+]i before and after application of heparine in PASMCs of CH groups was detected. CONCLUSION:Chronic hypoxia increased the [Ca2+]i in PASMCs. Chronic hypoxia induced increase in [Ca2+]i may relate to the influx of extracellular calcium, but not due to the L-type calcium channel or the IP3R modulation only. 相似文献
5.
AIM: To investigate the effect of neuropeptide Y (NPY) on intracellular free calcium([Ca2+]i) and Ca2+ sarcoplasmic reticulum of cardiomyocytes in rats.METHODS: Cardiomyocytes of neonatal Sprague-Dawley rats were incubated with NPY at concentration of 100 nmol/L for 24 h. Fluorescent indicator Fluo-4 AM was used to detect [Ca2+]i and Fluo-5N AM was used to detect Ca2+ in sarcoplasmic reticulum (SR). Calcium image was recorded by laser scanning confocal microscope. The SR Ca2+ load was estimated by caffeine-induced Ca2+ transient (CCT). RESULTS: 24 h after incubation with NPY, compared with control group, the concentration of [Ca2+]i was significantly elevated (P<0.05), and the concentration of free Ca2+ in SR ([Ca2+]SR) was significantly decreased (P<0.05), and the peak of CCT was attenuated.CONCLUSION: Stimulation with NPY for 24 h causes redistribution of free calcium in rat cardiomyocytes, namely the elevation in [Ca2+]i and decline in [Ca2+]SR. 相似文献
6.
AIM: To investigate the effects of high-fat diet on the level of intracellular free calcium ([Ca2+]i) and the activity of angiotensinⅠconverting enzyme (ACE) in alveolar macrophages (AMs) of rabbits.The association between asthma and high-fat diet was also observed.METHODS: Twelve male New Zealand rabbits were medially divided into normal diet group and 1.2% high-cholesterol diet group randomly.8 weeks later,bronchial alveolar lavage was performed in vitro.[Ca2+]i was determined by Fluo-2/am.The activity of ACE was detected with ultraviolet method.RESULTS: The levels of [Ca2+]i in AMs greatly increased (P<0.01).The activity of ACE both in BALF and in culture supernatants of AMs was all greatly increased compared with normal diet group (P<0.01).In hypercholesterolemic group the number of macrophages in BALF showed a positive correlation with the content of cholesterol in serum,such as the level of [Ca2+]i in AMs and the activity of ACE in the culture supernatants of AMs (all P<0.05).CONCLUSION: The results suggest that AMs of rabbits may be activated by hyperlipoidemia and become ease to be stimulated. 相似文献
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SHAO Jian-lin WANG Ling-ling WANG Jun-ke MA Hong-zhong WU Bin-yang SONG Da-yong 《园艺学报》2007,23(12):2317-2321
AIM: To investigate the effect of hydrogen sulfide on neuron apoptosis through PI3-K/Akt/P70S6K cell-survival signal transduction pathways after neuron anoxia-reoxygenation.METHODS: Newborn (24-48 h) Wistar rats were decapitated.The hippocampus tissue was dissected and cells were suspended.Cells were plated at 1.0×108 cells/L on poly-dlysine-treated 96-well (100 μL/well) plates and 6-well (2 mL/well) plates.Cells were used after 7 days.For anoxia-reoxygenation (oxygen glucose deprivation,OGD) experiments,cells were washed three times in a glucose-free balanced salt solution (BSS).They were then placed in deoxygenated glucose-free medium and cultured under 95% N2,5% CO2 in an anaerobic chamber equilibrated to 37 ℃ and 100% humidity for 45 min.OGD was terminated by replacement of stored medium and by returning the cultures to a standard incubator maintained at 37 ℃ in 95% air,5% CO2.In experimental group,cells were respectively carried out OGD,OGD+150 μmol/L NaHS,OGD+150 μmol/L NaHS+10 μmol/L triciribin,OGD+150 μmol/L NaHS+10 nmol/L rapamycin and OGD+150 μmol/L NaHS+10 μmol/L triciribin+10 nmol/L rapamycin.Control cells were cultured normally.24 h later,neuron viability and apoptosis were measured.The level of cAMP and protein expression of PI3-K,Akt and P70S6K were detected.RESULTS: NaHS enhanced concentration of cAMP and expression of PI3-K,Akt and P70S6K.Meanwhile,increased neuron viability and decreased neuron apoptosis (P<0.01 vs group C or group I/R) were observed.Triciribin inhibited Akt and P70S6K,as well as increased neuron apoptosis and decreased neuron viability (P<0.05,P<0.01 vs group NaHS).Rapamycin inhibited P70S6K,as well as increased neuron apoptosis and decreased neuron viability (P<0.05,P<0.01 vs group NaHS).CONCLUSION: H2S inhibits hippocampus neuron apoptosis and protects neuron from anoxia-reoxygenation injury through cAMP-mediated PI3-K/Akt/P70S6K kinase cell-survival signaling pathways. 相似文献
9.
