Pub Date : 2003-07-01DOI: 10.1046/J.1443-9573.2003.T01-1-00116.X
Guo Zhang, Y. Wang, Qiang Wang, Min Zhang, Ce-ran Han, Ying Rao
OBJECTIVE: To study the effects of the angiogenesis inhibitor SU5416 on the growth and liver metastasis of gastric cancer and to investigate its effects on the apoptosis of gastric cancer cells. METHODS: A model simulating the metastasis of human gastric cancer was established by orthotopic implantation of histologically intact human tumor tissue into the gastric wall of nude mice, which were randomly divided into four groups: control group (saline solution), 5-FU group (fluorouracil 30 mg/kg per day i.p), SU5416 group (SU5416 15 mg/kg per day i.p.), and combined treatment with 5-Fu and SU5416. Eight weeks after implantation, the tumor weight, inhibition rate, intratumoral microvessel density (MVD), apoptotic index (AI), and the status of metastasis were evaluated after the mice were killed. RESULTS: Compared with the control group, the growth of the orthotopically-implanted tumors was significantly inhibited, with reduced weight, and the tumor inhibition rate was 44.5%, 79.3%, and 84.4%, respectively, in the mice treated with 5-FU, SU5416 and both. The incidence of liver metastasis was also significantly decreased in the 5-Fu, SU5416, and combination groups compared with the control group (36.4%, 25.0%, and 0% vs 90.0%). The MVD of the 5-FU group, the SU5416 group and the combined group was 13.1 ± 4.7, 3.9 ± 1.8 and 2.1 ± 1.5, respectively, which was decreased significantly compared with the control group (14.6 ± 5.8). The AI was increased significantly in the treated mice (6.81 ± 4.92%, 9.82 ± 3.76% and 17.65 ± 9.85% vs 3.76 ± 2.25%). The growth of and liver metastasis of the human gastric cancer implanted in the nude mice were both more significantly inhibited in the SU5416 group and the combined group than in the control and 5-FU groups (P < 0.05). CONCLUSIONS: SU5416 can induce apoptosis in gastric cancer by inhibiting tumor angiogenesis and has a strong inhibitory effect on both the growth and liver metastasis of gastric cancer implanted in nude mice. The combination of SU5416 with other cytotoxic agents is more effective.
目的:研究血管生成抑制剂SU5416对胃癌生长和肝转移的影响，并探讨其对胃癌细胞凋亡的影响。方法:将组织学完整的人肿瘤组织原位植入裸鼠胃壁，建立模拟人胃癌转移的模型，将裸鼠随机分为4组:对照组(生理盐水)、5-FU组(氟尿嘧啶30 mg/kg / d i.p)、SU5416组(SU5416 15 mg/kg / d i.p)和5-FU与SU5416联合治疗。植入8周后处死小鼠，观察肿瘤重量、抑制率、瘤内微血管密度(MVD)、凋亡指数(AI)及转移情况。结果:与对照组相比，5-FU、SU5416及两者均能显著抑制原位植入肿瘤的生长，减轻肿瘤重量，肿瘤抑制率分别为44.5%、79.3%和84.4%。与对照组相比，5-Fu、SU5416和联合用药组的肝转移发生率也显著降低(36.4%、25.0%和0% vs 90.0%)。5-FU组、SU5416组和联合组的MVD分别为13.1±4.7、3.9±1.8和2.1±1.5，较对照组(14.6±5.8)明显降低。实验组小鼠的AI明显升高(分别为6.81±4.92%、9.82±3.76%和17.65±9.85% vs 3.76±2.25%)。与对照组和5-FU组相比，SU5416组和联合组对裸鼠移植人胃癌生长和肝转移的抑制作用更显著(P < 0.05)。结论:SU5416通过抑制肿瘤血管生成诱导胃癌细胞凋亡，对裸鼠移植胃癌细胞的生长和肝转移均有较强的抑制作用。SU5416与其他细胞毒药物合用效果更好。
{"title":"Effect of SU5416 on the inhibition of growth and metastasis of human gastric cancer implanted in nude mice","authors":"Guo Zhang, Y. Wang, Qiang Wang, Min Zhang, Ce-ran Han, Ying Rao","doi":"10.1046/J.1443-9573.2003.T01-1-00116.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2003.T01-1-00116.X","url":null,"abstract":"OBJECTIVE: To study the effects of the angiogenesis inhibitor SU5416 on the growth and liver metastasis of gastric cancer and to investigate its effects on the apoptosis of gastric cancer cells. \u0000 \u0000 \u0000 \u0000METHODS: A model simulating the metastasis of human gastric cancer was established by orthotopic implantation of histologically intact human tumor tissue into the gastric wall of nude mice, which were randomly divided into four groups: control group (saline solution), 5-FU group (fluorouracil 30 mg/kg per day i.p), SU5416 group (SU5416 15 mg/kg per day i.p.), and combined treatment with 5-Fu and SU5416. Eight weeks after implantation, the tumor weight, inhibition rate, intratumoral microvessel density (MVD), apoptotic index (AI), and the status of metastasis were evaluated after the mice were killed. \u0000 \u0000 \u0000 \u0000RESULTS: Compared with the control group, the growth of the orthotopically-implanted tumors was significantly inhibited, with reduced weight, and the tumor inhibition rate was 44.5%, 79.3%, and 84.4%, respectively, in the mice treated with 5-FU, SU5416 and both. The incidence of liver metastasis was also significantly decreased in the 5-Fu, SU5416, and combination groups compared with the control group (36.4%, 25.0%, and 0% vs 90.0%). The MVD of the 5-FU group, the SU5416 group and the combined group was 13.1 ± 4.7, 3.9 ± 1.8 and 2.1 ± 1.5, respectively, which was decreased significantly compared with the control group (14.6 ± 5.8). The AI was increased significantly in the treated mice (6.81 ± 4.92%, 9.82 ± 3.76% and 17.65 ± 9.85% vs 3.76 ± 2.25%). The growth of and liver metastasis of the human gastric cancer implanted in the nude mice were both more significantly inhibited in the SU5416 group and the combined group than in the control and 5-FU groups (P < 0.05). \u0000 \u0000 \u0000 \u0000CONCLUSIONS: SU5416 can induce apoptosis in gastric cancer by inhibiting tumor angiogenesis and has a strong inhibitory effect on both the growth and liver metastasis of gastric cancer implanted in nude mice. The combination of SU5416 with other cytotoxic agents is more effective.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81778871","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 : 2003-07-01DOI: 10.1046/J.1443-9573.2001.00119.X
