过氧化物酶体增殖物激活受体γ对人肝癌细胞生长和凋亡的影响及其机制

目的 检测过氧化物酶体增殖物激活受体γ(PPARγ)在人肝癌、癌旁和正常肝组织的表达,探讨激活或抑制PPARγ在肝癌细胞株生长和凋亡中的作用及其机制.方法 应用免疫组织化学方法检测20例肝癌、癌旁和正常肝组织中PPARγ的表达,Western blot检测2种肝癌和1种正常肝细胞株中PPARγ表达;PPARγ激动剂15dPGJ2和拮抗剂T0070907分别干预培养的2种肝癌细胞株,噻唑蓝(MTT)检测细胞生存率,流式细胞术(FCM)检测细胞周期及凋亡,试剂盒检测Caspase-3活性变化.结果 肝癌组织中PPARγ表达高于癌旁和正常肝组织(P＜0.05),PPARγ主要在肝癌细胞质中表达;肝癌细胞株PPARγ表达比正常肝细胞株高(P＜0.05);15dPG-J2抑制肝细胞增殖而T0070907则促进肝癌细胞增殖(P＜0.05).15dPG-J2可使肝癌HepG2和SMMC7721细胞G0/G1期细胞比例由(42.5±0.9)%和(49.0±3.8)%增高至(61.0±2.0)%和(67.5±2.2)%,(P＜0.05),S期由(30.5±0.3)%和(43.0±2.5)%降低至(6.6±1.1)%和(25.1±2.0)%(P＜0.05).而且,15dPG-J2可明显促进两种肝癌细胞凋亡,凋亡率分别增加约24.4%和22.4%,并可增强细胞Caspase-3活性(P＜0.05);Caspase抑制剂Z-VAD-FMK则可逆转15dPG-J2对肝癌细胞的促凋亡作用.结论 PPARγ在肝癌细胞中表达升高,其表达主要位于细胞质中,为无活性状态.PPARγ激动剂可活化PPARγ和Caspase通路,抑制肝癌细胞生长,促进细胞凋亡.

Abstract：

Objective To investigate the expression of peroxisome proliferator-activated receptor γ (PPARγ) in human liver cancer tissue and cells, and to explore the effects and mechanisms of PPARγ on growth and apoptosis in human hepatocellular carcinoma cells. Methods The expression of PPARγ in 20 cases of liver cancer, tumor adjacent tissue, normal liver, one liver cell line and two liver cancer cell lines were detected by immunohistochemistry or Western blotting. Two incubated malignant cell lines were exposed to PPARγ agonist 15dPGJ2 or antagonist T0070907, cell viability was determined by methyl thiazol tetrazolium (MTT) assay and cell cycle distribution and apoptosis were examined by flow cytometry (FCM). Consequently, the activity of caspase-3 following treatments of 15dPGJ2 or T0070907 was observed by the commercial Caspase-3 Activity Kit. Results The expression of PPARγin liver cancer was higher than that in adjacent and normal liver tissue ( P ＜ 0. 05) and PPART was predominantly expressed in the cytoplasm. Further,the expression of PPARγwas higher in hepatoma cell line than that in normal liver cell line (P＜ 0.05 ). PPARγ agonist 15dPG-J2 inhibited the proliferation while the antagonist T0070907 induced the growth of hepatoma cells (P ＜ 0. 05). G0/G1 phase of HepG2 and SMMC772 cells was blocked by 15dPG-J2, and the ratio were raised from (42.5 ±0.9)% and (49.0 ±3.8)% to (61.0 ±2. 0)% and (67.5 ±2. 2)% ,respectively. Meantime,S phase ratio were decreased from (30. 5 ± 0. 3 ) % and (43.0 ± 2. 5 ) % to ( 6. 6 ± 1. 1 ) % and ( 25. 1 ± 2. 0 ) %. Further, 15 dPG-J2 facilitated significant apoptosis in those cell lines and the increased apoptosis ratio were 24. 4% and 22. 4% respectively.Accordingly,the activity of Caspase-3 induced by 15dPGJ2 were 21-and 23-fold higher than those in control groups (P ＜ 0. 05 ). The Caspase inhibitor Z-VAD-fmk expectedly reversed the apoptosis induced by 15dPGJ2 in HepG2 and SMMC772 cells. Conclusion The expression of PPARγ increases in human hepatoma predominantly in cytoplasm with its inactivated form. 15dPG-J2 ,an agonist of PPART inhibits growth and induces apoptotic in hepatoma cells through activation of PPARγ pathway and the consequent Caspase3 signal.     