LIAO Xin-xue WANG Yan-li GUO Rui-xian SUN Sheng-nan HU Fen CHEN Pei-xi FENG Jian-qiang 《园艺学报》2008,24(9):1839-1844
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
10.
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
11.
AIM:To study the effect of VEGF on extracellular H2O2 production in HUVECs and the role of H2O2 in the VEGF-induced proliferation. METHODS:HUVECs was stimulated with 500 μg/L VEGF. Products of extracellular H2O2 was detected by H2DCFDA staining. MTT method was used to value the influences of 3×106 U/L catalase and 5-20 mmol/L H2O2 to VEGF function. RESULTS:After treatment for 15 min with VEGF, HUVECs appeared fluorescence, and continued to become stronger, peaked at 45 min then decreased. HUVECs, which was treated simultaneity with VEGF and 3×106 U/L catalase, only appeared very faint fluorescence. The proliferation of HUVECs by VEGF was restrained when treated with 3×106 U/L catalase. The extrinsic H2O2 at concentration of 5-10 mmol/L promoted the proliferation of HUVECs but inhibited the proliferation effect of VEGF on HUVECs (P<0.01). CONCLUSION:These findings indicate that VEGF induces HUVECs to produce extracellular H2O2 and plays role in proliferation, but extrinsic H2O2 restrains VEGF function. 相似文献
12.
XIE Tong-jie HONG Bing-zhe LI Sheng-fan WANG Li-ping PIAO Hai-nan GAO Li-jian LIU Xue-tian CHEN Yu-ting 《园艺学报》2008,24(9):1665-1669
AIM:The mechanism of angiopoietin-1 (Ang-1) in mediating increase in intracellular free magnesium ([Mg2+]i) in human umbilical vein endothelial cells (HUVECs) was investigated in this study. METHODS:The change of [Mg2+]i in HUVECs was quantitatively detected in intracellular cation measurement system via loaded with the fluorescent magnesium indicator mag-fura-2. RESULTS:Ang-1 increased [Mg2+]i, and there was not any significant difference among the groups of 0 mmol/L and 1 mmol/L of extracellular Mg2+. Similar results were obtained in groups done with Ca2+. Pretreatment with tyrosine kinase inhibitors (tyrphostin A23 and genistein), phosphatidylinositol 3-kinase (PI3K) inhibitors (wortmannin and LY294002) blocked the increase in [Mg2+]i induced by Ang-1. However, mitogen-activated protein kinase inhibitors (SB202190 and PD98059) had no effect on the Ang-1-induced [Mg2+]i increase. CONCLUSION:These results suggest that the increase in [Mg2+]i by Ang-1 come from intracellular Mg2+ pools mediated by tyrosine kinase/PI3K -dependent signaling pathways. 相似文献
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LIU Guo-tong YANG Cheng-ming WANG Xu-kai ZENG Chun-yu WANG Hong-yong FANG Yu-qiang FU Chun-jiang SHI Wei-bin 《园艺学报》2007,23(3):514-517
AIM:To investigate the changes of intracellular calcium ion (Ca2+) concentration in mouse H9c2 (2-1) cells transfected with or without FK506 binding protein 12.6(FKBP12.6) gene by ultrasound mediated destruction of microbubbles. METHODS:The pcDNA3.1-FKBP12.6 plasmid, mingled with albumin-coated microbubbles agents, was transfected into H9c2 (2-1) cells by ultrasound-mediated destruction of microbubbles. The H9c2 (2-1) cell growth state was investigated by inverted microscope. The changes of intracellular Ca2+ concentration was determined by laser scanning confocal microscope. The FKBP12.6 protein expression was checked by immunohistochemistry. RESULTS:As compared with control cells, the H9c2 (2-1) cells, transfected with FKBP12.6 gene, grew better, had higher gross intracellular Ca2+ concentration. CONCLUSION:FKBP12.6 gene augments Ca2+ concentration in mouse H9c2 (2-1) cells, enhances the contractibility of the myocardial cell, which may be helpful to improve the myocardial dysfunction. 相似文献
14.
