共查询到20条相似文献,搜索用时 140 毫秒
1.
AIM: To explore the localization and semi-quantification of the glomerular complement C5b-9 complexes and synthesis of some inflammatory mediators or cytokines such as nitric oxide (NO) and tumor necrosis factor α(TNFα) in the rats with anti-thymocyte serum nephritis(ATSN). METHODS: The animal model of rat ATSN was reproduced by a single intravenous injection of anti-thymocyte serum (ATS). Then, the deposits of glomerular C5b-9 complexes were localized and quantified by immunohistochemical staining and microscopic image scanning separately. And the glomerular mesangial cells (MC) surrounded by C5b-9 complexes were counted under microscope. In addition, the expression of glomerular MC inducible NO synthase(iNOS) mRNA and excretion of urinary NO metabolite (NO-2/NO-3) and TNF α in the rats with ATSN were detected. RESULTS: The MC in the rats with ATSN emerged necrosis followed by a rapid proliferation. In the early time of MC injury, the C5b-9 complexes were mainly seen in glomerular mesangium and MC surface. But with the progression of ATSN, the MC enclosed by C5b-9 appeared gradual decrease. Moreover, the expression of MC iNOS mRNA in early stage of ATSN obviously increased and the excretion of urinary NO-2/NO-3 and TNF α also significantly increased. However, the changes of parameters mentioned above in ATSN proliferative stage (after 7 days) alleviated gradually. CONCLUSION: The secondary lysis of MC has relation to the deposition of C5b-9 complexes and synthesis and release of NO and TNF α in rats with ATSN. 相似文献
2.
AIM: To study the effects of nitric oxide (NO) on mitochondrial damage caused by exogenous calcium. METHODS: Normal myocardial mitochondria were divided into three groups; L-arginine control group (CG), Ca2+-damaged group (DG) and L-NAME-preserved group (PG). Mitochondria of all groups were incubated at 30 ℃ with reaction medium containing 20 μmol/L EDTA, 100 μmol/L CaCl2 and 1 μmol/L L-NAME with 100 μmol/L CaCl2 respectively. Then the NO2-/NO3- contents, mitochondrial viability and membrane potential were investigated. RESULTS: The NO2-/NO3- contents of DG was obviously higher than that of CG and PG, meanwhile, there was no obvious difference between CG and PG. Mitochondrial viability and membrane potential of DG were significantly lower than that of CG and PG, and negatively related to NO-2/NO-3 contents (r=-0.5297, P<0.01; r=-0.6041, P<0.01). But, the mitochondrial viability and membrane potential of PG were still lower than that of CG. CONCLUSION: Exogenous calcium could activate mitochondrial nitric oxide synthase resulting in NO production and the latter play an important role in decreasing mitochondrial viability and membrane potential. 相似文献
3.
AIM: To investigate the effects of extract of Ginkgo biloba (EGB) on the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) induced by tumor necrosis factor a(TNF-α) in bovine aortic endothelial cells(BAECs). METHODS: The BAECs were incubated with TNF-α, followed by EGB treatment. The effect of EGB on LOX-1 expression was investigated by RT-PCR and Western blotting. The content of endothelial nitric oxide synthase (eNOS) was determined by Western blotting. Potential involvement of signaling pathways of the effects was explored by using related inhibitors of the signal molecules. The concentration of NO-2/NO-3 was also tested. RESULTS: Increased LOX-1 expression was induced by TNF-α. EGB markedly prevented the increase of LOX-1 expression induced by TNF-α (P<0.05), and this effect was inhibited by inhibitor of NOS (P<0.05). EGB significantly prevented the decrease of eNOS expression induced by TNF-α (P<0.05). EGB also significantly prevented the decrease of NO-2/NO-3 production induced by TNF-α (P<0.05). CONCLUSION: EGB markedly prevents the increase of LOX-1 expression induced by TNF-α and the effect is mediated by eNOS. 相似文献
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5.