雷帕霉素对炎性反应状态下肾小球系膜细胞内脂质稳态的影响

Objective To investigate the effect of rapamycin on cholesterol homeostasis of glomerular mesangial cells and the underlying mechanism. Methods Glomerular mesangial cell line (HMCL) cells were cultured and divided into control group, IL-1β group and different concentration rapamycin groups. Intracellular cholesterol accumulation was observed and measured by oil O staining and HPLC. Real-time quantitative PCR and Western blot were used to detect the mRNA and protein expression of LDLR, PPARγ, LXRα, ABCA1 in HMCL after the treatment with IL-1β and rapamycin. Results Rapamycin had no significant influence on intracellular cholesterol concentration under normal condition. IL-1β significantly increased the intracellular cholesterol concentration by 143％ of control (P<0.05), and 10, 50, 100 ?滋g/L rapamycin could significantly inhibit the effect of IL-1β (87％, 116％, 96％ of control respectively, all P<0.05). Rapamycin could suppress the increased expression of LDLR caused by IL-1β on both mRNA and protein level in a dose-dependent manner（P<0.01）. Rapamycin dose-dependently up-regulated the reduced mRNA and protein expression of ABCA1, the decreased mRNA expression of PPARγ and LXRα induced by IL-1β as well (P<0.01）. Conclusion Rapamycin may contribute to the maintenance of intracellular cholesterol homeostasis in glomerular mesangial cells under inflammatory state by both reducing cholesterol uptake and promoting cholesterol efflux.     

Expression and clinical significance of FPARγ and β-catenin in breast cancer

Objective To study the expression of peroxisome proliferator-activated receptor γ (PPARγ) and β-catenin in breast cancer, and their correlations with clinicopathological parameters and prognosis. Methods Tissue samples obtained from 70 patients with breast cancer and 20 patients with breast benign mass were immunohistochemically examined for the expression of PPARγ and p-catenin. Results Overexpression rate of PPARγ protein was 34. 3% in breast cancer, significantly lower than that in breast benign mass. Abnormal expression rate of β-catenin in breast cancer was 67. 1%. A significant negative-correlation was found between the expression of PPARγ and β-catenin (r=-0. 398,P<0.05 ). PPARγ expression was inversely associated with histologic grade, tumor size, axillary lymph node metastasis,TNM stage and Ki-67 expression (P<0. 05), while positively correlated with ER status and overall survival rate (P<0. 05). Abnormal β-catenin expression was positively associated with histologic grade, axillary lymph node metastasis and TNM stage (P<0. 05), while inversely correlated with overall survival rate (P<0.05). Conclusion PPARγ and β-catenin are correlated with development of breast carcinoma,suggesting that detection of PPARγ and β-catenin may be of value in evaluating the biological behaviors and the prognosis of breast cancer.     

Norcantharidin inhibits tumor growth and vasculogenic mimicry of human gallbladder carcinomas by suppression of the PI3-K /MMPs /Ln-5γ2 signaling pathway

