Pub Date : 2001-03-01DOI: 10.1046/J.1443-9573.2001.00023.X
M. Hua, Yuan Ai-li, Zhao Min-fang, Lai Zuosheng
OBJECTIVE: Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis, infiltration and metastasis in cancer. However, the associated signal transduction pathway remains unclear. The present study aimed to observe the effect of signal transduction induced by VEGF on p38 mitogen-activated protein kinase (MAPK) during metastasis in hepatocellular carcinoma. METHODS: The membrane invasion culture system (MICS) and SB203580, a blocker of p38 MAPK were used to observe the inhibitory effect of VEGF on metastasis in hepatocellular carcinoma. RESULTS: The numbers of cells in the lower compartment of the Boden chamber with or without SB203580 were 16 × 104 and 0.75 × 104/mL, respectively, after being cultured for 5 h with 5 ng/mL VEGF. These values were markedly higher than the number of cells (1.25 × 104/mL) in the control group (P < 0.01). Pretreatment with 5 μmol/L SB203580 was able to block metastatic potential by 95% in hepatic cancer, the hepatocarcinoma cell number cultured for 5 h with 1 ng/mL VEGF, 5 ng/mL VEGF, 10 ng/mL VEGF in amnia was 15, 42 and 28, respectively, as compared with the control (4 cells), these were highly significant (P < 0.05, P < 0.01). When compared with group of 1 ng/mL VEGF, and group 10 ng/mL VEGF, the carcinoma cell number of group of 5 ng/mL VEGF was also highly significant (P < 0.05). CONCLUSIONS: Via the p38 MAPK signal transduction pathway, VEGF is able to induce metastasis in hepatic carcinoma. However, when this particular pathway was blocked with SB203580, then metastasis was inhibited.
{"title":"Role of signal transduction pathway of mitogen‐activated protein kinase on metastasis of hepatocellular carcinoma induced by VEGF","authors":"M. Hua, Yuan Ai-li, Zhao Min-fang, Lai Zuosheng","doi":"10.1046/J.1443-9573.2001.00023.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00023.X","url":null,"abstract":"OBJECTIVE: Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis, infiltration and metastasis in cancer. However, the associated signal transduction pathway remains unclear. The present study aimed to observe the effect of signal transduction induced by VEGF on p38 mitogen-activated protein kinase (MAPK) during metastasis in hepatocellular carcinoma. \u0000 \u0000 \u0000 \u0000METHODS: The membrane invasion culture system (MICS) and SB203580, a blocker of p38 MAPK were used to observe the inhibitory effect of VEGF on metastasis in hepatocellular carcinoma. \u0000 \u0000 \u0000 \u0000RESULTS: The numbers of cells in the lower compartment of the Boden chamber with or without SB203580 were 16 × 104 and 0.75 × 104/mL, respectively, after being cultured for 5 h with 5 ng/mL VEGF. These values were markedly higher than the number of cells (1.25 × 104/mL) in the control group (P < 0.01). Pretreatment with 5 μmol/L SB203580 was able to block metastatic potential by 95% in hepatic cancer, the hepatocarcinoma cell number cultured for 5 h with 1 ng/mL VEGF, 5 ng/mL VEGF, 10 ng/mL VEGF in amnia was 15, 42 and 28, respectively, as compared with the control (4 cells), these were highly significant (P < 0.05, P < 0.01). When compared with group of 1 ng/mL VEGF, and group 10 ng/mL VEGF, the carcinoma cell number of group of 5 ng/mL VEGF was also highly significant (P < 0.05). \u0000 \u0000 \u0000 \u0000CONCLUSIONS: Via the p38 MAPK signal transduction pathway, VEGF is able to induce metastasis in hepatic carcinoma. However, when this particular pathway was blocked with SB203580, then metastasis was inhibited.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90660808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-03-01DOI: 10.1046/J.1443-9573.2001.00016.X
Qin Chengyong, Li Dongxing, Zhu Juren, Fu Lina, Wang Zhaohai, Z. Guoquan, Jia Tao
OBJECTIVE: To evaluate the therapeutic effect of release-controlled nifedipine on portal hypertension. METHODS: Thirty-two cirrhotic patients were enrolled to investigate, by using duplex Doppler ultrasonography, differences in portal hemodynamics before and after treatment with release-controlled nifedipine (30 mg once per day). RESULTS: After taking nifedipine, the diameter, blood velocity and blood flow of the portal vein decreased, but only the change in velocity was statistically significant. After treatment, the congestion index increased, and the blood velocity and blood flow of the splenic vein significantly decreased. The resistance and pulsatile indices of the right hepatic and splenic arteries also decreased markedly. The total hepatic blood flow was elevated slightly and there were no significant changes in mean arterial pressure and heart rate. CONCLUSIONS: The resistance and pulsatile indices of the hepatic and splenic arteries are representative indices of portal resistance. Release-controlled nifedipine may decrease portal pressure by the following mechanisms: (i) decrease of systemic blood pressure triggers the sympathetic reflex, leading to splanchnic artery constriction and portal blood flow reduction; (ii) dilatation of the portal vein and sinusoids leads to decrease portal resistance; and (iii) dilatation of the collateral veins. Nifedipine has no significant effect on systemic circulation in normotensive cirrhotic patients, therefore it has good prospects as a drug for clinical use in portal hypertension.