CHEN Xiao-ling HUANG Shan-sheng LI Ying-min LI Wen-bin WANG Xin-liang WANG Qiu-hong 《园艺学报》2001,17(6):534-537
AIM: To observe the kinetic alteration of nitric oxide formation in the lungs in the development of pulmonary fibrosis in the rat. METHODS: The contents of hydroxyproline in the lungs, NO2-/NO3- (nitrite/nitrate) in out-flowing and in-flowing pulmonary blood (OPB, IPB) were assayed on the day 7, 14, 21, 30 and 70 after intratracheal administration of bleomycin A5 . The content of NO2-/NO3- in supernatants of culture of the alveolar macrophages (AMs) and the amount of iNOS positive stain cells in lung tissue section were also observed in the rat on 14th day after-bleomycin A5 administration. RESULTS: The content of lung hydroxyproline had no change on the 7th day, increased on the 14th day (P<0.05), increased significantly on the 21th day, 30th day and 70th day post-bleomycin A5 compared with control rats. On the 7th day and 14th day, the content of NO- 2 /NO3- increased in OPB and decreased in IPB (P<0.01). On the 21th day, the content of NO2-/NO3- abated in OPB (P>0.05) but still decreased in IPB (P<0.01). On the 30th day and the 70th day, the NO2-/NO3- level recovered both in OPB and IPB. AMs from rats on the 14th day post-bleomycin A5 showed significant elevation (P<0.01) in NO2-/NO3- level. The amount of iNOS positive stain cells increased in rats on the 14th day post-bleomycin A5. CONCLUSION: The amount of NO in the lungs was high in the initial phase of fibroproliferative reaction induced by bleomycin A5 ,and these might be associated with the enhanced ability of AMs to release NO and the increased amount of iNOS. 相似文献
6.
AIM: To investigate the effects of Schisandrin B (Sch B) on apoptosis of lens epithelial cells (LEC) treated with H2O2. METHODS: Eyes in SDrats were excised and lenses were separated under operating microscope in sterilized condition. Lenses were divided randomly into four groups with different treatment: control group, hydrogen peroxide group (H2O2), pirenoxine sodium group (PS) and schisandrin Bgroup (Sch B). Lenses were incubated in CO2 incubator for 24 h with 300 μmol·L-1 H2O2 and with or without 0.5 mmol·L-1 Sch B. LECaoptosis and apoptosis rate were measured by TUNELmethod. Ultrastructure changes and apoptosis bodies of LECwere observed via transmitted electron microscope. RESULTS: (1) Apoptosis rate in H2O2 group (92.0±2.6) was significantly higher than that in control group (3.5±1.8). Apoptosis rate in Sch Bgroup (13.8±3.27) was remarkably lower than that in H2O2 group and PSgroup. (2) Ultrastructure observation indicated that apoptosis cells occurred in most LEC in H2O2 group and the changes were severe presenting different stages. While a few apoptosis cells were observed in Sch Bgroup, the changes were slight and most of them were in early and middle stages. CONCLUSION: These data indicated that Sch Bsignificantly inhibited apoptosis of LECduring experimental oxidative injury, the effects were stronger than PS. 相似文献
7.
AIM:To investigate the role of nuclear factor κB (NFκB) in the induction of iNOS gene by TNFα and LPS in endothelial cells and the effect of antioxidant on the induction of iNOS. METHODS:Nitrite was determined based on Griess reaction. iNOS mRNA was analyzed using Northern blot. NFκB in the cell nucleole was detected with electrophoretic mobility shift assay.RESULTS: (1)NO production and iNOS mRNA expression induced by LPS and TNFα was blocked by pyrrolidine dithiocarbamate(PDTC) or N-acetylcysteine(NAC). (2)LPS and TNFα triggered the activation and translocation of NFκB, and PDTC or NAC inhibited the activation of NFκB induced by LPS and TNFα. CONCLUSIONS:(1)The induction of iNOS gene by TNFα and LPS is dependent on the activation of NFκB.(2)Antioxidants may inhibit the induction of iNOS gene through the inhibition of NFκB activation. 相似文献
8.
AIM:To study the current density and function of Na+ channel in cells from the epicardial border zone of the 1-week infarcted rabbit heart.METHODS:Rabbits were infarcted by ligation of the left anterior descending coronary artery.1 week later, INa was recorded using whole cel patch-clamp techniques in ventricular my ocytes from infarcted heart(IZs)and compared with the INa from noninfarcted heart(NZs).RESULTS:Peak INa current density(at -30 mV) was significantly reduced in IZs(22.48±4.62 PA/PF, n=14) compared with NZs(45.50±5.33 PA/PF, n=12), P<0.01;V0.5 of the availability curve(I/Imax curve)was shifted significantly in the hyperpolarizing direction in IZs(-89.1±5.6 mV, n=6) compared with NZs (-76.2±5.3 mV, n=5), P<0.05.Recovery of INa from inactivation was significantly slower in IZs.CONCLUSIONS:INais reduced, and its kinetics are altered in IZs.These changes may underlie the altered excitability and postrepolarization refractoriness of ventricular fibers of the IZs, thus contributing to reentrant arrhymias in the infarcted heart. 相似文献
9.