Background:Vasculogenic mimicry(VM)is a novel tumor blood supply in some highly aggressive malignant tumors.Recently,we reported VM existed in gallbladder carcinomas(GBCs)and the formation of the special passage through the activation of the PI3K/MMPs/Ln-5γ2 signaling pathway.GBC is a highly aggressive malignant tumor with disappointing treatments and a poor prognosis.Norcantharidin(NCTD)has shown to have multiple antitumor activities against GBCs,etc;however the exact mechanism is not thoroughly elucidated.In this study,we firstly investigated the anti-VM activity of NCTD as a VM inhibitor for GBCs and its underlying mechanisms.Methods:In vitro and in vivo experiments to determine the effects of NCTD on proliferation,invasion,migration,VM formation,hemodynamic and tumor growth of GBC-SD cells and xenografts were respectively done by proliferation,invasion,migration assays,HE staining and CD31-PAS double staining,optic/electron microscopy,tumor assay,and dynamic microMRA.Further,immunohistochemistry,immunofluorescence,Western blotting and RT-PCR were respectively used to examine expression of VM signaling-related markers PI3-K,MMP-2,MT1-MMP and Ln-5γ2 in GBC-SD cells and xenografts in vitro and in vivo.Results:After treatment with NCTD,proliferation,invasion,migration of GBC-SD cells were inhibited;GBC-SD cells and xenografts were unable to form VM-like structures;tumor center-VM region of the xenografts exhibited a decreased signal in intensity;then cell or xenograft growth was inhibited.Whereas all of untreated GBC-SD cells and xenografts formed VM-like structures with the same conditions;the xenograft center-VM region exhibited a gradually increased signal;and facilitated cell or xenograft growth(Figure 1-6).Furthermore,expression of MMP-2 and MT1-MMP products from sections/supernates of 3-D matrices and the xenografts,and expression of PI3-K,MMP-2,MM1-MMP and Ln-5γ2 proteins/mRNAs of the xenografts were all decreased in NCTD or TIMP-2 group(Figure 7-10;all P0.01,vs.control group);NCTD down-regulated expression of these VM signaling-related markers in vitro and in vivo.Conclusions:NCTD inhibited tumor growth and VM formation of human gallbladder carcinoma GBC-SD cells and xenografts by suppression of the PI3-K/MMPs/Ln-5γ2 signaling pathway.It is firstly concluded that NCTD may be a potential anti-VM agent for human GBCs.     

Expression and clinical significance of FPARγ and β-catenin in breast cancer

Objective To study the expression of peroxisome proliferator-activated receptor γ (PPARγ) and β-catenin in breast cancer, and their correlations with clinicopathological parameters and prognosis. Methods Tissue samples obtained from 70 patients with breast cancer and 20 patients with breast benign mass were immunohistochemically examined for the expression of PPARγ and p-catenin. Results Overexpression rate of PPARγ protein was 34. 3% in breast cancer, significantly lower than that in breast benign mass. Abnormal expression rate of β-catenin in breast cancer was 67. 1%. A significant negative-correlation was found between the expression of PPARγ and β-catenin (r=-0. 398,P<0.05 ). PPARγ expression was inversely associated with histologic grade, tumor size, axillary lymph node metastasis,TNM stage and Ki-67 expression (P<0. 05), while positively correlated with ER status and overall survival rate (P<0. 05). Abnormal β-catenin expression was positively associated with histologic grade, axillary lymph node metastasis and TNM stage (P<0. 05), while inversely correlated with overall survival rate (P<0.05). Conclusion PPARγ and β-catenin are correlated with development of breast carcinoma,suggesting that detection of PPARγ and β-catenin may be of value in evaluating the biological behaviors and the prognosis of breast cancer.     