JIANG Yu-feng WANG Qiu-hua LIU Zhi-qin CAO Xu -quan REN Li-wei CAI Da-yong LIU Shi-jing HUANG Qi-fu 《园艺学报》2007,23(12):2300-2303
AIM: To explore the effects of salvianolic acid B (SalB) on the energy metabolism and hydrocephalus in mice with cerebral ischemia.METHODS: NIH mice were randomly divided into four groups: sham-operated group,cerebral ischemia group,SalB-treated group and nimodipine-treated group.The brain tissue energy charge (EC),phosphocreatine (PCr),the activity of ATPase,excitability amino acid (EAA) content and water content of brain were measured when cerebral ischemia for 30 min.RESULTS: EC (0.520±0.034),PCr content [(98.344±13.249) μmol/g],the activity of Na+-K+-ATPase [(0.593±0.013)×103 U/g] and Ca2+-ATPase [(0.484±0.053)×103 U/g] in SalB-treated group were significantly higher than those in cerebral ischemia group {EC (0.465±0.037),PCr content [(81.614±9.919) μmol/g] ,the activity of Na+-K+-ATPase [(0.244±0.065)×103 U/g],the activity of Ca2+-ATPase [(0.321±0.086)×103 U/g]} (P<0.01).The glutamate (Glu) content [(0.405±0.110) μmol/g],aspartate (Asp) content [(0.141±0.020) μmol/g] and water content of brain [(38.1±0.1)%] in SalB-treated group were markedly lower than those in cerebral ischemia group [ Glu content (0.550±0.140) μmol/g,Asp content (0.287±0.050) μmol/g,water content of brain (44.1±0.1)%] (P<0.05,P<0.01).CONCLUSION: The increase in cerebral energy metabolism and the activity of ATPase,and decrease in EAA content in brain tissue are the mechanism of SalB alleviating hydrocephalus at the early stage of cerebral ischemia in mice. 相似文献
15.