Tao Guo, J. Qian, A. Yang, J. Li, Xing-hua Lu
OBJECTIVE: To evaluate the role of imaging methods in the diagnosis of chronic pancreatitis (CP) in improving the accuracy of a clinical diagnosis of CP. METHODS: The results of the imaging methods used for 129 cases diagnosed as CP in Peking Union Medical College Hospital from 1991 to 2000 were retrospectively analyzed. The imaging methods included ultrasonography (US), computed tomography (CT), endoscopic retrograde cholangiopancreatography (ERCP), magnetic resonance cholangiopancreatography (MRCP) and endoscopic ultrasonography (EUS). RESULTS: The sensitivity of EUS and MRCP was high and was in good agreement with ERCP in the diagnosis of CP. The sensitivity of ERCP was superior to US and CT (P < 0.05). The sensitivity of US and CT for diagnosing dilation of the pancreatic duct was 59.4% and 60%, respectively, the specificity was 93.8% and 95.7%, respectively. BT-PABA had a better correlation with ERCP in the group with severe changes of the pancreatic duct than in the mild or moderate group. The more complications of CP that were present, the more severe the lesions of the pancreatic duct. CONCLUSION: Among the traditional imaging modalities for diagnosing CP, ERCP is the most sensitive. MRCP and EUS, the promising and novel examination techniques, have high sensitivity and good agreement with ERCP.
{"title":"Evaluating the role of imaging methods in the diagnosis of chronic pancreatitis","authors":"Tao Guo, J. Qian, A. Yang, J. Li, Xing-hua Lu","doi":"10.1046/J.1443-9573.2001.00119.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00119.X","url":null,"abstract":"OBJECTIVE: To evaluate the role of imaging methods in the diagnosis of chronic pancreatitis (CP) in improving the accuracy of a clinical diagnosis of CP. \u0000 \u0000 \u0000 \u0000METHODS: The results of the imaging methods used for 129 cases diagnosed as CP in Peking Union Medical College Hospital from 1991 to 2000 were retrospectively analyzed. The imaging methods included ultrasonography (US), computed tomography (CT), endoscopic retrograde cholangiopancreatography (ERCP), magnetic resonance cholangiopancreatography (MRCP) and endoscopic ultrasonography (EUS). \u0000 \u0000 \u0000 \u0000RESULTS: The sensitivity of EUS and MRCP was high and was in good agreement with ERCP in the diagnosis of CP. The sensitivity of ERCP was superior to US and CT (P < 0.05). The sensitivity of US and CT for diagnosing dilation of the pancreatic duct was 59.4% and 60%, respectively, the specificity was 93.8% and 95.7%, respectively. BT-PABA had a better correlation with ERCP in the group with severe changes of the pancreatic duct than in the mild or moderate group. The more complications of CP that were present, the more severe the lesions of the pancreatic duct. \u0000 \u0000 \u0000 \u0000CONCLUSION: Among the traditional imaging modalities for diagnosing CP, ERCP is the most sensitive. MRCP and EUS, the promising and novel examination techniques, have high sensitivity and good agreement with ERCP.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75187103","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 : 2003-07-01DOI: 10.1046/J.1443-9611.2003.X
Xiao-ling Kuai, Y. Bian, X. Cong, Xiu Lan Li, SH Xiao
OBJECTIVE: Embryonic stem (ES) cells have a pluripotent ability to differentiate into a variety of cell lineages. Cell-to-cell contact is important for cell differentiation. Mouse ES cells were cocultured with mouse fetal liver cells and the green fluorescent protein (GFP) positive ES cells were transplanted into rats liver through the portal vein in order to investigate their potential to differentiate into hepatocytes. METHODS: Mouse ES cells were cocultured with the mouse fetal liver cell line, BNL.CL2. They did not make direct contact; instead the culture media was exchanged freely. After coculture for 48 h, albumin, transthyretin, glucose 6 phosphates, hepatic nuclear factor 4 and SEK1 mRNA were assayed by RT-PCR, and alpha-fetoprotein by immunohistochemistry. The morphology was investigated by microscopy. After transplantion of the GFP-positive ES cells, the whole liver was removed from a rat every four days. The liver slices were examined under a fluorescent microscope to detect the GFP-positive cells. Albumin was detected on the same slices by immunohistochemistry. RESULTS: After coculture with BNL.CL2 cells, the differentiated ES cells had the same morphology as the BNL.CL2 cells, and albumin, transthyretin, glucose 6 phosphates and SEK-1 mRNA were found by RT-PCR, and alpha-fetoprotein was detected immunohistochemically. The transplanted GFP-positive ES cells were found in the rats’ liver slices by GFP fluorescence, and development of teratomas was not observed. The immunohistochemistry results indicated that the transplanted GFP-positive ES cells retained an albumin-producing ability. CONCLUSIONS: Cell-to-cell contact is important for the differentiation of ES cells. Mouse embryonic stem cells can differentiate into hepatocytes directly either in vitro or in vivo.