{"title":"Effect of release‐controlled nifedipine on portal hemodynamics in cirrhotic patients","authors":"Qin Chengyong, Li Dongxing, Zhu Juren, Fu Lina, Wang Zhaohai, Z. Guoquan, Jia Tao","doi":"10.1046/J.1443-9573.2001.00016.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00016.X","url":null,"abstract":"OBJECTIVE: To evaluate the therapeutic effect of release-controlled nifedipine on portal hypertension. \u0000 \u0000 \u0000 \u0000METHODS: Thirty-two cirrhotic patients were enrolled to investigate, by using duplex Doppler ultrasonography, differences in portal hemodynamics before and after treatment with release-controlled nifedipine (30 mg once per day). \u0000 \u0000 \u0000 \u0000RESULTS: After taking nifedipine, the diameter, blood velocity and blood flow of the portal vein decreased, but only the change in velocity was statistically significant. After treatment, the congestion index increased, and the blood velocity and blood flow of the splenic vein significantly decreased. The resistance and pulsatile indices of the right hepatic and splenic arteries also decreased markedly. The total hepatic blood flow was elevated slightly and there were no significant changes in mean arterial pressure and heart rate. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: The resistance and pulsatile indices of the hepatic and splenic arteries are representative indices of portal resistance. Release-controlled nifedipine may decrease portal pressure by the following mechanisms: (i) decrease of systemic blood pressure triggers the sympathetic reflex, leading to splanchnic artery constriction and portal blood flow reduction; (ii) dilatation of the portal vein and sinusoids leads to decrease portal resistance; and (iii) dilatation of the collateral veins. Nifedipine has no significant effect on systemic circulation in normotensive cirrhotic patients, therefore it has good prospects as a drug for clinical use in portal hypertension.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78653929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-03-01DOI: 10.1046/J.1443-9573.2001.00022.X
Yang Zhengbing, Ouyang Qin, W. Yuquan, Liu Xiaoqin, L. Song
OBJECTIVE: To investigate: (i) the effect of sulindac on the proliferation of HT-29 cells; and (ii) the antineoplastic mechanisms of sulindac. METHODS: The MTT colorimetric assay was used to examine the effect of sulindac on the proliferation of HT-29 cells. Flow cytometry was used for examining the cell cycle distribution. Flow cytometry, transmission electron microscopy and DNA electrophoresis were used to determine whether sulindac induces cell apoptosis. RESULTS: Sulindac inhibited cell proliferation in a time- and dose-dependent manner. After treatment with 0.3, 0.6, 0.9 and 1.2 mmol/L sulindac for 72 h, the inhibition rates reached 16, 38, 62.3 and 92.2%, respectively. After treatment with 1.2 mmol/L sulindac for 24, 48 and 72 h, the inhibition rates reached 32.4, 71.3 and 92.2%, respectively (P < 0.05). Sulindac increased the proportion of cells in the G0/G1 phase and decreased the proportion of cells in the S phase of the cell cycle. After treatment with 1.2 mmol/L sulindac for 48 h, the proportion of cells in the G0/G1 phase increased from 32.5 to 70.5% and the S phase decreased from 43.1 to 11.3% compared with the control cells (P < 0.01). Flow cytometry, DNA electrophoresis and transmission electron microscopy all demonstrated that sulindac could induce apoptosis of the HT-29 cell line. After treatment with 0.3, 0.6 and 1.2 mmol/L sulindac for 48 h, the proportion of apoptotic cells reached 5.8, 7.6 and 11.7%, compared with 2.9% in the control group; after treatment for 72 h, the proportion of apoptotic cells increased to 12.5, 15.4% and 24.2%, respectively (P < 0.05). All effects were time and dose dependent. CONCLUSIONS: The colon adenocarcinoma HT-29 cell line can be inhibited by sulindac and the antitumor mechanism may be related to changing cell cycle distribution and inducing cell apoptosis.
