HCCR-2反义核酸对肝癌HepG2细胞的作用

Objective To investigate the effects of antisense recombinant euraryotic expression vector of HCCR-2 on the proliferation and apoptosis of HepG2. Methods The antisense recombinant eukaryotic expression vector of HCCR-2 was constructed. The vector was stably transfected to the HepG2 cells, and positive clones were selected by G418 (antiseuse vector group), pIRES2-EGFP vector was transfected into the HepG2 cells in the same way (pIRES2-EGFP group). The conditions of the nontransfected HepG2 cells were used as control (HepG2 group). Changes in cell growth curve, cell cycle, cell apoptosis and morphology of HepG2 cells after the transfec-tion were detected by MTT method, flow cytometry and transmission electron microscopy, respectively. All the data were analyzed by one-way ANOVA and chi-square test. Results The expression level of HCCR-2 mRNA was down-regulated to 0.39±0.04 in antisense vector group, and the expression level of HCCR-2 mRNA in pIRES2-EGFP group and HepG2 group were 0.62±0.06 and 0.72±0.03, respectively, with significant difference among the 3 groups (F=43.701, P<0.05). The apoptotic rate of HepG2 cells in antisense vector group, pIRES2-EGFP grop and HepG2 group were 13.30%, 2.51% and 2.07%, respectively, with significant difference among the 3 group (χ2=6.793, 8.721, P<0.05). The growth of HepG2 cells in antisense vector group was retarded, and was blocked in G0/G1 stage. Conclusions The HCCR-2 antisense recombinant eukaryotic expression vector can inhibit the mRNA expression of HCCR-2 and promote the apoptosis of cells. HCCR-2 may be involved in cell regulation and the proliferation of hepatocellular carcinoma cells.     

HCCR-2反义核酸对肝癌HepG2细胞的作用

Objective To investigate the effects of antisense recombinant euraryotic expression vector of HCCR-2 on the proliferation and apoptosis of HepG2. Methods The antisense recombinant eukaryotic expression vector of HCCR-2 was constructed. The vector was stably transfected to the HepG2 cells, and positive clones were selected by G418 (antiseuse vector group), pIRES2-EGFP vector was transfected into the HepG2 cells in the same way (pIRES2-EGFP group). The conditions of the nontransfected HepG2 cells were used as control (HepG2 group). Changes in cell growth curve, cell cycle, cell apoptosis and morphology of HepG2 cells after the transfec-tion were detected by MTT method, flow cytometry and transmission electron microscopy, respectively. All the data were analyzed by one-way ANOVA and chi-square test. Results The expression level of HCCR-2 mRNA was down-regulated to 0.39±0.04 in antisense vector group, and the expression level of HCCR-2 mRNA in pIRES2-EGFP group and HepG2 group were 0.62±0.06 and 0.72±0.03, respectively, with significant difference among the 3 groups (F=43.701, P<0.05). The apoptotic rate of HepG2 cells in antisense vector group, pIRES2-EGFP grop and HepG2 group were 13.30%, 2.51% and 2.07%, respectively, with significant difference among the 3 group (χ2=6.793, 8.721, P<0.05). The growth of HepG2 cells in antisense vector group was retarded, and was blocked in G0/G1 stage. Conclusions The HCCR-2 antisense recombinant eukaryotic expression vector can inhibit the mRNA expression of HCCR-2 and promote the apoptosis of cells. HCCR-2 may be involved in cell regulation and the proliferation of hepatocellular carcinoma cells.     