GU Hong-jiao CHEN Xiao-hua KONG Tian-yu HU Huan LIU Ning-ning XIONG Xu-ming ZHANG Zhen-hui 《园艺学报》2017,33(7):1209-1213
AIM:To evaluate the effect of inhibiting ubiquitin-specific protease 14(USPl4) activity on oxidative stress induced by H2O2 of H9c2 cells.METHODS:The H9c2 cells were incubated with H2O2 at 25 μmol/L for 2 h to establish the oxidative stress injury model.The cells were divided into control group,H2O2 group,IU1 group (25 μmol/L or 50 μmol/L) and IU1+H2O2 group.The H9c2 cells activity was measured by MTS assay.The level of intracellular reactive oxygen species (ROS) and cell survival rate were analyzed by flow cytometry assay.The changes of the mitogen-activated protein kinase (MAPK) family related proteins were detected by Western blot.RESULTS:Compared with control group,the cell activity and the viability rate in H2O2 group were decreased (P<0.05),while the intracellular ROS,the protein levels of Bax/Bcl-2,P53,p-ERK1/2,p-JNK and p-P38 were increased (P<0.05).Compared with H2O2 group,the cell activity and the viability rate of the H9c2 cells in IU1+H2O2 group were increased (P<0.05),while the intracellular ROS,the protein levels of Bax/Bcl-2,P53,p-ERK1/2,p-JNK and p-P38 were decreased (P<0.05).CONCLUSION:Inhibition of USPl4 activity reduces the oxidative stress injury of the H9c2 cells.The mechanism may be related to inhibition of the MAPK signaling and down-regulation of apoptosis related proteins. 相似文献
10.
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
11.
AIM: To explore the role of endogenous and exogenous hydrogen sulfide (H2S) in acute lung injury (ALI) induced by ischmia-reperfusion (IR) of hind limbs in rats.METHODS: A Sprague-Dawley rat model of acute lung injury was induced by ischemia of the hind limbs for 4 h and reperfusion for another 4 h. The rats (n=120) were randomly divided into 4 groups: control, IR, NaHS (H2S donor)+IR, and propargylglycine +IR. The animals were sacrificed after reperfusion. Lung weight/body weight ratio (LW/BW) was measured and calculated. Morphological changes of the lung tissues were observed. The concentrations of H2S, nitric oxide (NO) and carbon monoxide (CO) in plasma were tested. The content of malondialdehyde (MDA), the activity of CSE, inducible nitric oxide synthase (iNOS) and hemeoxygenase (HO) in the lungs were determined. The polymorpho-nuclear neutrophils(PMN) and protein content in bronchoalveolar lavage fluid(BALF) were also measured. The correlation of H2S content with the above indices was analyzed.RESULTS: Compared with control group, severe injuries of the lung tissues, raised LW/BW, MDA concentration, PMN and protein contents in BALF were observed in IR group. Limb IR also made a drop in the concentration of plasma H2S and the activity of lung CSE, while the activity of iNOS and HO in the lung tissues and the levels of plasma NO and CO increased. Administration of NaHS before IR attenuated the changes induced by IR, while pre-administration of PPG exacerbated the IR injuries and increased the plasma NO level and lung iNOS activity. The H2S content was positively correlated with CSE activity, CO content and HO-1 activity (P<0.01), and negatively correlated with the other indices (P<0.01).CONCLUSION: Down-regulation of H2S/CSE is involved in the pathogenesis of acute lung injury induced by IR. Endogenous and exogenous H2S protects against lung injuries. The anti-injury effects of H2S are related with its anti-oxidative activity to attenuate the inflammatory over-reactions in the lung induced by PMN. Down-regulation of NO/iNOS system and up-regulation of CO/HO-1 system by H2S are also involved in the process of anti-injury to ALI. 相似文献
12.
