AIM： To assess long-term effects of Helicobacter pylori （H pylon} eradication on antral G cell morphology and function in patients with and without duodenal ulcer （DU）.METHODS： Consecutive dyspeptic patients refe...AIM： To assess long-term effects of Helicobacter pylori （H pylon} eradication on antral G cell morphology and function in patients with and without duodenal ulcer （DU）.METHODS： Consecutive dyspeptic patients referred to the endoscopy entered the study. Out of 39 Hpylori positive patients, 8 had DU （Hpylori ＋DU） and 31 gastritis （Hpylori＋G）. Control groups consisted of 11 uninfected dyspeptic patients （CG1） and 7 healthy volunteers （CG2）. Basal plasma gastrin （PGL）, antral tissue gastrin concentrations （ATGC）, immunohistochemical and electron microscopic characteristics of G cells were determined, prior to and 6 mo after therapy.RESULTS： We-demonstrated elevated PGL in infected patients compared to uninfected controls prior to therapy.Elevated PGL were registered in all Hpylori＋patients （Hpylori＋DU： 106.78＋22.72 pg/mL, Hpylori＋G： 74.95＋15.63,CGI： 68.59＋17.97, CG2：39.24＋5.59 pg/mL, P〈0.01）.Successful eradication （e） therapy in Hpylori＋patients lead to significant decrease in PGL （Hpylori＋DU： 59.93＋9.40 and Hpylori＋Ge： 42.36＋10.28 pg/mL, P〈0.001）. ATGC at the beginning of the study were similar in infected and uninfected patients and eradication therapy lead to significant decrease in ATGC in Hpylori＋gastritis, but not in DU patients. In the Hpylori＋DU patients, the mean number of antral G cells was significantly lower in comparison with all other groups （P〈0.01）, but after successful eradication was close to normal values found in controls. By contrast, G cell number and volume density were significantly decreased （P〈0.01） in Hpylori＋Ge group after successful eradication therapy （294＋32 and 0.31＋0.02,respectively）, in comparison to values before eradication （416~40 and 0.48~0.09）. No significant change of the G cell/total endocrine cell ratio was observed during the 6 mo of follow up in any of the groups. A reversible increase in G cell secretory function was seen in all infected individuals, demonstrated by a more prominent secretory apparatus. However, differences between DU and gastritis group were identified.CONCLUSION： H py/oriinfection induces antral G cell hyperfunction resulting in increased gastrin synthesis and secretion. After eradication therapy complete morphological and functional recovery is observed in patients with gastritis. In the DU patients some other factors unrelated to the Hpyloriinfection influence antral G cell morphology and function.展开更多
Objective: To investigate the association of changes in G and D cells in the antral mucosa with the production of gastrin and somatostatin during gastric ulcer and the healing process. Methods: Experimental gastric ul...Objective: To investigate the association of changes in G and D cells in the antral mucosa with the production of gastrin and somatostatin during gastric ulcer and the healing process. Methods: Experimental gastric ulcer was induced with acetic acid in 42 Wistar rats and another 7 normal rats served as control. Changes in the production of gastrin and somatostatin in the plasma, gastric fluid and the antral tissues of the rats were measured by radio immunoassay, and the number and distribution of G and D cells were respectively determined by immunochemistry and Quantimet500 image analysis system. Results: In rats with gastric ulcer, the gastrin levels in the plasma, gastric fluid and the antral tissues increased while somatostatin levels were reduced, which were corrected in the healing process. Immunochemistry demonstrated the increase in the number of G cells in the antral tissues with decrease in D cell number, and the area covered by both cells shrank. The G cell to D cell number and area ratios were both decreased after the onset of the ulcer and returned to the normal when the healing process took place. Conclusion; Secretion of gastrin by G cells increases and that of somatostatin by D cells declines during gastric ulcer in rats, and imbalance of G and D cells may be responsible for gastrointestinal dysfunction.展开更多