HCCR-2反义核酸对肝癌HepG2细胞的作用

Objective To investigate the effects of antisense recombinant euraryotic expression vector of HCCR-2 on the proliferation and apoptosis of HepG2. Methods The antisense recombinant eukaryotic expression vector of HCCR-2 was constructed. The vector was stably transfected to the HepG2 cells, and positive clones were selected by G418 (antiseuse vector group), pIRES2-EGFP vector was transfected into the HepG2 cells in the same way (pIRES2-EGFP group). The conditions of the nontransfected HepG2 cells were used as control (HepG2 group). Changes in cell growth curve, cell cycle, cell apoptosis and morphology of HepG2 cells after the transfec-tion were detected by MTT method, flow cytometry and transmission electron microscopy, respectively. All the data were analyzed by one-way ANOVA and chi-square test. Results The expression level of HCCR-2 mRNA was down-regulated to 0.39±0.04 in antisense vector group, and the expression level of HCCR-2 mRNA in pIRES2-EGFP group and HepG2 group were 0.62±0.06 and 0.72±0.03, respectively, with significant difference among the 3 groups (F=43.701, P<0.05). The apoptotic rate of HepG2 cells in antisense vector group, pIRES2-EGFP grop and HepG2 group were 13.30%, 2.51% and 2.07%, respectively, with significant difference among the 3 group (χ2=6.793, 8.721, P<0.05). The growth of HepG2 cells in antisense vector group was retarded, and was blocked in G0/G1 stage. Conclusions The HCCR-2 antisense recombinant eukaryotic expression vector can inhibit the mRNA expression of HCCR-2 and promote the apoptosis of cells. HCCR-2 may be involved in cell regulation and the proliferation of hepatocellular carcinoma cells.     

HCCR-2反义核酸对肝癌HepG2细胞的作用

Objective To investigate the effects of antisense recombinant euraryotic expression vector of HCCR-2 on the proliferation and apoptosis of HepG2. Methods The antisense recombinant eukaryotic expression vector of HCCR-2 was constructed. The vector was stably transfected to the HepG2 cells, and positive clones were selected by G418 (antiseuse vector group), pIRES2-EGFP vector was transfected into the HepG2 cells in the same way (pIRES2-EGFP group). The conditions of the nontransfected HepG2 cells were used as control (HepG2 group). Changes in cell growth curve, cell cycle, cell apoptosis and morphology of HepG2 cells after the transfec-tion were detected by MTT method, flow cytometry and transmission electron microscopy, respectively. All the data were analyzed by one-way ANOVA and chi-square test. Results The expression level of HCCR-2 mRNA was down-regulated to 0.39±0.04 in antisense vector group, and the expression level of HCCR-2 mRNA in pIRES2-EGFP group and HepG2 group were 0.62±0.06 and 0.72±0.03, respectively, with significant difference among the 3 groups (F=43.701, P<0.05). The apoptotic rate of HepG2 cells in antisense vector group, pIRES2-EGFP grop and HepG2 group were 13.30%, 2.51% and 2.07%, respectively, with significant difference among the 3 group (χ2=6.793, 8.721, P<0.05). The growth of HepG2 cells in antisense vector group was retarded, and was blocked in G0/G1 stage. Conclusions The HCCR-2 antisense recombinant eukaryotic expression vector can inhibit the mRNA expression of HCCR-2 and promote the apoptosis of cells. HCCR-2 may be involved in cell regulation and the proliferation of hepatocellular carcinoma cells.     

HCCR-2反义核酸对肝癌HepG2细胞的作用

Objective To investigate the effects of antisense recombinant euraryotic expression vector of HCCR-2 on the proliferation and apoptosis of HepG2. Methods The antisense recombinant eukaryotic expression vector of HCCR-2 was constructed. The vector was stably transfected to the HepG2 cells, and positive clones were selected by G418 (antiseuse vector group), pIRES2-EGFP vector was transfected into the HepG2 cells in the same way (pIRES2-EGFP group). The conditions of the nontransfected HepG2 cells were used as control (HepG2 group). Changes in cell growth curve, cell cycle, cell apoptosis and morphology of HepG2 cells after the transfec-tion were detected by MTT method, flow cytometry and transmission electron microscopy, respectively. All the data were analyzed by one-way ANOVA and chi-square test. Results The expression level of HCCR-2 mRNA was down-regulated to 0.39±0.04 in antisense vector group, and the expression level of HCCR-2 mRNA in pIRES2-EGFP group and HepG2 group were 0.62±0.06 and 0.72±0.03, respectively, with significant difference among the 3 groups (F=43.701, P<0.05). The apoptotic rate of HepG2 cells in antisense vector group, pIRES2-EGFP grop and HepG2 group were 13.30%, 2.51% and 2.07%, respectively, with significant difference among the 3 group (χ2=6.793, 8.721, P<0.05). The growth of HepG2 cells in antisense vector group was retarded, and was blocked in G0/G1 stage. Conclusions The HCCR-2 antisense recombinant eukaryotic expression vector can inhibit the mRNA expression of HCCR-2 and promote the apoptosis of cells. HCCR-2 may be involved in cell regulation and the proliferation of hepatocellular carcinoma cells.     

