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正《中国果菜》是由中华全国供销合作总社济南果品研究所主办,是国内外公开发行的科学技术期刊。《中国果菜》1981年创刊,设立流通保鲜、果蔬加工、综合利用、质量控制、产业发展、栽培技术等栏目,主要刊登果蔬方面创新性或实用性的学术论文、技术综述文章,为从事果蔬研究的科研人员发表和交流科研、教学成果提供平台;为果蔬贮藏保鲜、流通经营、种植加工等企业提供技术、信息、经验交流服务平台,推动果蔬行业技术进步和健康发展。《中国果菜》国内统一刊号:CN 37-1282/S,国际标准刊号:ISSN 1008-1038,邮发代号:24-137,月刊,国家级。全国各地邮局均可订阅,也可直接联系编辑部订阅。     

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<正>《中国果菜》是由中华全国供销合作总社济南果品研究所主办,是国内外公开发行的科学技术期刊。《中国果菜》1981年创刊,设立流通保鲜、果蔬加工、综合利用、质量控制、产业发展、栽培技术等栏目,主要刊登果蔬方面创新性或实用性的学术论文、技术综述文章,为从事果蔬研究的科研人员发表和交流科研、教学成果提供平台;为果蔬贮藏保鲜、流通经营、种植加工等企业提供技术、信息、经验交流服务平台,推动果蔬行业技术进步和健康发展。     

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<正>《中国果菜》是由中华全国供销合作总社济南果品研究所主办,是国内外公开发行的科学技术期刊。《中国果菜》1981年创刊,设立流通保鲜、果蔬加工、综合利用、质量控制、产业发展、栽培技术等栏目,主要刊登果蔬方面创新性或实用性的学术论文、技术综述文章,为从事果蔬研究的科研人员发表和交流科研、教学成果提供平台;为果蔬贮藏保鲜、流通经营、种植加工等企业提供技术、信息、经验交流服务平台,推动果蔬行业技术进步和健康发展。     

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<正>《中国果菜》是由中华全国供销合作总社济南果品研究所主办,是国内外公开发行的科学技术期刊。《中国果菜》1982年创刊,设立流通保鲜、果蔬加工、综合利用、质量控制、产业发展、栽培技术等栏目,主要刊登果蔬方面创新性或实用性的学术论文、技术综述文章,为从事果蔬研究的科研人员发表和交流科研、教学成果提供平台;为果蔬贮藏保鲜、流通经营、种植加工等企业提供技术、信息、经验交流服务平台,推动果蔬行业技术进步和健康发展。     

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正《中国果菜》是由中华全国供销合作总社济南果品研究所主办,是国内外公开发行的科学技术期刊。《中国果菜》1982年创刊,设立流通保鲜、果蔬加工、综合利用、质量控制、产业发展、栽培技术等栏目,主要刊登果蔬方面创新性或实用性的学术论文、技术综述文章,为从事果蔬研究的科研人员发表和交流科研、教学成果提供平台;为果蔬贮藏保鲜、流通经营、种植加工等     

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正《中国果蔬》是由中华全国供销合作总社济南果品研究院、山东供销合作社联合社、中国果蔬贮藏加工技术研究中心联合主办,是国内外公开发行的科学技术期刊。《中国果蔬》1982年创刊,设立流通保险、果蔬加工、综合利用、质量控制、产业发展、栽培技术等栏目,主要刊登果蔬方面创新性或实用性的学术论文、技术综述文章,为从事果蔬研     

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正《中国果菜》是由中华全国供销合作总社济南果品研究院、山东供销合作社联合社、中国果蔬贮藏加工技术研究中心联合主办,是国内外公开发行的科学技术期刊。《中国果菜》1982年创刊,设立流通保鲜、果蔬加工、综合利用、质量控制、产业发展、栽培技术等栏目,主要刊登果蔬方面创新性或实用性的学术论文、技术综述文章,为从事果蔬研究的科研人员发表和交流科研、教学成果提供平台;为果蔬贮藏保鲜、流通经营、种植加工等企业提供技术、信息、经验交流服务平台,推动果蔬行业技术进步和健康发展。     