{"title":"Differentiation of mouse embryonic stem cells into hepatocytes in vitro and in vivo","authors":"Xiao-ling Kuai, Y. Bian, X. Cong, Xiu Lan Li, SH Xiao","doi":"10.1046/J.1443-9611.2003.X","DOIUrl":"https://doi.org/10.1046/J.1443-9611.2003.X","url":null,"abstract":"OBJECTIVE: Embryonic stem (ES) cells have a pluripotent ability to differentiate into a variety of cell lineages. Cell-to-cell contact is important for cell differentiation. Mouse ES cells were cocultured with mouse fetal liver cells and the green fluorescent protein (GFP) positive ES cells were transplanted into rats liver through the portal vein in order to investigate their potential to differentiate into hepatocytes. \u0000 \u0000 \u0000 \u0000METHODS: Mouse ES cells were cocultured with the mouse fetal liver cell line, BNL.CL2. They did not make direct contact; instead the culture media was exchanged freely. After coculture for 48 h, albumin, transthyretin, glucose 6 phosphates, hepatic nuclear factor 4 and SEK1 mRNA were assayed by RT-PCR, and alpha-fetoprotein by immunohistochemistry. The morphology was investigated by microscopy. After transplantion of the GFP-positive ES cells, the whole liver was removed from a rat every four days. The liver slices were examined under a fluorescent microscope to detect the GFP-positive cells. Albumin was detected on the same slices by immunohistochemistry. \u0000 \u0000 \u0000 \u0000RESULTS: After coculture with BNL.CL2 cells, the differentiated ES cells had the same morphology as the BNL.CL2 cells, and albumin, transthyretin, glucose 6 phosphates and SEK-1 mRNA were found by RT-PCR, and alpha-fetoprotein was detected immunohistochemically. The transplanted GFP-positive ES cells were found in the rats’ liver slices by GFP fluorescence, and development of teratomas was not observed. The immunohistochemistry results indicated that the transplanted GFP-positive ES cells retained an albumin-producing ability. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: Cell-to-cell contact is important for the differentiation of ES cells. Mouse embryonic stem cells can differentiate into hepatocytes directly either in vitro or in vivo.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85730943","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 : 2003-07-01DOI: 10.1046/J.1443-9573.2003.T01-1-00123.X
Yu Wang, Ding-guo Li, Hong-shan Wei, Z. Wang, Xin Huang, Xin-Wei Zhou, Q. Xu, Han-ming Lu
OBJECTIVE: To investigate the effects of different doses of angiotensin II (AngII) on the proliferation of hepatic stellate cells (HSC) and collagen synthesis in rats. METHODS: Pronase E and collagen I were used to isolate the HSC, and 3H-TdR,3H-Leu and 3H-pro incorporation methods were used to evaluate the effects of the different doses of AngII on HSC DNA, protein and proline synthesis. RESULTS: It was found that 10-9−10−6 mol/L AngII could increase the 3H-TdR incorporation rate of the HSC (P < 0.05), but only 10−6 mol/L and 10−7 mol/L AngII could significantly increase the 3H-Leu incorporation rate of the HSC (P < 0.01); 10−9−10−6 mol/L AngII caused a significant increment of the 3H-pro incorporation rate of the HSC in a dose-dependent manner. CONCLUSIONS: The appropriate dose of AngII may promote HSC proliferation and collagen synthesis.