AIM: To investigate the effects of lipopolysaccharide (LPS) and interleukin-1 receptor antagonist (IL-1ra) on mesangial cells proliferation and nitric oxide synthesis. METHODS: Glomerular mesangial cells from SD rats were cultured. The first and second passages of cultured cells were used for the experiment. LPS and LPS plus IL-1ra were added in cell cultures, respectively. By using chemical method the nitrite in supernatants was measured, [3H]-TdR incorporation was determined to evaluate the GMC proliferation. Northern and slot hybridizations were performed to detect the expression of iNOS mRNA. RESULTS: There were expression of iNOS mRNA, more production of nitrite (0.64±0.25 vs 0.12±0.06 nmol/104 cell) in supernatants and GMC proliferation (3735±1177.9 vs 1785±280.6) in LPS group compared to the control. While compared with LPS group, in LPS+IL-1ra GMC group, expression of iNOS mRNA decreased by 40%, nitrite increased (3.28±0.33nmol/104 cell), proliferation of GMC decreased (818±77.27). CONCLUSION: LPS could activate the GMC to express iNOS mRNA and produce more nitrite. IL-1ra could partially inhibit the effects of LPS on the expression of iNOS mRNA in GMC, but not nitrite. There is no synchronous correlation between NO production and GMC proliferation. 相似文献
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AIM:To evaluate effects of inhaled nitric oxide(iNO) on adhesion molecule CD11b expression on lung neutrophils in experimental meconium aspiration syndrome(MAS) rabbits treated with conventional mechanical ventilation under room air or 100%O2. METHODS:Animals were randomly allocated to 8 groups(n=48) of 6 each: two MAS model groups(under room air or 100%O2 without iNO treatment), 6 treatment groups were treated with continuous NO inhalation at a dose of 0.2×10-6mol/L, 0.33×10-6mol/L or 0.67×10-6mol/L respectively for 12 hours under room air or 100%O2. Mean systemic arterial pressure(SAP) and methemoglobin (MeHb) were performed at basement time, 0, 2, 4, 12 hours. Expression of CD11b on neutrophils in the bronchoalveolar lavage fluid(BALF) was detected with flow cytometry. RESULTS:SAP, MeHb at different time among different groups were within the normal scale. CD11b expression on the neutrophils in the BALF significantly decreased in groups of inhalation 0.33×10-6 mol/L or 0.67×10-6 mol/L NO, compared with the two MAS model groups. (x±s: under 21%O2, 0.33×10-6 mol/L NO, 121±20 υs 392±204; 0.67×10-6 mol/L NO, 112±30 υs 392±204;under 100%O2, 0.33×10-6 mol/L NO, 113±24υs293±65; 0.67×10-6 mol/L 102±114 υs293±65, P<0.05). 0.2×10-6mol/L NO inhalation did no effect on CD11b expression. (x±s:21%O2, 190±101 υs 392±204; 100%O2, 222±85 υs 293±65; P>0.05). No statistic difference was observed between groups inhaled 0.33×10-6 mol/L NO and 0.67×10-6mol/L NO. CONCLUSION:0.33×10-6 mol/L or 0.67×10-6 mol/L NO inhalation down-regulated the CD11b expression on the neutrophils in BALF to reduce the sequestration of neutrophils in rabbit lung. 相似文献
14.
AIM: To study the up-regulation of inducible nitric oxide synthase (iNOS) in lung of pulmonary fibrosis and its relationship with fibrosis. METHODS: The changes of amount of iNOS positive stain cells and type Ⅰ?Ⅲ collagen were examined on the day 7, 14 and 30 after intratracheal administration of bleomycin A5. The contents of NO2-/NO3- (nitrite/nitrate) in out-flowing pulmonary blood (OPB), hydroxyproline in lung and the histological changes were detected after iNOS was blocked by aminoguanidine (AG). RESULTS: (1) The number of iNOS-positive stain cells increased significantly in BLMA5 7 d, 14 d and 30 d groups compared with that in control group (P<0.01). Furthermore, the increment of the number of iNOS-positive stain cells in BLMA5 7 d, 14 d groups was more than that in BLMA5 30 d group. There was an increment of collagen in BLMA5 14 d group and in BLMA5 30 d group , with an increase in type Ⅲ collagen in BLMA5 14 d group and an increase in type Ⅰcollagen in BLMA5 30 d group. (2) The high level of NO2-/NO3- in OPB and hydroxyproline level in lung could be reversed by AG, a selective inhibitor of iNOS. Large amount of fibroblasts and macrophages were also abated by AG. CONCLUSION: In the development of pulmonary fibrosis, the expression of iNOS is up-regulated, which induces nitric oxide (NO) production and promotes propagation of pulmonary fibrosis. 相似文献
15.