Objective： To examine the apoptotic effect of ent-llα-hydroxy-15-oxo-kaur-16-en-19-oic-acid （5F）, a compound isolated from Pteris semipinnata L （PsL）, in human lung cancer A549 cells. Methods： A549 cells were ...Objective： To examine the apoptotic effect of ent-llα-hydroxy-15-oxo-kaur-16-en-19-oic-acid （5F）, a compound isolated from Pteris semipinnata L （PsL）, in human lung cancer A549 cells. Methods： A549 cells were treated with 5F （0-80 lag/ml） for different time periods. Cytotoxicity was examined using a Ml-I- method. Cell cycle was examined using propidium iodide staining. Apoptosis was examined using Hoechst 33258 staining, enzyme-linked immunosorbent assay （ELISA） and caspase-3 activity analysis. Expression of representative apoptosis-related proteins was evaluated by Western blot analysis. Reactive oxygen species （ROS） level was measured using standard protocols. Potential interaction of 5F with cisplatin was also examined. Results： 5F inhibited the proliferation of A549 cells in a concentration- and time-dependent manner. 5F increased the accumulation of cells in sub-G1 phase and arrested the cells in the G2 phase. Exposure to 5F induced morphological changes and DNA fragmentation that are characteristic of apoptosis. The expression of p21 was increased. 5F exposure also increased Bax expression, release of cytochrome c and apoptosis inducing factor （AIF）, and activation of caspase-3. 5F significantly sensitized the cells to cisplatin toxicity. Interestingly, treatment with 5F did not increase ROS, but reduced ROS production induced by cisplatin. Conclusion： 5F could inhibit the proliferation of A549 cells by arresting the cells in G2 phase and by inducing mitochondrial-mediated apoptosis.展开更多
To study the mechanisms involved in the inhibition of chronic myeloid leukemic cells (K562) proliferation induced by arsenic trioxide (As 2O 3) and to explore the potential role of Survivin, an inhibitor of apoptosi...To study the mechanisms involved in the inhibition of chronic myeloid leukemic cells (K562) proliferation induced by arsenic trioxide (As 2O 3) and to explore the potential role of Survivin, an inhibitor of apoptosis protein, in the regulation of As 2O 3 induced cell apoptosis, K562 cells were cultured with As 2O 3 of different concentrations. Cells were collected for proliferation analysis by MTT assay. Cell cycle distribution and cell apoptosis were analyzed by flow cytometry. Expression of Survivin protein and mRNA were detected by flow cytometry and RT-PCR, respectively. Our results showed that As 2O 3 (2-10 μmol/L) inhibited K562 cells growth effectively, but it did not induce cells apoptosis significantly. The percentage of K562 cells at G 2/M phase increased in proportion to As 2O 3 concentrations, and the expression of Survivin mRNA and content of Survivin protein was up-regulated accordingly. It is concluded that As 2O 3 inhibited K562 cells growth by inducing cell cycle arrest mainly at G 2/M phase. Over-expression of Survivin gene and protein might be one of the possible mechanisms contributing to K562 cells' resistance to As 2O 3-induced apoptosis.展开更多
AIM: To investigate the relationship between gastric dysmotility,gastrointestinal hormone abnormalities, and neuroendocrine cells in gastrointestinal mucosa in patients with functional dyspepsia (FD).METHODS: Gastric ...AIM: To investigate the relationship between gastric dysmotility,gastrointestinal hormone abnormalities, and neuroendocrine cells in gastrointestinal mucosa in patients with functional dyspepsia (FD).METHODS: Gastric emptying was assessed with solid radiopaque markers in 54 FD patients, and the patients were divided into two groups according to the results, one with delayed gastric emptying and the other with normal gastric emptying. Seventeen healthy volunteers acted as normal controls. Fasting and postprandial plasma levels and gastroduodenal mucosal levels of gastrointestinal hormones gastrin, somatostatin (SS) and neurotensin (NT)were measured by radioimmunoassay in all the subjects.G cells (gastrin-producing cells) and D cells (SS-producing cells) in gastric antral mucosa were immunostained with rabbit anti-gastrin polyclonal antibody and rabbit anti-SS polyclonal antibody, respectively, and analyzed quantitatively by computerized image analysis.RESULTS: The postprandial plasma gastrin levels, the fasting and postprandial plasma levels and the gastric and duodenal mucosal levels of NT were significantly higher in the FD patients with delayed gastric emptying than in those with normal gastric emptying and normal controls. The number and gray value of G and D cells and the G cell/D cell number ratio did not differ significantly between normal controls and the FD patients with or without delayed gastric emptying.CONCLUSION: Our findings suggest that the abnormalities of gastrin and NT may play a role in the pathophysiology of gastric dysmotility in FD patients, and the abnormality of postprandial plasma gastrin levels in FD patients with delayed gastric emptying is not related to the changes both in the number and gray value of G cells and in the G cell/D cell number ratio in gastric antral mucosa.展开更多