{"title":"Angiotensin II stimulates the synthesis of nucleic acid, protein and collagen of cultured hepatic stellate cells in rats","authors":"Yu Wang, Ding-guo Li, Hong-shan Wei, Z. Wang, Xin Huang, Xin-Wei Zhou, Q. Xu, Han-ming Lu","doi":"10.1046/J.1443-9573.2003.T01-1-00123.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2003.T01-1-00123.X","url":null,"abstract":"OBJECTIVE: To investigate the effects of different doses of angiotensin II (AngII) on the proliferation of hepatic stellate cells (HSC) and collagen synthesis in rats. \u0000 \u0000 \u0000 \u0000METHODS: Pronase E and collagen I were used to isolate the HSC, and 3H-TdR,3H-Leu and 3H-pro incorporation methods were used to evaluate the effects of the different doses of AngII on HSC DNA, protein and proline synthesis. \u0000 \u0000 \u0000 \u0000RESULTS: It was found that 10-9−10−6 mol/L AngII could increase the 3H-TdR incorporation rate of the HSC (P < 0.05), but only 10−6 mol/L and 10−7 mol/L AngII could significantly increase the 3H-Leu incorporation rate of the HSC (P < 0.01); 10−9−10−6 mol/L AngII caused a significant increment of the 3H-pro incorporation rate of the HSC in a dose-dependent manner. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: The appropriate dose of AngII may promote HSC proliferation and collagen synthesis.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79852664","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 : 2002-02-01DOI: 10.1046/J.1443-9573.2002.00066.X
Z. Cui, Z. Li, Guo-ming Xu, X. Zhan
OBJECTIVE: To determine the role of endogenous nitric oxide (NO) in gastric mucosal tolerant cytoprotection under stress and its possible mechanism. METHODS: Sprague–Dawley rats were exposed to repeated water immersion and restraint stress (WRS), during which NG-nitro-L-arginine methyl ester (L-NAME), a non-selective NO synthase inhibitor, and L-arginine (L-Arg), a substrate for NO synthesis, were administered to inhibit or promote the synthesis of endogenous NO, respectively. Gastric mucosal blood flow (GMBF) was measured with an LDF-3 Flowmeter (Electronic Instrument Factory of Nankai University, Tianjin, China), the NO level in the gastric mucosa was monitored by the Griess reaction and gastric mucosal lesions were evaluated using the ulcer index (UI). The relationships between changes in GMBF, UI and NO content in the gastric mucosa were analyzed by linear correlation analysis. RESULTS: Repeated WRS induced gastric mucosal tolerant cytoprotection and this was accompanied by increased GMBF and NO levels in the gastric mucosa. Inhibition of endogenous NO synthesis by L-NAME worsened mucosal lesions induced by single WRS and, after repeated WRS, the adaptive incremence in GMBF was abolished and the NO content in the gastric mucosa was significantly reduced. In contrast, enhancement of endogenous NO synthesis by L-Arg attenuated mucosal erosions caused by single WRS. After repeated WRS, GMBF and the NO content in the mucosa increased gradually. Mucosal lesions were negligible after rats were exposed to the fourth WRS. CONCLUSIONS: During the tolerant cytoprotection, GMBF, UI and the NO content showed regular changes and there were good relationships between them. L-NAME and L-Arg changed the levels of endogenous NO, which, accordingly, affected GMBF and the gastric tolerance. By regulating GMBF, endogenous NO may play an important role in the gastric mucosal tolerant cytoprotection under stress. Inhibition of the synthesis of NO delayed the induction of tolerant cytoprotection, whereas increased NO synthesis promoted cytoprotection.
目的:探讨内源性一氧化氮(NO)在应激条件下胃粘膜耐受细胞保护中的作用及其可能机制。方法:将Sprague-Dawley大鼠置于反复水浸和约束应激(WRS)条件下，分别给予非选择性NO合成酶抑制剂ng -硝基- l -精氨酸甲酯(L-NAME)和合成NO的底物l -精氨酸(L-Arg)抑制或促进内源性NO的合成。采用LDF-3型流量计(中国天津南开大学电子仪表厂)测定胃黏膜血流量(GMBF)，采用Griess反应监测胃黏膜NO水平，采用溃疡指数(UI)评价胃黏膜病变。采用线性相关分析胃黏膜GMBF、UI与NO含量变化的关系。结果:重复WRS诱导胃粘膜耐受细胞保护，并伴有胃粘膜GMBF和NO水平升高。L-NAME对内源性NO合成的抑制使单次WRS诱导的粘膜病变加重，多次WRS后GMBF的适应性增加被消除，胃粘膜NO含量显著降低。相反，l -精氨酸增强内源性NO合成可减轻单一WRS引起的粘膜侵蚀。重复WRS后，黏膜GMBF和NO含量逐渐升高。大鼠暴露于第四次WRS后，粘膜病变可忽略不计。结论:在耐受性细胞保护过程中，GMBF、UI和NO含量均呈规律性变化，且三者之间存在良好的关系。L-NAME和L-Arg改变了内源性NO的水平，从而影响了GMBF和胃耐受。内源性NO通过调控GMBF，可能在应激条件下胃粘膜耐受细胞保护中发挥重要作用。抑制NO的合成延迟了耐受细胞保护的诱导，而增加NO的合成则促进了细胞保护。
{"title":"Influence of NG‐nitro‐L‐arginine methyl ester and L‐arginine on gastric mucosal tolerant cytoprotection under stress","authors":"Z. Cui, Z. Li, Guo-ming Xu, X. Zhan","doi":"10.1046/J.1443-9573.2002.00066.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2002.00066.X","url":null,"abstract":"OBJECTIVE: To determine the role of endogenous nitric oxide (NO) in gastric mucosal tolerant cytoprotection under stress and its possible mechanism. \u0000 \u0000 \u0000 \u0000METHODS: Sprague–Dawley rats were exposed to repeated water immersion and restraint stress (WRS), during which NG-nitro-L-arginine methyl ester (L-NAME), a non-selective NO synthase inhibitor, and L-arginine (L-Arg), a substrate for NO synthesis, were administered to inhibit or promote the synthesis of endogenous NO, respectively. Gastric mucosal blood flow (GMBF) was measured with an LDF-3 Flowmeter (Electronic Instrument Factory of Nankai University, Tianjin, China), the NO level in the gastric mucosa was monitored by the Griess reaction and gastric mucosal lesions were evaluated using the ulcer index (UI). The relationships between changes in GMBF, UI and NO content in the gastric mucosa were analyzed by linear correlation analysis. \u0000 \u0000 \u0000 \u0000RESULTS: Repeated WRS induced gastric mucosal tolerant cytoprotection and this was accompanied by increased GMBF and NO levels in the gastric mucosa. Inhibition of endogenous NO synthesis by L-NAME worsened mucosal lesions induced by single WRS and, after repeated WRS, the adaptive incremence in GMBF was abolished and the NO content in the gastric mucosa was significantly reduced. In contrast, enhancement of endogenous NO synthesis by L-Arg attenuated mucosal erosions caused by single WRS. After repeated WRS, GMBF and the NO content in the mucosa increased gradually. Mucosal lesions were negligible after rats were exposed to the fourth WRS. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: During the tolerant cytoprotection, GMBF, UI and the NO content showed regular changes and there were good relationships between them. L-NAME and L-Arg changed the levels of endogenous NO, which, accordingly, affected GMBF and the gastric tolerance. By regulating GMBF, endogenous NO may play an important role in the gastric mucosal tolerant cytoprotection under stress. Inhibition of the synthesis of NO delayed the induction of tolerant cytoprotection, whereas increased NO synthesis promoted cytoprotection.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87063360","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 : 2001-10-01DOI: 10.1046/J.1443-9573.2001.00060.X
Min Zhao, Lumei Sun, Ruolan Jiang
OBJECTIVE: To investigate the role of pituitary adenylate cyclase-activating polypeptide (PACAP) in the growth modulation of human pancreatic carcinoma and to determine whether sphingomyelin may act as a second messenger in post-receptor signal transduction. METHODS: Three human pancreatic cancer cell lines, JF305, HS766T and ASPC-1, were cultivated, propagated and then treated with various concentrations of PACAP1–38 (10–12–10–6 mol/L). The number of proliferating cancer cells was estimated by using Mosmann’s MTT method. The concentration of intracellular sphingomyelin was determined by thin layer chromatography. Levels of intracellular adenosine monophosphate and Ca2+ were measured by radioimmunoassay and Fura-2/AM, respectively. RESULTS: The proliferation of human pancreatic cancer cell lines was enhanced and the intracellular levels of sphingomyelin, cAMP and cytosolic Ca2+ were increased by treatment with PACAP1–38. The effect of PACAP1–38 on JF305, HS766T and ASPC-1 cells was inhibited by somatostatin. CONCLUSIONS: It is possible that PACAP1–38 plays a role in the proliferation of human pancreatic cancer cells. The post-receptor signal transduction of PACAP may be mediated by both the adenosine cyclinase and calcium–calmodulin pathways. Sphingomyelin may be a second messenger involved in this process.
{"title":"Role of pituitary adenylate cyclase-activating polypeptide in the growth modulation of human pancreatic carcinoma","authors":"Min Zhao, Lumei Sun, Ruolan Jiang","doi":"10.1046/J.1443-9573.2001.00060.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00060.X","url":null,"abstract":"OBJECTIVE: To investigate the role of pituitary adenylate cyclase-activating polypeptide (PACAP) in the growth modulation of human pancreatic carcinoma and to determine whether sphingomyelin may act as a second messenger in post-receptor signal transduction. \u0000 \u0000 \u0000 \u0000METHODS: Three human pancreatic cancer cell lines, JF305, HS766T and ASPC-1, were cultivated, propagated and then treated with various concentrations of PACAP1–38 (10–12–10–6 mol/L). The number of proliferating cancer cells was estimated by using Mosmann’s MTT method. The concentration of intracellular sphingomyelin was determined by thin layer chromatography. Levels of intracellular adenosine monophosphate and Ca2+ were measured by radioimmunoassay and Fura-2/AM, respectively. \u0000 \u0000 \u0000 \u0000RESULTS: The proliferation of human pancreatic cancer cell lines was enhanced and the intracellular levels of sphingomyelin, cAMP and cytosolic Ca2+ were increased by treatment with PACAP1–38. The effect of PACAP1–38 on JF305, HS766T and ASPC-1 cells was inhibited by somatostatin. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: It is possible that PACAP1–38 plays a role in the proliferation of human pancreatic cancer cells. The post-receptor signal transduction of PACAP may be mediated by both the adenosine cyclinase and calcium–calmodulin pathways. Sphingomyelin may be a second messenger involved in this process.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83167617","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 : 2001-10-01DOI: 10.1046/J.1443-9573.2001.00058.X
Jiaguo Wu, J. Si, Q. Cao, Wen Lu, Jian Wang, Bingjian Lu, N. Dai
OBJECTIVE: To study the effect of epidermal growth factor (EGF) on pathological changes of the gastric mucosa in rats with chronic atrophic gastritis (CAG). METHODS: The established CAG rat models were divided into groups A and B. The rats in group A received 10 μg/kg EGF subcutaneously. In group B, rats were subcutaneously injected with the same quantity of normal saline. Twelve weeks later, all rats were killed by cervical dislocation and their gastric mucosa were examined microscopically. RESULTS: The grading of the inflammatory cell infiltration in group A was lower than that in group B (P < 0.01). The thickness of the gastric mucosal gland layer was 215.0 ± 20.7 μm in group A and 139.2 ± 13.8 μm in group B (P < 0.01). The ratio of the thickness of the gastric mucosal glands to that of the muscularis mucosa (L1/L2) was 2.70 ± 0.34 in group A and 1.27 ± 0.27 in group B (P < 0.01). The number of gastric glands in a 1-mm length of mucosal layer was 26.20 ± 1.27 in group A and 19.90 ± 1.78 in group B (P < 0.01). In group A, the gastric glands were rearranged, without signs of malignant proliferation. The width of gastric mucosa expressing proliferating cell nuclear antigen (PCNA) was larger in group A than in group B (77.70 ± 4.16 μm vs 54.40 ± 4.54 μm; P < 0.01). CONCLUSIONS: Epidermal growth factor plays a therapeutic role in reversing gastric mucosal atrophy in rats with CAG. It promotes the expression of PCNA, which induces a protective proliferation in gastric mucosal lesions in rats with CAG.