{"title":"Inhibitory effect of sulindac on the proliferation of HT‐29 colon adenocarcinoma cells: Effects on cell cycle and apoptosis","authors":"Yang Zhengbing, Ouyang Qin, W. Yuquan, Liu Xiaoqin, L. Song","doi":"10.1046/J.1443-9573.2001.00022.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00022.X","url":null,"abstract":"OBJECTIVE: To investigate: (i) the effect of sulindac on the proliferation of HT-29 cells; and (ii) the antineoplastic mechanisms of sulindac. \u0000 \u0000 \u0000 \u0000METHODS: The MTT colorimetric assay was used to examine the effect of sulindac on the proliferation of HT-29 cells. Flow cytometry was used for examining the cell cycle distribution. Flow cytometry, transmission electron microscopy and DNA electrophoresis were used to determine whether sulindac induces cell apoptosis. \u0000 \u0000 \u0000 \u0000RESULTS: Sulindac inhibited cell proliferation in a time- and dose-dependent manner. After treatment with 0.3, 0.6, 0.9 and 1.2 mmol/L sulindac for 72 h, the inhibition rates reached 16, 38, 62.3 and 92.2%, respectively. After treatment with 1.2 mmol/L sulindac for 24, 48 and 72 h, the inhibition rates reached 32.4, 71.3 and 92.2%, respectively (P < 0.05). Sulindac increased the proportion of cells in the G0/G1 phase and decreased the proportion of cells in the S phase of the cell cycle. After treatment with 1.2 mmol/L sulindac for 48 h, the proportion of cells in the G0/G1 phase increased from 32.5 to 70.5% and the S phase decreased from 43.1 to 11.3% compared with the control cells (P < 0.01). Flow cytometry, DNA electrophoresis and transmission electron microscopy all demonstrated that sulindac could induce apoptosis of the HT-29 cell line. After treatment with 0.3, 0.6 and 1.2 mmol/L sulindac for 48 h, the proportion of apoptotic cells reached 5.8, 7.6 and 11.7%, compared with 2.9% in the control group; after treatment for 72 h, the proportion of apoptotic cells increased to 12.5, 15.4% and 24.2%, respectively (P < 0.05). All effects were time and dose dependent. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: The colon adenocarcinoma HT-29 cell line can be inhibited by sulindac and the antitumor mechanism may be related to changing cell cycle distribution and inducing cell apoptosis.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83435052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-03-01DOI: 10.1111/J.1443-9573.2001.00015.X
C. Long, Lin Yan-zhen, Jin Guoxiang, Yu Dehong, T. Yue, Gao Jun, Chen Xuehua, Y. Baoming
OBJECTIVE: To improve the efficacy of gene delivery and to determine an effective way to kill gastric cancer cells by using a suicide gene. METHODS: First, the cytosine deaminase (CD) gene was cloned into an adenovirus vector and the recombinant plasmid was packed, amplified and purified. Murine gastric cancer cell line MFC was injected subcutaneously into the flanks of 615 mice, and when tumors were palpable, 0.2 mL of the recombinant adenovirus solution was injected directly into xenografts following the daily administration of 5-fluorocytosine (5-Fc) for 35 days. RESULTS: Positive clones were selected by using endonucleases to digest the recombinants, and the concentration of viral particles containing the CD gene was 1.2 × 1012 particles/mL. An antitumor effect was observed in MFC–CD(+) tumors when the animals were given 5-Fc via intraperitoneal injection. Pathologically, the tumors generated from MFC–CD(+) cells had widespread hemorrhagic necrosis within the tumor regions as compared with those of untreated animals, which had few necrotic regions. CONCLUSIONS: The improved antitumor effect of this adenovirus vector suggests a basis for further research involving the direct transduction of the CD gene into tumors, as well as inducing an intensive bystander effect.