INTRODUCTIONKupffer cells are residential macrophages in the liver ,which play a critical role in the maintenance of normal liver function and in immunal surveilance of hepatocellular carcinoma (HCC) and other cancers...INTRODUCTIONKupffer cells are residential macrophages in the liver ,which play a critical role in the maintenance of normal liver function and in immunal surveilance of hepatocellular carcinoma (HCC) and other cancers[1].The biological immune modulants have cancers[2].In our previous studies ,the combined use of biological immune modulants showed better dffects .展开更多
基金Supported by a Grant From Serbian Ministry for Science, Technology and Development, No. 1752
文摘AIM： To assess long-term effects of Helicobacter pylori （H pylon} eradication on antral G cell morphology and function in patients with and without duodenal ulcer （DU）.METHODS： Consecutive dyspeptic patients referred to the endoscopy entered the study. Out of 39 Hpylori positive patients, 8 had DU （Hpylori ＋DU） and 31 gastritis （Hpylori＋G）. Control groups consisted of 11 uninfected dyspeptic patients （CG1） and 7 healthy volunteers （CG2）. Basal plasma gastrin （PGL）, antral tissue gastrin concentrations （ATGC）, immunohistochemical and electron microscopic characteristics of G cells were determined, prior to and 6 mo after therapy.RESULTS： We-demonstrated elevated PGL in infected patients compared to uninfected controls prior to therapy.Elevated PGL were registered in all Hpylori＋patients （Hpylori＋DU： 106.78＋22.72 pg/mL, Hpylori＋G： 74.95＋15.63,CGI： 68.59＋17.97, CG2：39.24＋5.59 pg/mL, P〈0.01）.Successful eradication （e） therapy in Hpylori＋patients lead to significant decrease in PGL （Hpylori＋DU： 59.93＋9.40 and Hpylori＋Ge： 42.36＋10.28 pg/mL, P〈0.001）. ATGC at the beginning of the study were similar in infected and uninfected patients and eradication therapy lead to significant decrease in ATGC in Hpylori＋gastritis, but not in DU patients. In the Hpylori＋DU patients, the mean number of antral G cells was significantly lower in comparison with all other groups （P〈0.01）, but after successful eradication was close to normal values found in controls. By contrast, G cell number and volume density were significantly decreased （P〈0.01） in Hpylori＋Ge group after successful eradication therapy （294＋32 and 0.31＋0.02,respectively）, in comparison to values before eradication （416~40 and 0.48~0.09）. No significant change of the G cell/total endocrine cell ratio was observed during the 6 mo of follow up in any of the groups. A reversible increase in G cell secretory function was seen in all infected individuals, demonstrated by a more prominent secretory apparatus. However, differences between DU and gastritis group were identified.CONCLUSION： H py/oriinfection induces antral G cell hyperfunction resulting in increased gastrin synthesis and secretion. After eradication therapy complete morphological and functional recovery is observed in patients with gastritis. In the DU patients some other factors unrelated to the Hpyloriinfection influence antral G cell morphology and function.
基金Supported by Guangdong Provincial Key Project for Scientific Research (No. 99-13)
文摘Objective: To investigate the association of changes in G and D cells in the antral mucosa with the production of gastrin and somatostatin during gastric ulcer and the healing process. Methods: Experimental gastric ulcer was induced with acetic acid in 42 Wistar rats and another 7 normal rats served as control. Changes in the production of gastrin and somatostatin in the plasma, gastric fluid and the antral tissues of the rats were measured by radio immunoassay, and the number and distribution of G and D cells were respectively determined by immunochemistry and Quantimet500 image analysis system. Results: In rats with gastric ulcer, the gastrin levels in the plasma, gastric fluid and the antral tissues increased while somatostatin levels were reduced, which were corrected in the healing process. Immunochemistry demonstrated the increase in the number of G cells in the antral tissues with decrease in D cell number, and the area covered by both cells shrank. The G cell to D cell number and area ratios were both decreased after the onset of the ulcer and returned to the normal when the healing process took place. Conclusion; Secretion of gastrin by G cells increases and that of somatostatin by D cells declines during gastric ulcer in rats, and imbalance of G and D cells may be responsible for gastrointestinal dysfunction.