{"title":"Effect of epidermal growth factor on pathological changes of the gastric mucosa in rats with chronic atrophic gastritis","authors":"Jiaguo Wu, J. Si, Q. Cao, Wen Lu, Jian Wang, Bingjian Lu, N. Dai","doi":"10.1046/J.1443-9573.2001.00058.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00058.X","url":null,"abstract":"OBJECTIVE: To study the effect of epidermal growth factor (EGF) on pathological changes of the gastric mucosa in rats with chronic atrophic gastritis (CAG). \u0000 \u0000 \u0000 \u0000METHODS: The established CAG rat models were divided into groups A and B. The rats in group A received 10 μg/kg EGF subcutaneously. In group B, rats were subcutaneously injected with the same quantity of normal saline. Twelve weeks later, all rats were killed by cervical dislocation and their gastric mucosa were examined microscopically. \u0000 \u0000 \u0000 \u0000RESULTS: The grading of the inflammatory cell infiltration in group A was lower than that in group B (P < 0.01). The thickness of the gastric mucosal gland layer was 215.0 ± 20.7 μm in group A and 139.2 ± 13.8 μm in group B (P < 0.01). The ratio of the thickness of the gastric mucosal glands to that of the muscularis mucosa (L1/L2) was 2.70 ± 0.34 in group A and 1.27 ± 0.27 in group B (P < 0.01). The number of gastric glands in a 1-mm length of mucosal layer was 26.20 ± 1.27 in group A and 19.90 ± 1.78 in group B (P < 0.01). In group A, the gastric glands were rearranged, without signs of malignant proliferation. The width of gastric mucosa expressing proliferating cell nuclear antigen (PCNA) was larger in group A than in group B (77.70 ± 4.16 μm vs 54.40 ± 4.54 μm; P < 0.01). \u0000 \u0000 \u0000 \u0000CONCLUSIONS: Epidermal growth factor plays a therapeutic role in reversing gastric mucosal atrophy in rats with CAG. It promotes the expression of PCNA, which induces a protective proliferation in gastric mucosal lesions in rats with CAG.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76385830","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 : 2001-10-01DOI: 10.1046/J.1443-9573.2001.00054.X
Y. Ni, Houyu Liu, Dechang Hu, Weirong Zhe, Mingsheng Li
OBJECTIVE: Based on liver biopsy samples collected during the past 10 years, the present study aimed to investigate the incidence of fatty liver, the relationship between fatty liver and other underlying liver diseases, and the clinical and pathological characteristics, and the risk factors of fatty liver. METHODS: From a total of 658 liver biopsy specimens collected from 1988 to 1997, there were 71 cases of fatty liver and 68 cases of non-alcoholic fatty liver. Matched by sex and age, 155 specimens of non-fatty liver were used as controls. All patients from which the biopsies were taken were tested for liver function, blood lipid profile, blood glucose and hepatitis virus markers. The liver biopsy samples were all investigated by the same pathologist. RESULTS: The prevalence of fatty liver among all the liver biopsies was 10.8%. The alanine aminotransferase, aspartate aminotransferase, total bilirubin and con-jugated bilirubin levels in the fatty liver group were significantly lower than those in the non-fatty liver group, whereas the triglyceride levels were higher. Pathologically, steatosis in patients with fatty liver was mainly located around the hepatic lobules, and macrovesicular steatosis was common. Of the 68 cases of non-alcoholic fatty liver, hepatic cell necrosis was found in 35 cases (51.5%), inflammatory cell infiltration in 46 cases (67.6%) and fibrosis to various degrees in 19 cases (27.9%). CONCLUSION: Non-alcoholic fatty liver is closely related to hyperlipidemia. In asymptomatic subjects with abnormal liver function, a liver biopsy is the only way to establish the type and severity of liver lesions.