{"title":"Cytotoxic effect of the cytosine deaminase gene delivered by the adenovirus vector in murine gastric cancer","authors":"C. Long, Lin Yan-zhen, Jin Guoxiang, Yu Dehong, T. Yue, Gao Jun, Chen Xuehua, Y. Baoming","doi":"10.1111/J.1443-9573.2001.00015.X","DOIUrl":"https://doi.org/10.1111/J.1443-9573.2001.00015.X","url":null,"abstract":"OBJECTIVE: To improve the efficacy of gene delivery and to determine an effective way to kill gastric cancer cells by using a suicide gene. \u0000 \u0000 \u0000 \u0000METHODS: First, the cytosine deaminase (CD) gene was cloned into an adenovirus vector and the recombinant plasmid was packed, amplified and purified. Murine gastric cancer cell line MFC was injected subcutaneously into the flanks of 615 mice, and when tumors were palpable, 0.2 mL of the recombinant adenovirus solution was injected directly into xenografts following the daily administration of 5-fluorocytosine (5-Fc) for 35 days. \u0000 \u0000 \u0000 \u0000RESULTS: Positive clones were selected by using endonucleases to digest the recombinants, and the concentration of viral particles containing the CD gene was 1.2 × 1012 particles/mL. An antitumor effect was observed in MFC–CD(+) tumors when the animals were given 5-Fc via intraperitoneal injection. Pathologically, the tumors generated from MFC–CD(+) cells had widespread hemorrhagic necrosis within the tumor regions as compared with those of untreated animals, which had few necrotic regions. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: The improved antitumor effect of this adenovirus vector suggests a basis for further research involving the direct transduction of the CD gene into tumors, as well as inducing an intensive bystander effect.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83541577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-03-01DOI: 10.1046/J.1443-9573.2001.00019.X
Jiang Xuhuai, D. Burroni, Xu Guoming, C. Pagliaccia, J. Reyrat, Tu Zhen-xing, Ding Hua, Du Yiqi, R. Rappuoli, J. Telford
OBJECTIVE: To characterize the vacA alleles present in Chinese Helicobacter pylori strains and to compare the allelic variation in the vacA gene of Chinese strains with that of Western strains. METHODS: Twenty-two single colonies of H. pylori isolated from five biopsy specimens with different gastric disorders were characterized for the expression of VacA protein and for evaluating the cytotoxic activity in HeLa cells. Five representative strains were selected and the vacA gene was amplified by PCR and subjected to automatic DNA sequencing using a primer walking strategy. RESULTS: Four strains expressed the VacA protein. Only one of the five strains induced vacuole degeneration in HeLa cells. All five vacA genes coded for identical signal peptides of the sla allele and had similar sequences encoding a 37 kDa subunit and outer membrane exporter. One of the five strains expressed a VacA protein with a middle region of the m1 allele and the others of the m2 allele. The four m2 allele strains had little vacuolating activity in HeLa cells. Phylogenetic analysis indicated that the homology of the Chinese vacA genes was 97.6–99.2% compared with 91.3–92.0% in the Western strains. CONCLUSIONS: There are allelic variations in the vacA gene between Chinese and Western H. pylori. Chinese H. pylori strains form a phylogenetically independent cluster separated from Western isolates. The m2-type strains seem to be more prevalent in China. Cytotoxicity in HeLa cells appear to associate with the middle region but not the signal sequence.
{"title":"Allelic variation in the vacA gene of Helicobacter pylori isolated from Chinese patients","authors":"Jiang Xuhuai, D. Burroni, Xu Guoming, C. Pagliaccia, J. Reyrat, Tu Zhen-xing, Ding Hua, Du Yiqi, R. Rappuoli, J. Telford","doi":"10.1046/J.1443-9573.2001.00019.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00019.X","url":null,"abstract":"OBJECTIVE: To characterize the vacA alleles present in Chinese Helicobacter pylori strains and to compare the allelic variation in the vacA gene of Chinese strains with that of Western strains. \u0000 \u0000 \u0000 \u0000METHODS: Twenty-two single colonies of H. pylori isolated from five biopsy specimens with different gastric disorders were characterized for the expression of VacA protein and for evaluating the cytotoxic activity in HeLa cells. Five representative strains were selected and the vacA gene was amplified by PCR and subjected to automatic DNA sequencing using a primer walking strategy. \u0000 \u0000 \u0000 \u0000RESULTS: Four strains expressed the VacA protein. Only one of the five strains induced vacuole degeneration in HeLa cells. All five vacA genes coded for identical signal peptides of the sla allele and had similar sequences encoding a 37 kDa subunit and outer membrane exporter. One of the five strains expressed a VacA protein with a middle region of the m1 allele and the others of the m2 allele. The four m2 allele strains had little vacuolating activity in HeLa cells. Phylogenetic analysis indicated that the homology of the Chinese vacA genes was 97.6–99.2% compared with 91.3–92.0% in the Western strains. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: There are allelic variations in the vacA gene between Chinese and Western H. pylori. Chinese H. pylori strains form a phylogenetically independent cluster separated from Western isolates. The m2-type strains seem to be more prevalent in China. Cytotoxicity in HeLa cells appear to associate with the middle region but not the signal sequence.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73042973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-03-01DOI: 10.1046/J.1443-9573.2001.00021.X
Cui Rutao, C. Gan, C. Yong, Yang Qiuhong, T. Tao
OBJECTIVE: To study the mechanism and effect of all-trans retinoic acid on apoptosis and the expression of Bcl-2, Fas and ICE in experimentally induced dysplastic gastric epithelial cells. METHODS: Apoptosis and expression of Bcl-2, Fas and ICE in gastric epithelial cells was studied using the terminal dUTP nucleotide end-labeling (TUNEL) technique. The immunohistochemistry of Wistar rats enrolled in three groups was studied: group 1, blank controls; group 2, dysplasia induced by N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and then treated with all-trans retinoic acid; and group 3, dysplasia induced by MNNG and treated with a placebo. RESULTS: In the three groups, the rates of dysplasia were 0, 26.7 and 73.3%; the apoptosis indices were 8.3 ± 3.1, 7.8 ± 2.6 and 2.2 ± 0.4; the expression of Bcl-2 was 13.3, 33.3 and 66.7%; and overexpression of Bcl-2 was 6.7, 6.7 and 33.3%, respectively. There were significant differences between group 2 and group 3 (P 0.05). The expression rates of Fas were 46.7, 40 and 6.7%; the overexpression rates were 13.3, 26.7 and 13.3%, respectively; the expression rates of ICE were 20, 60 and 13.3%; the overexpression rates were 0, 13.3 and 6.7% in the three groups, respectively. The expression rates of Fas and ICE in group 2 were significantly different from that of group 3 (P < 0.05), but there were no significant differences in overexpression rates between group 2 and group 3. No significant differences were found either in expression or overexpression of Fas and ICE between group 2 and group 1. CONCLUSIONS: These results suggest that all-trans retinoic acid inhibits Bcl-2 expression, promotes Fas expression, enhances ICE expression and gastric mucosal epithelial cell apoptosis, and thus may reverse or inhibit the progression to cancer.
{"title":"Effect of all‐trans retinoic acid on apoptosis and expression of regulatory genes (Bcl‐2, Fas, ICE) in experimentally induced gastric epithelial cell dysplasia in rats","authors":"Cui Rutao, C. Gan, C. Yong, Yang Qiuhong, T. Tao","doi":"10.1046/J.1443-9573.2001.00021.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00021.X","url":null,"abstract":"OBJECTIVE: To study the mechanism and effect of all-trans retinoic acid on apoptosis and the expression of Bcl-2, Fas and ICE in experimentally induced dysplastic gastric epithelial cells. \u0000 \u0000 \u0000 \u0000METHODS: Apoptosis and expression of Bcl-2, Fas and ICE in gastric epithelial cells was studied using the terminal dUTP nucleotide end-labeling (TUNEL) technique. The immunohistochemistry of Wistar rats enrolled in three groups was studied: group 1, blank controls; group 2, dysplasia induced by N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and then treated with all-trans retinoic acid; and group 3, dysplasia induced by MNNG and treated with a placebo. \u0000 \u0000 \u0000 \u0000RESULTS: In the three groups, the rates of dysplasia were 0, 26.7 and 73.3%; the apoptosis indices were 8.3 ± 3.1, 7.8 ± 2.6 and 2.2 ± 0.4; the expression of Bcl-2 was 13.3, 33.3 and 66.7%; and overexpression of Bcl-2 was 6.7, 6.7 and 33.3%, respectively. There were significant differences between group 2 and group 3 (P 0.05). The expression rates of Fas were 46.7, 40 and 6.7%; the overexpression rates were 13.3, 26.7 and 13.3%, respectively; the expression rates of ICE were 20, 60 and 13.3%; the overexpression rates were 0, 13.3 and 6.7% in the three groups, respectively. The expression rates of Fas and ICE in group 2 were significantly different from that of group 3 (P < 0.05), but there were no significant differences in overexpression rates between group 2 and group 3. No significant differences were found either in expression or overexpression of Fas and ICE between group 2 and group 1. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: These results suggest that all-trans retinoic acid inhibits Bcl-2 expression, promotes Fas expression, enhances ICE expression and gastric mucosal epithelial cell apoptosis, and thus may reverse or inhibit the progression to cancer.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83974693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-03-01DOI: 10.1046/J.1443-9573.2001.00028.X