罗格列酮对人多囊肾囊肿衬里上皮细胞增殖的抑制作用

Objective To investigate the antiproliferative effect of rosiglitazone, a thiazolidinedione (TZD) on autosomal dominant polycystic kidney disease (ADPKD) cystic lining epithelial cells and to explore the underlying molecular mechanism. Methods ADPKD cysticlining immortalized epithelial (WT9-12) cells were stimulated by rosiglitazone with different concentrations. After treatment, MTT method was performed to detect the level of proliferation; flow cytometry was used to determine the cell cycle distribution and the apoptosis rate. Western blotting was used to detect the protein expressions of mTOR, p70S6K, 4E-Bp1, PPARγ PPARγ siRNA was transfected into WT9-12 cells to knock down the expression of PPARγ Results Treatment of WT9-12 cells with rosiglitazone resulted in a dose-dependent and time-dependent strong inhibition of cell proliferation, an accumulation of cells in the G0/G1 phase (rosiglitazone 50 μmol/L 65.43%,rosiglitazone 100 μmol/L 64.02%, control 49.65% ) and 6% apoptosis at high concentration (rosiglitazone 200 μmol/L). Rosiglitazone reduced the phosphorylation of p70S6K in a dosedependent and time-dependent manner. The levels of phosphorylated mTOR and 4E-Bp1, the latter being a downstream substrate of mTOR related mRNA translation initiation, were not changed by rosiglitazone. Cells were pre-incubated with GW9662, a PPARγ antagonist, before the treatment with rosiglitazone, the inhibition of p70S6 kinase phosphorylation by rosiglitazone was partially prevented by GW9662 (P＜0.01). Then PPARγ siRNA was transfected into WT9-12 cells, in contrast to untransfected control or cells transfected with an irrelevant siRNA, rosiglitazone did not cause an obvious inhibition of p70S6 kinase phosphorylation in PPARγ knock-down.Conclusion Rosiglitazone inhibits the proliferation of ADPKD cystic lining epithelial cells, and down-regulates p70S6 kinase phosphorylation through mTOR-independent and PPARγ-dependent signal pathway.     

罗格列酮对人多囊肾囊肿衬里上皮细胞增殖的抑制作用

Objective To investigate the antiproliferative effect of rosiglitazone, a thiazolidinedione (TZD) on autosomal dominant polycystic kidney disease (ADPKD) cystic lining epithelial cells and to explore the underlying molecular mechanism. Methods ADPKD cysticlining immortalized epithelial (WT9-12) cells were stimulated by rosiglitazone with different concentrations. After treatment, MTT method was performed to detect the level of proliferation; flow cytometry was used to determine the cell cycle distribution and the apoptosis rate. Western blotting was used to detect the protein expressions of mTOR, p70S6K, 4E-Bp1, PPARγ PPARγ siRNA was transfected into WT9-12 cells to knock down the expression of PPARγ Results Treatment of WT9-12 cells with rosiglitazone resulted in a dose-dependent and time-dependent strong inhibition of cell proliferation, an accumulation of cells in the G0/G1 phase (rosiglitazone 50 μmol/L 65.43%,rosiglitazone 100 μmol/L 64.02%, control 49.65% ) and 6% apoptosis at high concentration (rosiglitazone 200 μmol/L). Rosiglitazone reduced the phosphorylation of p70S6K in a dosedependent and time-dependent manner. The levels of phosphorylated mTOR and 4E-Bp1, the latter being a downstream substrate of mTOR related mRNA translation initiation, were not changed by rosiglitazone. Cells were pre-incubated with GW9662, a PPARγ antagonist, before the treatment with rosiglitazone, the inhibition of p70S6 kinase phosphorylation by rosiglitazone was partially prevented by GW9662 (P＜0.01). Then PPARγ siRNA was transfected into WT9-12 cells, in contrast to untransfected control or cells transfected with an irrelevant siRNA, rosiglitazone did not cause an obvious inhibition of p70S6 kinase phosphorylation in PPARγ knock-down.Conclusion Rosiglitazone inhibits the proliferation of ADPKD cystic lining epithelial cells, and down-regulates p70S6 kinase phosphorylation through mTOR-independent and PPARγ-dependent signal pathway.     

Effect of decoy-oligodeoxynucleotides on expression of inflammation mediators in pMΦ cells from rats

Objective: To study the effect of decoyoligodeoxynucleotides (decoy-ODNs) in dumbbell shape with the oligodeoxynucleotide sequence similar to nuclear factor kappa B (NF-KB) cis-elements on expression of inflammation mediators in pMcP cells from rats. Methods： With carriers of cationic liposomes, decoy-ODNs were transfected into pMΦ cells of rats. Then the inhibiting effects of the decoy-ODNs on tumor necrosis factor α (TNFα), interleukin-6 (IL-6) and IL-10 were analyzed. Results. Decoy-ODNs could decrease the expression of TNFα and IL-6 in dose-dependent fashion but had weaker inhibiting effect on IL-10. Conclusions: Decoy-ODNs targeting NF-κB can decrease the expression of inflammatory mediators in pMΦ cells from rats.     