{"title":"Clinicopathological analysis of non-alcoholic steatohepatitis","authors":"Y. Ni, Houyu Liu, Dechang Hu, Weirong Zhe, Mingsheng Li","doi":"10.1046/J.1443-9573.2001.00054.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00054.X","url":null,"abstract":"OBJECTIVE: Based on liver biopsy samples collected during the past 10 years, the present study aimed to investigate the incidence of fatty liver, the relationship between fatty liver and other underlying liver diseases, and the clinical and pathological characteristics, and the risk factors of fatty liver. \u0000 \u0000METHODS: From a total of 658 liver biopsy specimens collected from 1988 to 1997, there were 71 cases of fatty liver and 68 cases of non-alcoholic fatty liver. Matched by sex and age, 155 specimens of non-fatty liver were used as controls. All patients from which the biopsies were taken were tested for liver function, blood lipid profile, blood glucose and hepatitis virus markers. The liver biopsy samples were all investigated by the same pathologist. \u0000 \u0000RESULTS: The prevalence of fatty liver among all the liver biopsies was 10.8%. The alanine aminotransferase, aspartate aminotransferase, total bilirubin and con-jugated bilirubin levels in the fatty liver group were significantly lower than those in the non-fatty liver group, whereas the triglyceride levels were higher. Pathologically, steatosis in patients with fatty liver was mainly located around the hepatic lobules, and macrovesicular steatosis was common. Of the 68 cases of non-alcoholic fatty liver, hepatic cell necrosis was found in 35 cases (51.5%), inflammatory cell infiltration in 46 cases (67.6%) and fibrosis to various degrees in 19 cases (27.9%). \u0000 \u0000CONCLUSION: Non-alcoholic fatty liver is closely related to hyperlipidemia. In asymptomatic subjects with abnormal liver function, a liver biopsy is the only way to establish the type and severity of liver lesions.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83265781","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 : 2001-10-01DOI: 10.1046/J.1443-9573.2001.00032.X
Dong-Ping Liu, Bingyuan Wang, Ruolan Jiang
OBJECTIVE: The purpose of the present study was to investigate the correlation between the expression of vascular endothelial growth factor (VEGF), the expression of its receptors, Flt and KDR, and the biological behavior of gastric cancer. METHODS: Sixty cases of gastric cancer that had been diagnosed by surgery and pathology were studied with the method of semiquantitative reverse transcriptase–polymerase chain reaction (RT-PCR), to determine the expression of VEGF, Flt and KDR in gastric cancer tissue. RESULTS: The positive rates of VEGF, Flt and KDR in gastric cancer were 73.3, 86.7 and 80.0%, respectively. In pericancerous tissue, the rates were 43.3, 33.0 and 30.0%, respectively. There were significant differences between the groups with and without lymph node metastasis (P < 0.01). For gastric cancer patients with lymphatic metastasis, the positive rates for VEGF, Flt and KDR were 90.3, 80.6 and 96.8%, respectively; for patients without lymphatic metastasis, the rates were 51.7, 41.3 and 55.1%; there were significant differences between the groups with and without lymph node metastasis (P < 0.01). The positive rates of VEGF and KDR in well-differentiated gastric cancer were 40.0 and 46.7%, markedly lower than those of the poorly differentiated and undifferentiated gastric cancer groups. The rate of positive expression of Flt in the well-differentiated gastric cancer group was 73.3%. There was no significant difference between this rate and that of the poorly differentiated and undifferentiated groups (87.5%). The positive expression of VEGF, Flt and KDR was unrelated to the depth of infiltration. CONCLUSIONS: There are some correlations between VEGF, Flt and KDR and the biological behavior of gastric cancer. Knowing where they are expressed at high rates may be of help in evaluating the prognosis of gastric cancer.
{"title":"Expression of VEGF and its receptors Flt and KDR in gastric cancer","authors":"Dong-Ping Liu, Bingyuan Wang, Ruolan Jiang","doi":"10.1046/J.1443-9573.2001.00032.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00032.X","url":null,"abstract":"OBJECTIVE: The purpose of the present study was to investigate the correlation between the expression of vascular endothelial growth factor (VEGF), the expression of its receptors, Flt and KDR, and the biological behavior of gastric cancer. \u0000 \u0000 \u0000 \u0000METHODS: Sixty cases of gastric cancer that had been diagnosed by surgery and pathology were studied with the method of semiquantitative reverse transcriptase–polymerase chain reaction (RT-PCR), to determine the expression of VEGF, Flt and KDR in gastric cancer tissue. \u0000 \u0000 \u0000 \u0000RESULTS: The positive rates of VEGF, Flt and KDR in gastric cancer were 73.3, 86.7 and 80.0%, respectively. In pericancerous tissue, the rates were 43.3, 33.0 and 30.0%, respectively. There were significant differences between the groups with and without lymph node metastasis (P < 0.01). For gastric cancer patients with lymphatic metastasis, the positive rates for VEGF, Flt and KDR were 90.3, 80.6 and 96.8%, respectively; for patients without lymphatic metastasis, the rates were 51.7, 41.3 and 55.1%; there were significant differences between the groups with and without lymph node metastasis (P < 0.01). The positive rates of VEGF and KDR in well-differentiated gastric cancer were 40.0 and 46.7%, markedly lower than those of the poorly differentiated and undifferentiated gastric cancer groups. The rate of positive expression of Flt in the well-differentiated gastric cancer group was 73.3%. There was no significant difference between this rate and that of the poorly differentiated and undifferentiated groups (87.5%). The positive expression of VEGF, Flt and KDR was unrelated to the depth of infiltration. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: There are some correlations between VEGF, Flt and KDR and the biological behavior of gastric cancer. Knowing where they are expressed at high rates may be of help in evaluating the prognosis of gastric cancer.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80641458","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 : 2001-10-01DOI: 10.1046/J.1443-9573.2001.00055.X