Wang Xingpeng, Wang Bingxian, Wu Jianxin, W. Guoliang
OBJECTIVE: Because bacterial translocation from the gut is one of the important sources of bacterial infection in acute necrotizing pancreatitis (ANP), and growth hormone (GH) has the ability to promote intestinal epithelial proliferation, we investigated the effects of GH on bacterial translocation in a rat ANP model. METHODS: Acute necrotizing pancreatitis was induced in rats via injection of 5% sodium taurocholate into the biliopancreatic duct. The rats with ANP were treated with either human recombinant GH or a placebo. Laparotomized animals without ANP induction (sham operation) served as controls. Twenty-four hours after the operation, blood was drawn for bacterial culture and determinations of amylase, lipase and endotoxin. Peritoneal fluid and specimens of mesenteric lymph nodes (MLN), liver, pancreas and spleen were taken for bacterial culture by standard techniques. Intestinal mucosal permeability was assessed by measuring the movement of [125I]-labeled albumin from blood to the intestinal lumen. Insulin-like growth factor-1 (IGF-1) mRNA was detected in the liver and ileum by reverse transcription–polymerase chain reaction (RT-PCR). Morphological changes in the pancreas and ileum were also analyzed. RESULTS: Administration of GH significantly decreased the activity of serum amylase and lipase, decreased the plasma endotoxin level and reduced the incidence of bacterial translocation. Moreover, the survival rate of ANP rats was improved. The severity of inflammation in the pancreas and ileum was reduced by GH treatment. Ileal mucosal thickness, villus height and crypt depth in GH-treated rats were obviously increased as compared with those of ANP rats. The intestinal permeability was markedly decreased in the GH group as compared with the ANP group. GH treatment resulted in upregulation of IGF-1 mRNA expression in ileum, but not in liver. CONCLUSIONS: These results suggest that exogenous GH has beneficial effects in maintaining the integrity of the intestinal mucosal barrier and reducing the incidence of bacterial translocation in rats with ANP. One of the mechanisms might be the upregulation of IGF-1 mRNA in the intestine by GH.
{"title":"Beneficial effects of growth hormone on bacterial translocation during the course of acute necrotizing pancreatitis in rats","authors":"Wang Xingpeng, Wang Bingxian, Wu Jianxin, W. Guoliang","doi":"10.1046/J.1443-9573.2001.00028.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00028.X","url":null,"abstract":"OBJECTIVE: Because bacterial translocation from the gut is one of the important sources of bacterial infection in acute necrotizing pancreatitis (ANP), and growth hormone (GH) has the ability to promote intestinal epithelial proliferation, we investigated the effects of GH on bacterial translocation in a rat ANP model. \u0000 \u0000METHODS: Acute necrotizing pancreatitis was induced in rats via injection of 5% sodium taurocholate into the biliopancreatic duct. The rats with ANP were treated with either human recombinant GH or a placebo. Laparotomized animals without ANP induction (sham operation) served as controls. Twenty-four hours after the operation, blood was drawn for bacterial culture and determinations of amylase, lipase and endotoxin. Peritoneal fluid and specimens of mesenteric lymph nodes (MLN), liver, pancreas and spleen were taken for bacterial culture by standard techniques. Intestinal mucosal permeability was assessed by measuring the movement of [125I]-labeled albumin from blood to the intestinal lumen. Insulin-like growth factor-1 (IGF-1) mRNA was detected in the liver and ileum by reverse transcription–polymerase chain reaction (RT-PCR). Morphological changes in the pancreas and ileum were also analyzed. \u0000 \u0000RESULTS: Administration of GH significantly decreased the activity of serum amylase and lipase, decreased the plasma endotoxin level and reduced the incidence of bacterial translocation. Moreover, the survival rate of ANP rats was improved. The severity of inflammation in the pancreas and ileum was reduced by GH treatment. Ileal mucosal thickness, villus height and crypt depth in GH-treated rats were obviously increased as compared with those of ANP rats. The intestinal permeability was markedly decreased in the GH group as compared with the ANP group. GH treatment resulted in upregulation of IGF-1 mRNA expression in ileum, but not in liver. \u0000 \u0000CONCLUSIONS: These results suggest that exogenous GH has beneficial effects in maintaining the integrity of the intestinal mucosal barrier and reducing the incidence of bacterial translocation in rats with ANP. One of the mechanisms might be the upregulation of IGF-1 mRNA in the intestine by GH.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89314951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2000-11-01DOI: 10.1046/J.1443-9573.2000.00013.X