HCCR-2反义核酸对肝癌HepG2细胞的作用

Objective To investigate the effects of antisense recombinant euraryotic expression vector of HCCR-2 on the proliferation and apoptosis of HepG2. Methods The antisense recombinant eukaryotic expression vector of HCCR-2 was constructed. The vector was stably transfected to the HepG2 cells, and positive clones were selected by G418 (antiseuse vector group), pIRES2-EGFP vector was transfected into the HepG2 cells in the same way (pIRES2-EGFP group). The conditions of the nontransfected HepG2 cells were used as control (HepG2 group). Changes in cell growth curve, cell cycle, cell apoptosis and morphology of HepG2 cells after the transfec-tion were detected by MTT method, flow cytometry and transmission electron microscopy, respectively. All the data were analyzed by one-way ANOVA and chi-square test. Results The expression level of HCCR-2 mRNA was down-regulated to 0.39±0.04 in antisense vector group, and the expression level of HCCR-2 mRNA in pIRES2-EGFP group and HepG2 group were 0.62±0.06 and 0.72±0.03, respectively, with significant difference among the 3 groups (F=43.701, P<0.05). The apoptotic rate of HepG2 cells in antisense vector group, pIRES2-EGFP grop and HepG2 group were 13.30%, 2.51% and 2.07%, respectively, with significant difference among the 3 group (χ2=6.793, 8.721, P<0.05). The growth of HepG2 cells in antisense vector group was retarded, and was blocked in G0/G1 stage. Conclusions The HCCR-2 antisense recombinant eukaryotic expression vector can inhibit the mRNA expression of HCCR-2 and promote the apoptosis of cells. HCCR-2 may be involved in cell regulation and the proliferation of hepatocellular carcinoma cells.     

HCCR-2反义核酸对肝癌HepG2细胞的作用

Objective To investigate the effects of antisense recombinant euraryotic expression vector of HCCR-2 on the proliferation and apoptosis of HepG2. Methods The antisense recombinant eukaryotic expression vector of HCCR-2 was constructed. The vector was stably transfected to the HepG2 cells, and positive clones were selected by G418 (antiseuse vector group), pIRES2-EGFP vector was transfected into the HepG2 cells in the same way (pIRES2-EGFP group). The conditions of the nontransfected HepG2 cells were used as control (HepG2 group). Changes in cell growth curve, cell cycle, cell apoptosis and morphology of HepG2 cells after the transfec-tion were detected by MTT method, flow cytometry and transmission electron microscopy, respectively. All the data were analyzed by one-way ANOVA and chi-square test. Results The expression level of HCCR-2 mRNA was down-regulated to 0.39±0.04 in antisense vector group, and the expression level of HCCR-2 mRNA in pIRES2-EGFP group and HepG2 group were 0.62±0.06 and 0.72±0.03, respectively, with significant difference among the 3 groups (F=43.701, P<0.05). The apoptotic rate of HepG2 cells in antisense vector group, pIRES2-EGFP grop and HepG2 group were 13.30%, 2.51% and 2.07%, respectively, with significant difference among the 3 group (χ2=6.793, 8.721, P<0.05). The growth of HepG2 cells in antisense vector group was retarded, and was blocked in G0/G1 stage. Conclusions The HCCR-2 antisense recombinant eukaryotic expression vector can inhibit the mRNA expression of HCCR-2 and promote the apoptosis of cells. HCCR-2 may be involved in cell regulation and the proliferation of hepatocellular carcinoma cells.     