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《中国果菜》是由中华全国供销合作总社济南果品研究所主办,是国内外公开发行的科学技术期刊。《中国果菜》1981年创刊,设立流通保鲜、果蔬加工、综合利用、质量控制、产业发展、栽培技术等栏目,主要刊登果蔬方面创新性或实用性的学术论文、技术综述文章,为从事果蔬研究的科研人员发表和交流科研、教学成果提供平台。     

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正《中国果菜》是由中华全国供销合作总社济南果品研究所主办,是国内外公开发行的科学技术期刊。《中国果菜》1982年创刊,设立流通保鲜、果蔬加工、综合利用、质量控制、产业发展、栽培技术等栏目,主要刊登果蔬方面创新性或实用性的学术论文、技术综述文章,为从事果蔬研究的科研人员发表和交流科研、教学成果提供平台;为果蔬贮藏保鲜、流通经营、种植加工等企业提供技术、信息、经验交流服务平台,推动果蔬行业技术进步和健康发展。《中国果菜》单月刊、国家级;国内统一刊号:CN37-1282/S,国际标准刊号:ISSN     

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<正>《中国果菜》是由中华全国供销合作总社济南果品研究所主办,是国内外公开发行的科学技术期刊。《中国果菜》1981年创刊,设立流通保鲜、果蔬加工、综合利用、质量控制、产业发展、栽培技术等栏目,主要刊登果蔬方面创新性或实用性的学术论文、技术综述文章,为从事果蔬研究的科研人员发表和交流科研、教学成果提供平台;为果蔬贮藏保鲜、流通经营、种植加工等企业提供技术、信息、经验交流服务平台,推动果蔬行业技术进步和健康发展。     

Effects of AZD8055 on autophagy and apoptosis in cholangiocarcinoma cells

AIM: To explore the effects of mammalian target of rapamycin (mTOR) double inhibitor AZD8055 on autophagy and apoptosis of human cholangiocarcinoma cell line HuCCT1. METHODS: The effect of AZD8055 on the viability of HuCCT1 cells was detected by MTT assay. Autophagosome was detected by acridine orange (AO) staining. After treated with AZD8055, the expression levels of apoptosis-related proteins Bcl-2, Bax and cleaved caspase-3 and auto-phagy marker proteins beclin 1, LC3 and p62 were determined by Western blot. Apoptotic rate was analyzed by flow cyto-metry with Annexin V-FITC/PI double staining. RESULTS: AZD8055 significantly inhibited the viability of HuCCT1 cells (P<0.05). AO staining showed that AZD8055 significantly increased orange granules in the cytoplasm. After treated with AZD8055, compared with the control group, the protein level of beclin 1 and the ratio of LC3-Ⅱ/LC3-I were enhanced, while p62 was attenuated (P<0.05). The protein expression level of pro-apoptotic regulator Bax was down-regulated and anti-apoptotic regulator Bcl-2 was increased. The protein level of cleaved caspase-3 was reduced (P<0.05). The results of flow cytometry showed that AZD8055 inhibited cell apoptosis. CONCLUSION: AZD8055 inhibits the viability of cholangiocarcinoma cells, and the mechanism is closely related with autophagy induced by AZD8055.     

Role of calreticulin-induced mitochondrial damage in high glucose-induced apoptosis of myocardial cells

AIM: To observe the effect of high glucose on the protein expression of calreticulin (CRT) and its association with cell apoptosis and mitochondrial dysfunction in the cardiomyocytes. METHODS: AC-16 cardiomyocytes were randomly divided into normal glucose group, high glucose group, high glucose+ CRT siRNA group and isotonic control group. The cell apoptotic rate, reactive oxygen species (ROS), mitochondrial membrane potential level, respiratory enzyme activity, and protein expression of CRT were observed. RESULTS: Compared with the cardiomyocytes in normal glucose group, the apoptotic rate and ROS production of cardiomyocytes increased in high glucose group, accompanying with the decreases in the mitochondrial membrane potential level and enzyme activitiy of the respiratory chain. The protein expression of CRT was significantly increased in high glucose group. However, compared with high glucose group, high glucose+ CRT siRNA decreased the expression of CRT and attenuated the damage of mitochondria, but CRT siRNA did not reduce the ROS level in cardiomyocytes. CONCLUSION: High glucose brings about CRT over-expression to induce mitochondrial injury, thus increasing myocardial apoptosis.     