携带γ-干扰素的溶瘤病毒CNHK300-mIFN-γ治疗肝癌

目的 观察鼠源γ-干扰素(mIFN-γ)基因插入溶瘤腺病毒CNHK300后,该病毒对不同的肝癌细胞株及其裸鼠移植瘤的增殖力及特异性杀伤作用.方法 用噻唑蓝(MTT)法观察CNHK300-mIFN-γ(简称CNHK300-Mγ)对人正常肝细胞WRL-68、人肝癌细胞SMMC-7721、HepG Ⅱ的特异性杀伤作用.裸鼠肝癌SMMC-7721模型观察CNHK300-Mγ、CNHK300和ONYX-015的抗肿瘤疗效,并用酶联免疫吸附试验(ELISA)检测血清中mIFN-γ的表达量.结果 CNHK300-Mγ能选择性地杀伤肝癌细胞,在肿瘤细胞中半数抑制浓度(IC50)＜1,而在正常肝细胞中为370.肝癌模型中,CNHK300-Mγ治疗组能表达mIFN-γ,治疗结束后第3天和第7天血清中的mIFN-γ分别为(231±101)ng/L和(1733±191)ng/L.CNHK300-Mγ具有明显的肿瘤生长抑制作用,与CNHK300、ONYX2015和对照组的差异均有统计学意义(P＜0.05).结论 mIFN-γ的插入使病毒对肿瘤细胞的杀伤能力提高,CNHK300-Mγ具有明显的肿瘤生长抑制作用.

Abstract：

Objective To study the effect of mouse interferon-γ (mIFN-γ) insertion on the selective replication and cytotoxicity of a tumor-specific oncolytic adenovirus CNHK300 in hepatocellular carcinoma (HCC) cells and HCC xenografts. Methods The cytotoxicity of CNHK300-mIFN-γ (CNHK300-Mγ) was examined by methyl thiazol tetrazolium (MTT) colorimetric assay in normal and HCC cells.Healthy nude BALB/C mice were injected with the SMMC-7221 cells. Forty mice with tumors of 5-8 mm in diameter were randomly divided into 4 groups of 10 mice: CNHK300-Mγ group (CNHK300-Mγ was injected into the tumor once every other day for 5 times) , CNHK300 group ( CNHK300 was injected) , ONYX-015 group (ONYX-015 was injected) , and control group (diluent of virus was injected). Seven, 14, 21, 28, 35, and 42 days after the initial injection the size of tumor was examined ( Tumor volume was estimated as a × b2 × 0. 5 , where a and b were the maximal and minimal diameters, respectively). Forty-eighth after the finish of the whole course of treatment, the mice were killed. Twenty-four mice with the same tumors were randomly divided into 3 groups of 8 mice: CNHK300-Mr group, CHNK300 group and control group.The mice were killed in half, 3, 7 days after the last injection. Enzyme linked immunosorbent assay (ELISA) was used to detect the expression of mIFN-γ in blood. Results CNHK300-Mγ could selectively kill tumor cell lines, whose 50% inhibitory concentration (IC50) was under 1 in tumor cells and 370 in normal liver cells. ELISA showed that the expression of mIFN-γ in the blood of the CNHK300-Mγ group was (231 ± 101) ng/L or (1733 ± 191) ng/L in 3 days or 7 days after virus infection, while no mIFN-γ could be detected in CHNK300 group and control group. The tumor size in the CNHK300-Mr group was significantly smaller than in the CNHK300 group, ONYX-015 group, and control group (P＜0. 05). Conclusion Being capable of specifically killed HCC cells and mediating effective expression of therapeutic gene in vivo, CNHK300-Mγ holds a splendid future as a potential antitumor agent.     