AIM: To investigate the effects of the sera from the rats after limb ischemic preconditioning (LIPC) on human umbilical vein endothelial cells (HUVECs) injured by hydrogen peroxide (H2O2). METHODS: The HUVECs were divided into 5 groups: the cells in control group were cultured without any intervention; the cells in model group (M) were damaged by 1 mmol/L H2O2 for 2 h; the cells in early preconditioning serum (EPS) group, delayed preconditioning serum (DPS) group or sham limb ischemic preconditioning serum (SPS) group were treated with the corresponding serum at 5% for 12 h, respectively, and then treaed with H2O2 for 2 h. The viability of the HUVECs was analyzed by flow cytometry. The lactate dehydrogenase (LDH) in the culture media was detected. The cell adhesion molecules in the HUVECs were detected by real-time PCR. The mRNA and protein expression of heme oxygenase-1 (HO-1) was also determined. RESULTS: The viability of HUVECs incubated with 1 mmol/L H2O2 for 2 h significantly decreased compared with the control cells, which was accompanied with the augmentations of LDH in the medium and the cell adhesion molecules in cells, such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Preincubation with EPS and DPS derived from the rats subjected LIPC attenuated these injuries. Furthermore, pretreatment with EPS and DPS increased the expression of HO-1 at mRNA and protein levels. CONCLUSION: LIPC protects the HUVECs from H2O2-induced injury. 相似文献
16.
AIM: To investigate the effect of acetyl-L-carnitine (ALC) on H2O2-induced oxidative damage in PC12 cells and its possible mechanism. METHODS: A moderate oxidative damage PC12 cell model was induced by exposure of the PC12 cells to H2O2. ALC at different concentrations (100, 200 and 400 μmol/L) was applied to the PC12 cells cultured in vitro, and CCK8 assay was used to detect the cell viability. The cells were divided into control group, H2O2 group, and low-ALC, medium-ALC and high-ALC groups. The apoptosis of the cells was analyzed by flow cytometry. The protein levels of Nrf2 and cleaved caspase-3 were determined by Western blot. The nuclear translocation of Nrf2 was observed by immunofluorescence staining. RESULTS: ALC at different concentrations (100, 200 and 400 μmol/L) significantly inhibited H2O2-induced PC12 cell apoptosis, and the medium concentration group had the best effect. Compared with H2O2 group, low, medium and high concentrations of ALC significantly increased the viability of the PC12 cells induced by H2O2, inhibit cell apoptosis (P<0.05), significantly down-regulated the protein level of cleaved caspase-3 (P<0.05), up-regulated the protein level of Nrf2 (P<0.05), and promoted the translocation of Nrf2 from the cytoplasm to the nucleus. CONCLUSION: Acetyl-L-carnitine attenuates H2O2-induced oxidative damage of PC12 cells, inhibits the apoptosis and increases the viability, which is related to the activation of Nrf2 signaling pathway. 相似文献
17.
ZHANG Yan-mei YANG Quan LI Kang-sheng XU Chong-tao LI Wei-qiu ZHENG Zhi-chao WU Cai-ru 《园艺学报》2002,18(8):981-984
AIM: To investigate the changes in nNOS and iNOS expression of hippocampal CA3 pyramidal neurons and NO2-/NO3- level of hippocampal homogenate of rats induced by stress, and to explore the effect of phenytoin on them. METHODS: Rats were subjected to forced-swimming stress, phenytoin was administered(ip) at 30 min before stress. Using the immunohistochemistry and the computerized image technique, the expression levels of nNOS and iNOS of rat hippocampal CA3 pyramidal neurons were assayed quantitatively, and the NO2-/NO3- level of hippocampal homogenate was also measured using nitric acid deoxidize enzyme method. RESULTS: The nNOS average grey degree of hippocampal CA3 pyramidal neurons was significantly lower in stress group (155.42±3.77)than that in control group(164.54±4.62)and in stress plus phenytoin group(164.27±2.55)(P<0.01); The iNOS relative sectional area proportion of hippocampal CA3 pyramidal neuron was significantly larger in stress group(5.87%±2.90%) than that in control group (0.90%±0.89%) and in strers plus phenytoin groups (0.90%±0.88%)(P<0.01); The NO2-/NO3- level of hippocampal homogenate was significantly higher in stress group(42.75 umol/L±14.49 umol/L)than that in control group(21.23 umol/L±6.99 umol/L)and in stress plus phenytoin group(18.40 umol/L±8.11 umol/L)(P<0.01). CONCLUSION: It is suggested that the stress could induce nNOS and iNOS expression in CA3 pyramidal neurons and excessive production of NO in hippocampus of rats, which could be inhibited by phenytoin. 相似文献
18.