Effects of Panax quinquefolium saponin on mitochondrial membrane potential and cardiomyocyte apoptosis in ischemia/reperfusion rats

AIM：To investigate whether mitochondrial membrane potential (ΔΨm) and the mitochondrial apoptotic pathway are involved in the protective mechanism of Panax quinquefolium saponin (PQS) against cardiomyocyte apoptosis after ischemia/reperfusion (I/R) injury in rat myocardium. METHODS：Ninety healthy male SD rats were randomly divided into sham group, I/R group, PQS (200 mg·kg-1·d-1) +I/R group, cyclosporine A (CsA) group, CsA (10 mg·kg-1) +I/R group and PQS +CsA +I/R group. The model of myocardial I/R injury in vivo was established by ligating the left anterior descending artery (LAD) for 30 min followed by 120 min of reperfusion in the rats. The serum activity of lactate dehydrogenase (LDH) was measured by automatic chemistry analyzer. The myocardial infarct size was measured by Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) staining. Cardiomyocyte apoptosis was detected by in situ TDT-mediated dUTP nick end labeling (TUNEL). The protein levels of Bcl-2, Bax, cleaved caspase-3 and cytosolic cytochrome C were determined by Western blotting. ΔΨm was measured by laser scanning confocal microscopy and fluorescence microplate reader. RESULTS：Compared with I/R group, the serum content of LDH,the infarction size in PQS+I/R group, CsA+I/R group and PQS+CsA+I/R group and the myocardial apoptotic index were decreased. Compared with I/R group, the fluorescence intensity of mitochondria after JC-1 staining was enhanced in PQS+I/R group, CsA+I/R group and PQS+CsA+I/R group, and the relative fluorescence units (RFU) of ΔΨm were improved in those 3 groups. In PQS+I/R group, CsA+I/R group and PQS+CsA+I/R group, the protein expression of Bcl-2 was increased, and that of Bax was decreased compared with I/R group. Moreover, in those 3 groups, the protein levels of cleaved-caspase-3 and cytosolic cytochrome C were decreased compared to I/R group, respectively. CONCLUSION：PQS attenuates myocardial injury and cardiomyocyte apoptosis during I/R, and the protective mechanisms of PQS were associated with the modulation of ΔΨm and the inhibition of mitochondrial apoptosis pathway.     

Effects of intermittent high glucose on apoptosis and PTEN expression in islet cells

AIM: To investigate whether the increase in PTEN expression is related to apoptosis, and whether it is regulated by reactive oxygen species(ROS). METHODS: The rat islet cells were divided into constant low glucose group (group L), constant high glucose group (group H), glucose fluctuation group (group F), low glucose after high glucose group (group HL) and low glucose after fluctuation group (group FL). The ROS level, apoptotic rate, intracellular calcium, insulin release and PTEN protein expression were analyzed. RESULTS: Compared with groups H and L, the insulin secretion decreased, and intracellular calcium, ROS level, PTEN protein expression and apoptotic rate increased in group F (P<0.05). Compared with group H, the intracellular calcium, ROS level, PTEN protein expression and apoptotic rate in group HL decreased, but were still higher than those in group L (P<0.05). Compared with group F, the intracellular calcium, ROS level, PTEN protein expression and apoptotic rate in group FL decreased, but were still higher than those in group L (P<0.05). CONCLUSION: Glucose fluctuation can cause the apoptosis of islet cells more easily than constant high glucose. This may be related to the change of intracellular calcium and increase in oxidative stress which promotes PTEN expression. The recovery of glucose level to some extent relieves oxidative stress, decrease PTEN expression and reduce cell damage.     

Effects of soybean isflavones on mitochondrial damage and neuronal apoptosis induced by cerebral ischemia/reperfusion