Cheng Shuqun, Z. Xinda, T. Zhao-you, Yu Yao, Bao Susu, Qian Dechu
OBJECTIVE: To assess the efficacy of high-intensity focused ultrasound (HIFU) when combined with heparin and cortisone acetate in treating experimental liver cancer LTNM4 implanted subcutaneously in nude mice. METHODS: High-intensity focused ultrasound treatment was administered with a focused 1.1 MHz transducer at a peak intensity of 750 W/cm2 for a continuous exposure of 20 s and, 1 day later, heparin (300 U/mL) was given orally in drinking water and an initial dose of 250 mg/kg cortisone acetate was injected subcutaneously into each mouse. Forty-eight mice with tumors were randomly divided into four groups. Group I (n = 12) were controls; Group II (n = 12) received heparin and cortisone therapy; Group III (n = 12) received HIFU therapy only; Group IV (n = 12) received both HIFU, heparin and cortisone therapy. RESULTS: Significant inhibition of tumor growth was seen in groups II, III and IV as compared with group I (P < 0.05), with the tumor growth inhibition rate on the 28th day being 86, 90 and 99%, respectively. All mice in group IV were cured, with no evidence of tumors by the 35th day and, histologically, no tumor cells remained. CONCLUSIONS: The data suggest that HIFU can destroy liver cancer effectively and that HIFU combined with treatment using the anti-angiogenic agents heparin and cortisone may constitute a comprehensive treatment to ablate liver cancer.
{"title":"Effects of high‐intensity focused ultrasound and anti‐angiogenic agents on the ablation of experimental liver cancers","authors":"Cheng Shuqun, Z. Xinda, T. Zhao-you, Yu Yao, Bao Susu, Qian Dechu","doi":"10.1046/J.1443-9573.2000.00013.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2000.00013.X","url":null,"abstract":"OBJECTIVE: To assess the efficacy of high-intensity focused ultrasound (HIFU) when combined with heparin and cortisone acetate in treating experimental liver cancer LTNM4 implanted subcutaneously in nude mice. \u0000 \u0000 \u0000 \u0000METHODS: High-intensity focused ultrasound treatment was administered with a focused 1.1 MHz transducer at a peak intensity of 750 W/cm2 for a continuous exposure of 20 s and, 1 day later, heparin (300 U/mL) was given orally in drinking water and an initial dose of 250 mg/kg cortisone acetate was injected subcutaneously into each mouse. Forty-eight mice with tumors were randomly divided into four groups. Group I (n = 12) were controls; Group II (n = 12) received heparin and cortisone therapy; Group III (n = 12) received HIFU therapy only; Group IV (n = 12) received both HIFU, heparin and cortisone therapy. \u0000 \u0000 \u0000 \u0000RESULTS: Significant inhibition of tumor growth was seen in groups II, III and IV as compared with group I (P < 0.05), with the tumor growth inhibition rate on the 28th day being 86, 90 and 99%, respectively. All mice in group IV were cured, with no evidence of tumors by the 35th day and, histologically, no tumor cells remained. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: The data suggest that HIFU can destroy liver cancer effectively and that HIFU combined with treatment using the anti-angiogenic agents heparin and cortisone may constitute a comprehensive treatment to ablate liver cancer.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87629582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2000-11-01DOI: 10.1046/J.1443-9573.2000.00009.X
Lu Lungen, Zeng Min-de, Fan Jiangao, Hua Jing, L. Jiqiang, Qiu Dekai, Fan Zhuping
OBJECTIVE: To explore the expression of intercellular adhesion molecule-1 (ICAM-1) in hepatic stellate cells (HSC). METHODS: Via in situ perfusion with proteinase and collagenase and density-gradient centrifugation with Nycodenz, HSC were isolated and cultured from the livers of both normal Wistar rats and the livers of rats treated with carbon tetrachloride. Expression of ICAM-1 in HSC was detected by an immunohistochemistry assay and reverse transcription–polymerase chain reaction (RT-PCR). RESULTS: No ICAM-1 was expressed in the freshly isolated HSC of normal rats, but ICAM-1 was found in primary cultures of HSC at day 10 and in secondary cultures of HSC at day 7. Additionally, the intensity of the expression increased over time. Expression of ICAM-1 was observed in freshly isolated HSC from the livers of rats treated with carbon tetrachloride. CONCLUSIONS: Expression of ICAM-1 is related to the activation of HSC, hepatic inflammation and hepatic fibrogenesis.