YUAN Zhen-yu YE Chun-ling JIN Yong-liang SUN Jing-bo YE Kai-he JIANG Jia-hua 《园艺学报》2006,22(7):1295-1299
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
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AIM: To explore the role of endothelin-1 (ET-1) in initiating transdifferentiation of sub-epithelial fibroblasts (SEFs) into myofibroblasts and its ionic and signal transduction mechanism.METHODS: Human SEFs or SEFs plated in collagen gels were co-cultured with human bronchial epithelial cells (16HBE) treated with lipopolysaccharide (LPS) plus mechanical scratch. ET receptor A inhibitor (BQ123) or the inhibitors specific for p38 MAPK, ERK1/2 were added, repectively. The expression of α-smooth muscle actin (α-SMA) in the SEFs and contractility of the collagen gels containing with SEFs as well as the effects of p38 MAPK or ERK1/2 on α-SMA expression were evaluated. Using Ca2+ sensitive Fluo-3/AM, dynamic changes of intracellular calcium concentration ([Ca2+]i) were observed in the SEFs by laser confocal microscopy.RESULTS: Injured 16HBE induced the transdifferentiation of myofibroblasts, which expressd α-SMA and increased contractility. BQ123 blocked the induction to a certain extent. Injured 16HBE activated p38 MAPK and ERK1/2 pathways in SEFs, both inhibitors of p38 MAPK and ERK1/2 attenuated the induction of α-SMA by injured 16HBE. The addition of exogenous ET-1 enhanced α-SMA expression and activated p38 MAPK, ERK1/2 pathways in the SEFs. Additionally, ET-1 significantly facilitated Ca2+ inflow into the fibroblasts.CONCLUSION: Injured 16HBE induces the transdifferentiation of SEFs into myofibroblasts, which is involved in the activation of p38 MAPK and ERK1/2 pathways. The ET-induced influx of Ca2+ may be an early signal for initiating the myofibroblasts transdifferentiation. 相似文献
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AIM: To study the mechanisms of salvianolic acid B (Sal B)antagonizing mesangial cell activation and kidney fibrosis through investigating the effect of Sal B on expression of transforming growth factor-β1 (TGF-β1) receptors and Smad2 in TGF-β1-stimulated renal mesangial cell activation. METHODS: Mesangial cells was isolated and purified from rat kidney. TGF-β1 was used to establish rat primary mesangial cell activation model and Smad2,Smad7 protein expression was detected. Sal B (10-6 mol/L and 10-5 mol/L) was employed to treat the cells; α-smooth muscle actin(α-SMA) expression was analyzed by immunofluorescence staining and Western blotting. Mesangial cells were treated with Sal B alone or additional with TGF-β1,and TGF-β1 receptor Ⅰ (TβRⅠ),TGF-β1 receptorⅡ (TβRⅡ),Smad2 phosphorylation and Smad2 protein expression was determined by Western blotting. RESULTS: Cell ular model was established by incubating with 5 μg/L TGF-β1 for 24 h,and in early stage Smad2 was significantly phosphorylated. Sal B (10-6 mol/L and 10-5 mol/L) could inhibit α-SMA expression,which was the biomarker of activated mesangial cells. In addition,in Sal B group,the protein expression of TβRⅠand TβRⅡ was significantly down-regulated while Smad2 phosphorylation in mesangial cells was inhibited. CONCLUSION: Sal B inhibits the TGF-β1-Smad pathway,the protein expression of TβRⅠ,TβRⅡ and Smad2 phosphorylation in mesangial cells,which is probably one of the mechanisms of Sal B alleviating kidney fibrosis. 相似文献
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Upregulatory effect of isopsoralen on expression of estrogen receptor in human lens epithelial cells
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
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AIM: To investigate the antitumor effect and mechanism of trichosanthin (TCS) on melanoma B-16 cells.METHODS: (1) The injury of B-16 cells by trichosanthin was observed with SCGE and hoechst33258 staining method.(2) LCSM and specificity fluorescent probe Fluo-3/AM,H2DCF-DA,DAF-FM diacetate were applied to analyze the dynamic changes of Ca2+,ROS and NO in single cell cultured with TCS.Simultaneously,the relationship between ROS,NO and increase of Ca2+ was also revealed.RESULTS: (1)When treated with TCS (50 mg/L) for 3 h and 6 h,neither cytotoxicity assay nor SCGE showed the differences compared with control group.After 12 h incubation,specificity phenomena of DNA injury-comet tail appeared in SCGE and chromatin condensation even apoptotic body formation were seen by Hoechst33258 staining.(2) TCS (50 mg/L) evoked rapid enhancement of the production of Ca2+,ROS and NO in the cell and the differences between TCS and control group had statistical significance (P<0.01).Augment of ROS and NO was involved in the increase of Ca2+.CONCLUSION: Trichosanthin has relatively strong cytotoxicity on melanoma B-16 cells and contributes to apoptosis as well.Trichosanthin-induced apoptosis is related to the increase of Ca2+,NO and ROS in the cells. 相似文献