RhoA基因沉默对肝癌HepG2细胞增殖和迁移能力的影响

Objective To construct a RhoA-siRNA expression vector and determine its role on the malig-nant behavior of HepG2 cells.Methods A RhoA-siRNA DNA fragment was synthesized and cloned into the expression vector of pGenesil-1.The constructed Rhon-siRNA DNA plasmid was stably transfected into HerG2 cells by lipofectamine,and then HepG2 cells were divided into the HepG2/RhoA-siRNA group (HepG2 cells were transfected with pGenesil-1-RhoA-siRNA),HepG2/control group(HepG2 cells were transfected with control plasmid) and HepG2 group (without plasmid transfection).The inbibitory effect of RhoA-siRNA on RhoA protein expression was shown by Western blot.The proliferation,migration,growth potentiality and cell cycle of transfected HepG2 cells were evaluated by MTT assay,wounded healing,the plate cloning formation test and flow cytometry,respectively.All data were analyzed by one-way analysis of variance (ANOVA) and chi-square test.Results The expression of RhoA protein in the HepG2/RhoA-siRNA group was,significantly decreased compared with that in the other two groups (F=178.19,P<0.05).Scratched cells were healed within 48 hours in the HepG2/control group and HepG2 group,but not in the HepG2/RhoA-siRNA group.The clone formation rates in the HepG2/RhoA-siRNA group,HepG2 group and HepG2/control group were 39%±3%,67%±5%and 70%±6%,respectively,with a significant difference among the three groups(χ2=33.34,38.69,P<0.05).Flow cytometry showed that the number of cells transfected with RhoA-siRNA was highest in the G0/G1 phase and lowest in the S phase(F=70.46,76.57.P<0.05).Conclusion The RhoA-siRNA expression vector can effectively suppress the proliferation and migration of HepG2 cells,which may provide a novel gene therapy for hepatocellular carcinoma.     

RhoA基因沉默对肝癌HepG2细胞增殖和迁移能力的影响

Objective To construct a RhoA-siRNA expression vector and determine its role on the malig-nant behavior of HepG2 cells.Methods A RhoA-siRNA DNA fragment was synthesized and cloned into the expression vector of pGenesil-1.The constructed Rhon-siRNA DNA plasmid was stably transfected into HerG2 cells by lipofectamine,and then HepG2 cells were divided into the HepG2/RhoA-siRNA group (HepG2 cells were transfected with pGenesil-1-RhoA-siRNA),HepG2/control group(HepG2 cells were transfected with control plasmid) and HepG2 group (without plasmid transfection).The inbibitory effect of RhoA-siRNA on RhoA protein expression was shown by Western blot.The proliferation,migration,growth potentiality and cell cycle of transfected HepG2 cells were evaluated by MTT assay,wounded healing,the plate cloning formation test and flow cytometry,respectively.All data were analyzed by one-way analysis of variance (ANOVA) and chi-square test.Results The expression of RhoA protein in the HepG2/RhoA-siRNA group was,significantly decreased compared with that in the other two groups (F=178.19,P<0.05).Scratched cells were healed within 48 hours in the HepG2/control group and HepG2 group,but not in the HepG2/RhoA-siRNA group.The clone formation rates in the HepG2/RhoA-siRNA group,HepG2 group and HepG2/control group were 39%±3%,67%±5%and 70%±6%,respectively,with a significant difference among the three groups(χ2=33.34,38.69,P<0.05).Flow cytometry showed that the number of cells transfected with RhoA-siRNA was highest in the G0/G1 phase and lowest in the S phase(F=70.46,76.57.P<0.05).Conclusion The RhoA-siRNA expression vector can effectively suppress the proliferation and migration of HepG2 cells,which may provide a novel gene therapy for hepatocellular carcinoma.     