{"title":"Expression of intercellular adhesion molecule-1 in hepatic stellate cells","authors":"Lu Lungen, Zeng Min-de, Fan Jiangao, Hua Jing, L. Jiqiang, Qiu Dekai, Fan Zhuping","doi":"10.1046/J.1443-9573.2000.00009.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2000.00009.X","url":null,"abstract":"OBJECTIVE: To explore the expression of intercellular adhesion molecule-1 (ICAM-1) in hepatic stellate cells (HSC). \u0000 \u0000 \u0000 \u0000METHODS: Via in situ perfusion with proteinase and collagenase and density-gradient centrifugation with Nycodenz, HSC were isolated and cultured from the livers of both normal Wistar rats and the livers of rats treated with carbon tetrachloride. Expression of ICAM-1 in HSC was detected by an immunohistochemistry assay and reverse transcription–polymerase chain reaction (RT-PCR). \u0000 \u0000 \u0000 \u0000RESULTS: No ICAM-1 was expressed in the freshly isolated HSC of normal rats, but ICAM-1 was found in primary cultures of HSC at day 10 and in secondary cultures of HSC at day 7. Additionally, the intensity of the expression increased over time. Expression of ICAM-1 was observed in freshly isolated HSC from the livers of rats treated with carbon tetrachloride. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: Expression of ICAM-1 is related to the activation of HSC, hepatic inflammation and hepatic fibrogenesis.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78870102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2000-11-01DOI: 10.1046/J.1443-9573.2000.00002.X
Ma Jinping, Zhan Wen-hua, C. Shirong, Peng Junsheng, W. Jianping
OBJECTIVE: To examine telomerase activity and its clinical significance in human gastric carcinoma and to evaluate the feasibility of non-radioisotopic TRAP (telomeric repeat amplification protocol) assays to detect telomerase activity. METHODS: Telomerase activity in tissue samples from 58 gastric carcinomas (and their matched normal tissues), 12 gastric adenomas and nine gastric ulcers was examined by using a modified non- radioisotopic PCR (polymerase chain reaction)-based TRAP assay. RESULTS: Forty-nine of 58 gastric cancer specimens were positive for telomerase activity, with a positive rate of 84.5%. In contrast, none of the normal tissues exhibited telomerase activity (P < 0.001). One of each of the 12 gastric adenomas and nine gastric ulcers was also positive. The prevalence of telomerase activity in gastric carcinoma tissues was not correlated with age, tumor diameter, histological grade, tumor invasion depth, lymph node metastasis or tumor node metastasis (TNM) stage. CONCLUSIONS: Telomerase activity could be a good diagnostic marker for the detection of gastric carcinoma. The non-radioisotopic TRAP assay is a feasible method for detecting telomerase activity.
{"title":"Telomerase activity in gastric cancer","authors":"Ma Jinping, Zhan Wen-hua, C. Shirong, Peng Junsheng, W. Jianping","doi":"10.1046/J.1443-9573.2000.00002.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2000.00002.X","url":null,"abstract":"OBJECTIVE: To examine telomerase activity and its clinical significance in human gastric carcinoma and to evaluate the feasibility of non-radioisotopic TRAP (telomeric repeat amplification protocol) assays to detect telomerase activity. \u0000 \u0000 \u0000 \u0000METHODS: Telomerase activity in tissue samples from 58 gastric carcinomas (and their matched normal tissues), 12 gastric adenomas and nine gastric ulcers was examined by using a modified non- radioisotopic PCR (polymerase chain reaction)-based TRAP assay. \u0000 \u0000 \u0000 \u0000RESULTS: Forty-nine of 58 gastric cancer specimens were positive for telomerase activity, with a positive rate of 84.5%. In contrast, none of the normal tissues exhibited telomerase activity (P < 0.001). One of each of the 12 gastric adenomas and nine gastric ulcers was also positive. The prevalence of telomerase activity in gastric carcinoma tissues was not correlated with age, tumor diameter, histological grade, tumor invasion depth, lymph node metastasis or tumor node metastasis (TNM) stage. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: Telomerase activity could be a good diagnostic marker for the detection of gastric carcinoma. The non-radioisotopic TRAP assay is a feasible method for detecting telomerase activity.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78425809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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