基金supported by the National Natural Science Foundation of China(No.3987099)the Guangdong-Hong Kong Technology Cooperation Funding Scheme(No.GHP/022/06)the Research Committee,Guangdong Medica College(No.XB0601)
文摘Objective： To examine the apoptotic effect of ent-llα-hydroxy-15-oxo-kaur-16-en-19-oic-acid （5F）, a compound isolated from Pteris semipinnata L （PsL）, in human lung cancer A549 cells. Methods： A549 cells were treated with 5F （0-80 lag/ml） for different time periods. Cytotoxicity was examined using a Ml-I- method. Cell cycle was examined using propidium iodide staining. Apoptosis was examined using Hoechst 33258 staining, enzyme-linked immunosorbent assay （ELISA） and caspase-3 activity analysis. Expression of representative apoptosis-related proteins was evaluated by Western blot analysis. Reactive oxygen species （ROS） level was measured using standard protocols. Potential interaction of 5F with cisplatin was also examined. Results： 5F inhibited the proliferation of A549 cells in a concentration- and time-dependent manner. 5F increased the accumulation of cells in sub-G1 phase and arrested the cells in the G2 phase. Exposure to 5F induced morphological changes and DNA fragmentation that are characteristic of apoptosis. The expression of p21 was increased. 5F exposure also increased Bax expression, release of cytochrome c and apoptosis inducing factor （AIF）, and activation of caspase-3. 5F significantly sensitized the cells to cisplatin toxicity. Interestingly, treatment with 5F did not increase ROS, but reduced ROS production induced by cisplatin. Conclusion： 5F could inhibit the proliferation of A549 cells by arresting the cells in G2 phase and by inducing mitochondrial-mediated apoptosis.
文摘To study the mechanisms involved in the inhibition of chronic myeloid leukemic cells (K562) proliferation induced by arsenic trioxide (As 2O 3) and to explore the potential role of Survivin, an inhibitor of apoptosis protein, in the regulation of As 2O 3 induced cell apoptosis, K562 cells were cultured with As 2O 3 of different concentrations. Cells were collected for proliferation analysis by MTT assay. Cell cycle distribution and cell apoptosis were analyzed by flow cytometry. Expression of Survivin protein and mRNA were detected by flow cytometry and RT-PCR, respectively. Our results showed that As 2O 3 (2-10 μmol/L) inhibited K562 cells growth effectively, but it did not induce cells apoptosis significantly. The percentage of K562 cells at G 2/M phase increased in proportion to As 2O 3 concentrations, and the expression of Survivin mRNA and content of Survivin protein was up-regulated accordingly. It is concluded that As 2O 3 inhibited K562 cells growth by inducing cell cycle arrest mainly at G 2/M phase. Over-expression of Survivin gene and protein might be one of the possible mechanisms contributing to K562 cells' resistance to As 2O 3-induced apoptosis.
文摘AIM: To investigate the relationship between gastric dysmotility,gastrointestinal hormone abnormalities, and neuroendocrine cells in gastrointestinal mucosa in patients with functional dyspepsia (FD).METHODS: Gastric emptying was assessed with solid radiopaque markers in 54 FD patients, and the patients were divided into two groups according to the results, one with delayed gastric emptying and the other with normal gastric emptying. Seventeen healthy volunteers acted as normal controls. Fasting and postprandial plasma levels and gastroduodenal mucosal levels of gastrointestinal hormones gastrin, somatostatin (SS) and neurotensin (NT)were measured by radioimmunoassay in all the subjects.G cells (gastrin-producing cells) and D cells (SS-producing cells) in gastric antral mucosa were immunostained with rabbit anti-gastrin polyclonal antibody and rabbit anti-SS polyclonal antibody, respectively, and analyzed quantitatively by computerized image analysis.RESULTS: The postprandial plasma gastrin levels, the fasting and postprandial plasma levels and the gastric and duodenal mucosal levels of NT were significantly higher in the FD patients with delayed gastric emptying than in those with normal gastric emptying and normal controls. The number and gray value of G and D cells and the G cell/D cell number ratio did not differ significantly between normal controls and the FD patients with or without delayed gastric emptying.CONCLUSION: Our findings suggest that the abnormalities of gastrin and NT may play a role in the pathophysiology of gastric dysmotility in FD patients, and the abnormality of postprandial plasma gastrin levels in FD patients with delayed gastric emptying is not related to the changes both in the number and gray value of G cells and in the G cell/D cell number ratio in gastric antral mucosa.
基金Supported by the National Natural Science Foundation of China,No.39270379
文摘INTRODUCTIONKupffer cells are residential macrophages in the liver ,which play a critical role in the maintenance of normal liver function and in immunal surveilance of hepatocellular carcinoma (HCC) and other cancers[1].The biological immune modulants have cancers[2].In our previous studies ,the combined use of biological immune modulants showed better dffects .