Construction of recombinant baculovirus Ac-CMV-hSox9 for gene therapy of intervertebral disc degeneration

Objective： To construct the recombinant baculovirus Ac-cytomegalovirus （CMV）-hSox9 for gene therapy of intervertebral disc degeneration. Methods： Bac-to-Bac system was used for the construction of baculovirus Ac-CMV-hSox9. The cDNA of hSox9 was first cloned into a plasmid vector under the control of CMV promotor to generate the donor plasmid pFastBacDul-green fluorescene protein （ GFP ）-CMV （pgGC）-hSox9. The resultant plasmid was transformed into DH10Bac cells and then the transformation mixture was spread on Luria-Bertani （LB） agarose culture medium containing isopropyl-β-D-thiogalactoside （IPTG）, X-gal, gentamicin, kanamycin and tetracycline. The white colonies were selected and cultured for amplification, and the hSox9 Bacmid DNA was extracted. After verification, recombinant baculovirns Ac-CMV-hSox9 was obtained through transfecting Sf 21 cells. The expression of hSox9 gene in the intervertebral disc cells in rabbits was determined by Western blotting and immunohistochemical staining. Results： Polymerase chain reaction （ PCR ） confirmed the presence of hSox9 gene in the recombinant baculovirus and the Sf 21 cells transfected by the baculovirus showed the expression of fluorescence protein. Western blotting and indicated that exogenous hSox9 disc cells. staining analysis Conclusions： The successful construction of the recombinant baculovirus Ac-CMV-hSox9 and the confirmation of the target gene expression provides a novel expression vector system for basic research and clinical treatment of intervertebral degenerative disc disease.     

Changes of pulmonary intercellular adhesion molecule-1 and CD11b／CD18 in peripheral polymorphonuclear neutrophils and their significance at the early stage of burns

Objective: To investigate the role of intercellular adhesion molecule-1 (ICAM-1) in the accumulation of polymorphonuclear neutrophils (PMN) in the lungs at the early stage of burns. Methods: Myeloperoxidase content in lung tissues and bronchoalveolar lavage fluid (BALF) were detected.ICAM-1 and its mRNA expression in lung tissues were determined bycal method and in situ hybridization. CD11b/CD18 expression on the peripheral PMNs was measured by flowcytometry. Results : The levels of myeloperoxidase in lung tissues and BALF after burn injury were markedly higher than those of control. Expression of ICAM-1 and its mRNA in the lung tissues and CD11b/CD18 on peripheral PMNs surface was significantly increased at 2, 6, 12, 24 h after burns. Conclusions. PMNs accumulation in the lungs is related to increased ICAM-1 expression on pulmonary microvascular endothelial cells and CD11b/CD18 expression on PMN at the early stage of burn injury.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.     

Effects of laparoscopy-assisted radical gastrectomy on the expression of intercellular adhesion molecule β1 and integrin 1 in peritoneal mesothelial cells and its significance

Objective To investigate the changes of the expression of intercellular adhesion molecule-1 (ICAM-1) and integrin β1 in peritoneal mesothelial cells during laparoscopy-assisted radical gastrectomy (LARG) and to explore the possible effects of LARG on the peritoneal metastasis. Methods From April to August 2008, LARG was performed for 26 patients with gastric cancer (laparoscopy group), while 20 cases underwent open radical gastrectomy (open group). Peritoneum of right upper belly was collected at 3 operation time points (the beginning, 2 hours, 4 hours). The expressions of ICAM-1 and integrin β1 in peritoneal mesothelial cells at 3 time points were detected by immunohistochemistry. Results With the operation prolonging, the expression of ICAM-1 and integrin β1 was increased gradually in both LARG and open groups. The expression of integrin β1 in two groups was obviously increased at 4-hour time point as compared to the beginning (P<0.05). Besides, there were no significant differences of these two adhesion molecules among the three operation time points between two groups (P>0.05). Conclusions Compared with open surgery, LARG is not associated with a greater effect on the expression of ICAM-1 and integrin β1 in peritoneal mesothelial cells, and may not promote peritoneal metastasis of gastric cancer through increasing the expression of adhesion molecule in peritoneal mesothelial cells.