靶向Survivin的siRNA联合吉西他滨抑制胰腺癌细胞增殖

Objective To construct the siRNA eukaryotic expression vector targeting Survivin gene, and investigate the chemotherapy sensitivity of pancreatic cancer line Panc-1 treated by gemcitabine. Methods The siRNA eukaryotic expression vector targeting Survivin gene was constructed. Panc-1 cells were transfected with negative control vector or siRNA vector and selected by G418, and the cell growth curve was drawn. The expression of Survivin mRNA and protein was detected by RT-PCR and Western blot respectively. Panc-1 cells or transfected cells were treated with gemcitabine for 24 h,and then the growth inhibition rate was measured by MTT assay, and cell apeptosis rate was measured by flow cytometry. Results The result of endonuclease digestion and DNA sequencing revealed that the recombinant plasmid psiRNA-Survivin was constructed successfully. Survivin mRNA and protein levels were reduced by 79.2% and 83.6% respectively in stably transfected Panc-1 cells as compared with control group, and the cell growth curve was much smoother, and the growth inhibition rate [ ( 24.6±4.5 ) % / (38.7±5.2 ) % ] and apoptosis rate of these cells [ ( 16.7±2.5 ) %/( 26.8±3.4 ) % ] were significantly increased after treatment by gemcitabine (P < 0.05 ). Conclusion The constructed siRNA eukaryotie expression vector targeting Survivin could decrease the Survivin expression,inhibit the growth of Panc-1 cells significantly,and increase the chemotherapy sensitivity to gemcitabine.     

P2Y2 receptors and GRK2 are involved in oscillatory fluid flow induced ERK1/2 responses in chondrocytes

Mechanical loading is an important factor regulating cartilage metabolism maintained by chondrocytes. However, some of its underlying mechanisms remain poorly understood. In this study, we employed a chondrogenic cell line ATDC5 to investigate roles of P2Y₂ and GRK2 in chondrocyte mechanotransduction. We first confirmed the expression of chondrocyte markers in differentiated ATDC5 cells. We then exposed both differentiated and undifferentiated ATDC5 cells to oscillatory fluid flow, and found that differentiated ATDC5 cells responded to oscillatory fluid flow by increasing COX‐2 and aggrecan expressions. More importantly, fluid flow induced ERK1/2 response in differentiated cells was increased more than 10 times compared to those in undifferentiated cells. Furthermore, we found that P2Y₂ mRNA and protein levels in differentiated ATDC5 cells were significantly higher than those in undifferentiated cells. In contrast, GRK2 protein levels in differentiated cells were significantly lower than those in undifferentiated cells. Finally, overexpressions of P2Y₂ and GRK2 in differentiated ATDC5 cells result in a 34% increase and a 21% decrease of the ERK1/2 phosphorylation, respectively, in response to oscillatory fluid flow, suggesting important roles of P2Y₂ and GRK2 in chondrocyte mechanotransduction. © 2010 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29:828–833     

23 COX-2和 HER-2在结直肠癌中的表达及其意义

为研究COX 2和HER 2在结直肠癌中的表达及其临床意义以及两者的相互关系，笔者采用免疫组化法检测123例结直肠腺癌及其中的25例淋巴结转移灶组织、12例远癌肠黏膜组织、15例结直肠腺瘤性息肉组织COX 2和HER 2的表达情况。结果示，COX 2在远癌组织、腺瘤性息肉、腺癌中的高表达率分别为0%，33.3％，81.3％，三者差异有统计学意义（P<0.001）;腺癌中COX 2的高表达与Dukes分期、淋巴结转移和浸润层次有关;HER 2的高表达在腺癌（67.5％）与腺瘤性息肉（80.0%）之间差异无统计学意义，但均高于远癌肠黏膜（33.3%）（P<0.05）;HER 2的胞膜高表达与浸润层次有关;在淋巴结转移灶中COX 2和HER 2具有相关性(χ2=3.949，P<0.05，c=0.3693）。提示 COX 2在正常组织、腺瘤性息肉及腺癌中的表达逐步上调;COX 2可能是结直肠癌发生的早期事件;COX 2的高表达及HER 2胞膜的高表达均与肿瘤侵袭性增高有关。     