AIM: To study the effects of soybean isoflavones on mitochondrial ultrastructure, neuronal apoptosis and expression of cytochrome C, caspase-9 and caspase-3 in the rats with cerebral ischemia/reperfusion.METHODS: Adult healthy SD rats (n=60) were randomly divided into 3 groups: sham group, ischemia/reperfusion injury (I/R) group and soybean isoflavone (SI) pretreatment group. Soybean isoflavones (120 mg·kg-1·d-1) were fed by gastric lavage for 21 d. The global ischemia/reperfusion model of the rats was established by blocking 3 vessels, and then reperfused for 1 h after 1 h of ischemia. The morphological change of the cerebral cortex cells was observed under light microscope. The mitochondrial ultrastructure of the cerebral cortex cells was determined by transmission electron microscope. The apoptotic rate of the cerebral cortex cells was detected by flow cytometry. The expression of cytochrome C, caspase-9 and caspase-3 in the cerebral cortex cells was determined by semi-quantitative RT-PCR and immunohistochemical techniques.RESULTS: Disintegration of mitochondria membrane and disappearance of the mitochondrial cristae were seen in I/R group. Compared with I/R group, the change of ultrastructure of mitochondria was significantly improved by soybean isoflavone pretreatment, and the neuronal apoptotic rate was also significantly decreased (P<0.01). The mRNA expression and protein content of cytochrome C, caspase-9 and caspase-3 in I/R group were obviously higher than those in sham group (P<0.01). Compared with I/R group, the mRNA expression and protein content of cytochrome C, caspase-9 and caspase-3 in SI group were significantly decreased (P<0.01).CONCLUSION: Soybean isoflavones attenuate cerebral ischemia/reperfusion injury by stabilizing the structure of mitochondria, preventing cytochrome C release to the cytoplasm, inhibiting the activation of caspase-9 and caspase-3 and decreasing cell apoptosis．     

Effects of Arg-Gly-Asp-Ser tetrapeptide on proliferation and apoptosis of hepatic stellate cells in vitro

AIM:To investigate the effects of Arg-Gly-Asp-Ser (RGDS) tetrapeptide on proliferation, apoptosis and caspase 3 expression in FN-stimulated HSCs in vitro. METHODS:[³H]-thymidine incorporation, Annexin-V/Propidium Iodide double-labeled flow cytometry(FCM), TUNEL, scanning electron microscope and transmission electron microscopy were employed to estimate the influence of RGDS on proliferation and apoptosis of HSCs. The adhesion rates were observed by toluidine blue colorimetric assay. The expression of caspase-3 protein was detected by FCM. RESULTS:①Compared with control and FN groups, RGDS tetrapeptide at concentrations of 25 mg·L^-1, 50mg·L^-1 and 100 mg·L^-1 inhibited the proliferation of HSCs (P<0.01), and the inhibition rates of 100 mg·L^-1 at 12 h, 24 h and 48 h were 62.73%, 74.23%, 80.22%, respectively.②RGDS tetrapeptide induced the HSC apoptosis in dose-dependent and time-dependent manners(P<0.01). Observed with scanning electron microscope, the cell bodies and cellular processes of HSCs exposed to RGDS tetrapeptide were seen to be diminished. Microvilli on the cell surface decreased, became short even disappeared. Observed with transmission electron microscopy, the chromatins condensed, shrunk and aggregated along inside of nuclear membrane to exist in the form of ball, petal and crescent. Sometimes, apoptotic bodies formed. ③After exposure of HSCs to RGDS tetrapeptide for 2 h, the inhibition rates of adhesion were 8.82%, 29.41% and 45.59%, respectively, but that of RGES group was only 4.41%, P<0.01. ④ The expression of caspase 3 was obviously higher in RGDS tetrapeptide group than that in FN group, RGES tetrapeptide. CONCLUSION: These results suggest that RGDS tetrapeptide may inhibit proliferation and induce apoptosis of HSCs in both dose- dependent and time- dependent manners in vitro, which may be related to the abrogation of cell adhesion and caspase 3.     

Effects of silymarin on homocysteine-induced apoptosis in human umbilical vein endothelial cells