J. Sheng, S. Shen, Shirong Li, Xia Wu, G. Gao, Shiyong Li, Zhimin Chen
OBJECTIVE: To assess the value of Fourier-transform infrared (FT-IR) spectroscopic analysis in detecting colorectal carcinoma. METHODS: Fifty pairs of specimens of exfoliated cells from patients with colorectal carcinoma, who had undergone colorectal resection, were analyzed by using FT-IR spectrometry. Exfoliated cells were obtained by scraping off: (i) the foci of the colorectal carcinoma; and (ii) the normal mucosa more than 5 cm away from the foci. Cell specimens were fixed and smeared onto two slides: a gold-coated slide for the infrared spectrometry and a conventional one for histopathological evaluation. The spectra from 28 pairs of specimens were analyzed by logistic regression with multiple factors to establish a statistical model for predicting the probability of colorectal cancers, and then the spectra of the remaining 22 pairs were judged according to the model. Their corresponding diagnostic accuracy was calculated. RESULTS: Substantial differences were found in the spectral properties of cancer and non-cancer cells, which were evident in the frequency region of 1000–1350/cm. A shift of the phosphodiester groups of nucleic acids was noted: compared with the spectral features of non-cancerous cells, the distance between VsPO2– and VasPO2– was shorter in cancerous cells. The C–O stretching bonds of cell proteins were significantly changed in the frequency region of 1140–1180/cm. In non-cancerous cells, the peak intensity of 1155/cm was stronger than that of 1174/cm, whereas in cancerous cells the peak intensity of 1155/cm was weaker than that of 1174/cm; the peak intensity ratio of 1174/cm : 1155/cm was increased in cancerous cells. The spectral characteristics of the spectrometric data from the 22 pairs of specimens were consistent with those of the base-model data. The other 22 pairs of specimens were analyzed according to the model, indicating that Fourier-transform infrared spectrometry can be used to discriminate cancerous cells from non-cancerous cells with a sensitivity of 90.91%, a specificity of 86.36%, a positive prediction value of 86.96% and a negative predictive value of 90.48%. CONCLUSIONS: Fourier-transform infrared spectrometry is of value in detecting colorectal cancer cells and it could be used as a rapid method for the clinical screening of malignant cells.
{"title":"Fourier-transform infrared spectrometric analysis for detecting colorectal carcinoma","authors":"J. Sheng, S. Shen, Shirong Li, Xia Wu, G. Gao, Shiyong Li, Zhimin Chen","doi":"10.1046/J.1443-9573.2001.00055.X","DOIUrl":"https://doi.org/10.1046/J.1443-9573.2001.00055.X","url":null,"abstract":"OBJECTIVE: To assess the value of Fourier-transform infrared (FT-IR) spectroscopic analysis in detecting colorectal carcinoma. \u0000 \u0000 \u0000 \u0000METHODS: Fifty pairs of specimens of exfoliated cells from patients with colorectal carcinoma, who had undergone colorectal resection, were analyzed by using FT-IR spectrometry. Exfoliated cells were obtained by scraping off: (i) the foci of the colorectal carcinoma; and (ii) the normal mucosa more than 5 cm away from the foci. Cell specimens were fixed and smeared onto two slides: a gold-coated slide for the infrared spectrometry and a conventional one for histopathological evaluation. The spectra from 28 pairs of specimens were analyzed by logistic regression with multiple factors to establish a statistical model for predicting the probability of colorectal cancers, and then the spectra of the remaining 22 pairs were judged according to the model. Their corresponding diagnostic accuracy was calculated. \u0000 \u0000 \u0000 \u0000RESULTS: Substantial differences were found in the spectral properties of cancer and non-cancer cells, which were evident in the frequency region of 1000–1350/cm. A shift of the phosphodiester groups of nucleic acids was noted: compared with the spectral features of non-cancerous cells, the distance between VsPO2– and VasPO2– was shorter in cancerous cells. The C–O stretching bonds of cell proteins were significantly changed in the frequency region of 1140–1180/cm. In non-cancerous cells, the peak intensity of 1155/cm was stronger than that of 1174/cm, whereas in cancerous cells the peak intensity of 1155/cm was weaker than that of 1174/cm; the peak intensity ratio of 1174/cm : 1155/cm was increased in cancerous cells. The spectral characteristics of the spectrometric data from the 22 pairs of specimens were consistent with those of the base-model data. The other 22 pairs of specimens were analyzed according to the model, indicating that Fourier-transform infrared spectrometry can be used to discriminate cancerous cells from non-cancerous cells with a sensitivity of 90.91%, a specificity of 86.36%, a positive prediction value of 86.96% and a negative predictive value of 90.48%. \u0000 \u0000 \u0000 \u0000CONCLUSIONS: Fourier-transform infrared spectrometry is of value in detecting colorectal cancer cells and it could be used as a rapid method for the clinical screening of malignant cells.","PeriodicalId":10082,"journal":{"name":"Chinese journal of digestive diseases","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77389351","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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