AIM: To investigate the effect of salvianolic acid B (Sal B) on apoptosis of rat bone mesenchymal stem cells(BMSCs) induced by hydrogen peroxide(H2O2). METHODS: BMSCs were incubated with Sal B at the concentration of 1, 10 or 100 μmol/L while treated with lethal concentration of H2O2 (500 μmol/L). The effect of Sal B at different concentrations on the viability of BMSCs was detected by MTT. Flow cytometry were used to determine the protective role of Sal B in apoptosis of BMSCs. The changes of chromatin distribution in BMSCs were observed by Hoechst 33342 staining. The expression of p-ERK1/2 was detected by Western blotting. RESULTS: Sal B protected the BMSCs against H2O2 as the cell viability was increased from (53.60±4.21)% to (85.33±9.08)% or (75.78±6.28)% in a dose-dependent manner. After exposed to H2O2, about 50%-65% BMSCs displayed apoptotic morphology. Treatment with Sal B at the concentrations of 10 and 100 μmol/L reduced the cytotoxic effect of H2O2 on BMSCs to about 32% and 47%, respectively. The results of flow cytometric analysis confirmed the cytoprotective effect of Sal B. This protective effect was concomitant with significant reduction of ROS generation. Moreover, H2O2 time-dependently induced a pronounced increase in ERK1/2 phosphorylation,which was effectively inhibited by Sal B.CONCLUSION: Sal B protects BMSCs against H2O2-induced apoptosis. Sal B may exert its protective effect on BMSCs by triggering intracellular anti-apoptosis mechanism as well as reducing the oxidative stress. 相似文献
19.
AIM: To investigate the effects of astragalosides on autophagy and apoptosis of rat cardiomyocytes induced by hydrogenperoxide (H2O2).METHODS: The injury model of H9c2 cells induced by H2O2 was established, and the cells in astragalosides group and rapamycin group were treated with 20 mg/L astragalosides and 0.1 mg/L rapamycin, respectively. The apoptotic rate was detected by flow cytometry. The autophagy was observed by acridine orange staining. Western blot was used to detect the protein levels of p-mTOR, P70S6K, LC3 and caspase-3. RESULTS: Compared with H2O2 group and rapamycin group, the viability of H9c2 cells in astragalosides group was significantly increased (P<0.05). The shape of the H9c2 cells in astragalosides group was complete, the nuclei were stained with yellow-green fluorescence, and the chromatin was distributed evenly. The protein levels of p-mTOR and P70S6K in the H9c2 cells of astragalosides group were significantly increased (P<0.05), whereas the protein levels of LC3, cleaved caspase-3 and caspase-3 in the H9c2 cells of astragalosides group were decreased significantly (P<0.05). CONCLUSION: Astragalosides enhance the viability, inhibit the apoptosis, increase the protein levels of p-mTOR and P70S6K, and decrease the protein levels of LC3, cleaved caspase-3 and caspase-3 in the H2O2-induced rat myocardial H9c2 cells. The mechanism is related to the mTOR signaling pathway. 相似文献
20.
AIM: To investigate the role of autophagy inhibitor 3-methyladenine(3-MA) in the injury of U251 glioma cells induced by H2O2. METHODS: The following groups in this study were set up: control group, 10 mmol/L 3-MA group, 1 mmol/L H2O2 group and 1 mmol/L H2O2 +10 mmol/L 3-MA group. The viability of U251 cells in each group was detected by MTT assay. Autophagic vacuoles in the cells were observed by staining with MDC. The cells were stained with Hoechst 33342 to determine the chromatin condensation. Cell apoptotic ratio was measured by flow cytometry analysis. RESULTS: Compared with control group, no effect of 3-MA on the viability of U251 cells was observed. In H2O2 group, the cell viability decreased and cell apoptotic ratio increased.The autophagic vacuoles and nuclear chromatin condensation in the cells were also detected. Compared with H2O2 group, addition of 3-MA inhibited the increase in autophagic vacuoles but exacerbated the apoptosis. CONCLUSION: Autophagy inhibitor 3-MA inhibits autophagy partially, but exacerbates apoptosis in U251 cells, indicating that autophagy exerts protective effect in the process of injury in U251 cells induced by H2O2. 相似文献