AIM:To investigate the effect of silymarin on homocysteine-induced cell viability and apoptosis in human umbilical vein endothelial cells (HUVECs). METHODS:Cell viability was analyzed by using MTT and LDH assay. Apoptotic cells were detected by using DNA fragmentation and flow cytometric analysis. The level of intracellular reactive oxygen species (ROS) and the potential of mitochondrial membrane were determined by flow cytometric assay. The activity of caspase-3, -6 and -9 were measured with microplate spectrofluorometer. Protein levels were examined by Western blotting. RESULTS:Treatment of cultured HUVECs with HCY for 48 h induced a significant decrease in cell viability, and the percentage of apoptosis increased to 76.8%. The level of intracellular ROS and activity of caspase-3, -6 and -9 enhanced, and the red/green ratios of mitochondrial membrane decreased. However, simultaneous treatment with silymarin exhibited cytoprotective effects, reduced formation of the DNA ladder, prevented the levels of Bax and Bcl-2 proteins and the accumulation of ROS as well as caspase-3, -6 and -9 activation, reconverted the potential of mitochondrial membrane, and the percentage of apoptosis/necrosis was significantly decreased to 12.7% in a dose-dependent manner. CONCLUSION:These results demonstrate that silymarin has the protective capacity to antagonize HCY-induced apoptosis in HUVECs. The antiapoptotic action of silymarin may be partially dependent on an anti-oxidative stress effects, inhibition of caspases activity, and maintenance of mitochondria function.     

Effects of down-regulation of X-linked inhibitor of apoptosis protein gene on docetaxel-induced apoptosis in bladder cancer cells

AIM: To observe the effects of down-regulation of X-linked inhibitor of apoptosis protein ( XIAP ) gene on the chemotherapeutic sensitivity of bladder cancer cells. METHODS: The shRNA and shRNA-XIAP were transfected into bladder cancer T24T cells. The fluorescence microscopy was used to detect the transfection effects. XIAP gene expression was detected by RT-PCR and Western blotting. Docetaxel was administrated to T24T, T24T shRNA and T24T shRNA-XIAP bladder cancer cells. ATPase methods was performed to measure in vitro cell viability. Morphological changes and apoptotic rates were determined by phase contrast microscopy and flow cytometry assay. Cellular poly(ADP-ribose) polymerase (PARP) and caspase-3 protein expression and their cleavage were assayed by Western blotting. RESULTS: The fluorescence was obvious in the T24T shRNA and T24T shRNA-XIAP cells under the fluorescence microscope. Using Western blotting and RT-PCR methods, the protein and mRNA levels of XIAP gene in T24T shRNA-XIAP cells were significantly decreased,respectively. After treated with various concentrations of docetaxel for 24 h, the IC₅₀ of T24T shRNA-XIAP cells was (1.23?0.62) nmol/L, lower than that of T24T and T24T shRNA cells, which were (8.22?1.23) and (8.35?0.98) nmol/L (P<0.01), respectively. Compared with control group, the typical morphological changes of apoptosis were observed in T24T shRNA-XIAP cells. Detected by flow cytometry assay, the apoptotic rates in shRNA-XIAP group were (41.45?6.23)% and (74.82?5.46)% after exposed to docetaxel at the concentrations of 2 nmol/L and 5 nmol/L for 24 h, which were significantly higher than that in T24T shRNA group with (25.34?3.81)% and (34.14?6.25)%, respectively (P<0.01). Compared with T24T shRNA cells, the cleavage of PARP and caspase-3 proteins in the cells transfected with shRNA-XIAP was significantly increased. CONCLUSION: XIAP gene is significantly down-regulated via shRNA-XIAP, which could increase the docetaxel-induced apoptosis and cytotoxic activity.     

Effects of low-dose mifepristone on apoptosis in human ovarian luteinized granulosa cells

AIM: To investigate the effect of different low-dose mifepristone on apoptosis in granulosa cells and to test low-dose mifepristone as an orally contraceptive drug. METHODS: By using immunofluorescence, terminal deoxynucleotidyl transferase-mediated nick end labelling (TUNEL) and flow cytometry technique, the nuclear morphologic features and ratio of apoptosis and fluorescent intensity of caspase-3 in granulosa cells cultured in vitro treated with different low-doses of mifepristone were observed, respectively. RESULTS: By the display of immunofluorescence, the granulosa cells in treatment group were classified as apoptotic cells on the basis of their morphologic features contained a single condensed chromatin, multiple nuclear fragments. The results of TUNEL showed significant difference between control group and groups treated with different concentration of mifepristone (P<0.01). A significant difference (P<0.01) was also observed between the treatment groups with 1.25 μmol/L and 2.50 μmol/L mifepristone. The fluorescent intensity of caspase-3, observed by flow cytometry showed significant difference (P<0.01) between control group and treatment groups. CONCLUSION: Granulosa cells are induced to apoptosis by low-dose mifepristone, which may be regulated by the activation of caspase-3.