SIRT2 Regulates LPS-Induced Renal Tubular CXCL2 and CCL2 Expression

Sirtuin 2 (SIRT2), a NAD⁺-dependent histone deacetylase, is involved in carcinogenesis and genomic instability and modulates proinflammatory immune responses. However, its role in renal inflammatory injury has not been demonstrated. In this study, we explored the expression patterns of CXCL2 and CCL2 in kidney tissue from Sirt2^−/− and Sirt2^+/+ mice and in mouse proximal tubular epithelial (MPT) cells. CXCL2 and CCL2 were significantly downregulated at both the mRNA and the protein levels in kidneys of LPS-treated Sirt2^−/− mice compared with those of LPS-treated Sirt2^+/+ mice. Furthermore, SIRT2 deficiency ameliorated LPS-induced infiltration of neutrophils and macrophages, acute tubular injury, and decrease of renal function. Supporting these observations, CXCL2 and CCL2 expression levels were lower in MPT cells treated with SIRT2-siRNA than in cells treated with control-siRNA, and adenovirus-mediated overexpression of SIRT2 in MPT cells significantly increased the LPS-induced expression of CXCL2 and CCL2 at the mRNA and protein levels. In addition, SIRT2 interacted with mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1), and SIRT2-knockdown increased the acetylation of MKP-1 and suppressed the phosphorylation of p38 MAPK and c-Jun N-terminal kinase in LPS-treated MPT cells. SIRT2 also regulated p65 binding to the promoters of CXCL2 and CCL2. Taken together, these findings indicate that SIRT2 is associated with expression of renal CXCL2 and CCL2 and that regulation of SIRT2 might be an important therapeutic target for renal inflammatory injury.     

环氧合酶-2及血管生成素-2在大肠癌中的表达及临床意义

目的 研究环氧合酶-2（cyclooxygenase-2，Cox-2）及血管生成素-2（angiopoietin-2，Ang-2）在大肠癌组织、癌旁组织及正常大肠组织中的表达及其与大肠癌临床病理特征之间的关系。方法 采用免疫组化SP法检测45例大肠癌组织、45例癌旁组织及15例正常大肠组织中Cox-2和Ang2的表达情况。结果 大肠癌组织中的Cox-2和Ang-2的表达阳性率（80.0％，66.7％）均分别高于癌旁组织（35．6％，11．1％）及正常大肠组织（0，0），P均〈0.01。在大肠癌组织中Cox-2和Ang-2蛋白表达与淋巴结转移及Dukes分期有关（P〈0．05），且二者的表达具有相关性（P〈0．01）。结论 Cox-2和Ang-2在大肠癌发生、发展中起重要作用，二者在表达上密切相关。     

膀胱移行细胞癌中Dab2／DOC-2与GRB2表达的相关性及临床意义

目的探讨Dab2、GRB2在膀胱移行细胞癌中表达的临床意义及其相关性。方法应用免疫组织化学方法检测Dab2、GRB2在64例膀胱移行细胞癌中的表达,采用卡方检验分析两者表达与膀胱移行细胞癌临床病理学特征之间的关系。结果膀胱移行细胞癌中Dab2和GRB2阳性表达率分别是43．8％和81．3％,表达呈负相关（r=-0．383,P=0．002）。Dab2表达水平与肿瘤病理学分期有关,GRB2表达与肿瘤的病理学分级有关。结论Dab2、GRB2蛋白表达可作为判断膀胱移行细胞癌生物学行为的重要指标。     

PGE2和IL-2/IL-2R 在胃癌患者手术前后的动态变化和相互关系

目的　探讨胃癌患者外周血中白细胞介素２ （ＩＬ２）、白细胞介素２ 受体（ｓＩＬ２Ｒ） 水平及ＣＤ２５ 表达三者手术前后的动态变化情况和相互关系,以及前列腺素Ｅ２（ＰＧＥ２） 与ＩＬ２／ＩＬ２Ｒ系统的关系。方法　分别采用ＥＬＩＳＡ法、１２５ＩＲＩＡ法及免疫荧光法对５０ 例胃癌患者手术前后外周血中ＩＬ２、ｓＩＬ２Ｒ、ＰＧＥ２ 水平及ＣＤ２５ 表达进行检测。结果　胃癌患者手术前后外周血中ＩＬ２ 水平及ＣＤ２５ 表达均低于对照组,而ｓＩＬ２Ｒ与ＰＧＥ２ 水平均高于对照组;切除肿瘤后ＩＬ２ 水平及ＣＤ２５ 表达较术前升高,而ｓＩＬ２Ｒ及ＰＧＥ２ 水平较术前下降;６ 例术后发生肿瘤转移或复发的患者中,再次出现ＩＬ２ 水平及ＣＤ２５ 表达下降,而ｓＩＬ２Ｒ及ＰＧＥ２ 水平上升,胃癌患者术前ＩＬ２ 水平与术前ＰＧＥ２ 水平呈显著负相关,术前ｓＩＬ２Ｒ水平与ＩＬ２ 水平亦呈显著负相关。结论　ＰＧＥ２ 与ｓＩＬ２Ｒ 参与了胃癌患者术前存在的免疫抑制过程。非甾体抗炎药（ＮＳＡＩＤ）与外源性ＩＬ２ 联合应用以预防胃癌转移或复发理论上具有可行性。     

HCCR-2反义核酸对肝癌HepG2细胞的作用

目的 研究反义HCCR-2真核表达载体对肝癌HepG2细胞增殖及凋亡的影响.方法 构建反义HCCR-2真核表达载体(反义载体组),转染肝癌HepG2细胞,G418筛选阳性克隆,同样方法获得空载体pIRES2-EGFP稳定表达的细胞株(空载体组),取肝癌HepG2细胞为对照(肝癌HepG2组),用MTT法、流式细胞仪、透射电镜观察反义HCCR-2转染前后肝癌HepG2细胞生长曲线、细胞周期、细胞凋亡及细胞形态的变化.采用单因素方差分析和χ2检验比较各组差异.结果 反义载体组、空载体组、肝癌HepG2组HCCR-2 mRNA表达水平分别为0.39±0.04、0.62±0.06、0.72±0.03,3组比较差异有统计学意义(F=43.701,P<0.05);细胞凋亡率分别为13.30%、2.51%、2.07%,反义载体组与空载体组、肝癌HepG2组比较,差异有统计学意义(χ2=6.793,8.721,P<0.05);反义载体组细胞生长减慢,阻滞于G0/G1期.结论 HCCR-2反义核酸真核表达载体能抑制HCCR-2 mRNA的表达,促进细胞凋亡,HCCR-2蛋白可能参与肝癌细胞的周期调控,并与细胞的生长增殖有关.     

异丙酚麻醉下PaCO2对SjvO2影响的年龄差异

目的研究异氟醚和异丙酚维持神经外科手术中低碳酸和高碳酸血症对颈静脉球血氧饱和度(SjvO     

MMP-2和TIMP-2在大肠癌组织中的表达及其意义

目的探讨基质金属蛋白酶-2(MMP-2)和组织基质金属蛋白抑制剂-2(TIMP-2)在大肠癌组织中的表达及其意义。方法应用免疫组织化学SP法对60例大肠癌组织MMP-2和TIMP-2表达情况进行检测。结果MMP-2和TIMP-2在大肠癌组织中表达的阳性率分别为64.3%和30.3%。MMP-2的表达与大肠癌的病理分期和淋巴转移呈正相关(P<0.05),而TIMP-2的表达与其呈负相关,MMP-2和TIMP-2的表达呈负相关(P<0.05)。结论MMP-2和TIMP-2的表达与大肠癌的病理分期和淋巴转移密切相关,可作为判断大肠癌生物学行为的参考指标。     

NRF2与MRP2在原发性胆囊癌中的表达

Objective To detect the expressions of Nuclear factor-erythroid 2 p45-related factor 2 (NRF2) and multidrug resistance-associated protein 2 (MRP2), and investigate their significance in primary gallbladder carcinoma. Methods Immunohistochemistry SP assay and image analysis were used to detect the expressions of NRF2 and MRP2 protein in 59 patients with primary gallbladder carcinoma. Results A highly positive expression rates of NRF2 and MRP2 were found (76.3% and 74. 6%, respectively) in primary gallbladder carcinoma. The expressions of NRF2 and MRP2 had a significantly correlation with metastases, Nevin staging, and differentiation (P＜0.05), but there was no statistical association with sex and age. The expression of NRF2 had a positive correlation with MRP2 (r=0. 589,P＜0.05). Conclusion Both NRF2 and MRP2 were overexpressed in primary gallbladder carcinoma and they may play a role in the development of primary gallbladder carcinoma.