Objective: To study the expressions of Bcl-2 and Bax proteins and explore the relationships between them and apoptosis in gastric carcinoma and precancerous lesions. Methods: TUNEL method was used to detect apoptosis ...Objective: To study the expressions of Bcl-2 and Bax proteins and explore the relationships between them and apoptosis in gastric carcinoma and precancerous lesions. Methods: TUNEL method was used to detect apoptosis and im- munohistochemical staining method was used to detect the expressions of Bcl-2 and Bax proteins in 70 cases of chronic gastritis, 49 cases of intestinal metaplasia, 64 cases of dysplasia and 81 cases of gastric carcinoma. Results: The positive incidences of Bcl-2 and Bax were the highest in severe dysplasia. In intestinal metaplasia and dysplasia, positive incidences of Bcl-2 and Bax were higher than those in chronic gastritis and gastric carcinoma. During the process of evolvement from chronic gastritis to intestinal metaplasia then to dysplasia, apoptosis indexes gradually rise up to mid-high dysplasia, which reached the highest point, then it began to fall down, when it reached the lowest point in gastric carcinoma. There were nega- tive correlations between the expressions of Bcl-2, Bax proteins and apoptosis. Conclusion: The expression of Bcl-2 may be an early behavior in the gastric carcinogenesis. Bax had antagonistic effect to Bcl-2. Detections of Bcl-2 and Bax may be beneficial to the early diagnosis of gastric tumor and precancerous lesions.展开更多
Objective: To investigate the apoptosis effect of TNF-α on HepG2 cells and its mechanism in vitro. Methods: HepG2 cells were treated with TNF-α (400 U/mL). HepG2 cells treated with TNF-α for 24 h and apoptosis was ...Objective: To investigate the apoptosis effect of TNF-α on HepG2 cells and its mechanism in vitro. Methods: HepG2 cells were treated with TNF-α (400 U/mL). HepG2 cells treated with TNF-α for 24 h and apoptosis was proved by DNA fragments on gel electrophoresis. Fluorescent quantitative real-time PCR was used to detect Fas and FasL expression. HepG2 cells treated by TNF-α were co-cultivated with normal HepG2 cells. Apoptosis of HepG2 cells was determined by the method of FACS. Results: After 24 h TNF-α treatment, DNA was collapsed into fragments to form DNA ladder in gel elec- trophoresis; FasL expression increases and induces HepG2 cells apoptosis. By FACS, 98.4% of the co-cultivated cells were apoptosis, but 16.5% cells in control group were apoptosis. Conclusion: TNF-α can induce apoptosis of HepG2 cells in vitro. FasL expression on TNF-α pre-treated HepG2 cells increased and these cells can lead normal HepG2 cells to apoptosis. This may attribute to the cure of virus hepatitis and hepatoma.展开更多
文摘Objective: To study the expressions of Bcl-2 and Bax proteins and explore the relationships between them and apoptosis in gastric carcinoma and precancerous lesions. Methods: TUNEL method was used to detect apoptosis and im- munohistochemical staining method was used to detect the expressions of Bcl-2 and Bax proteins in 70 cases of chronic gastritis, 49 cases of intestinal metaplasia, 64 cases of dysplasia and 81 cases of gastric carcinoma. Results: The positive incidences of Bcl-2 and Bax were the highest in severe dysplasia. In intestinal metaplasia and dysplasia, positive incidences of Bcl-2 and Bax were higher than those in chronic gastritis and gastric carcinoma. During the process of evolvement from chronic gastritis to intestinal metaplasia then to dysplasia, apoptosis indexes gradually rise up to mid-high dysplasia, which reached the highest point, then it began to fall down, when it reached the lowest point in gastric carcinoma. There were nega- tive correlations between the expressions of Bcl-2, Bax proteins and apoptosis. Conclusion: The expression of Bcl-2 may be an early behavior in the gastric carcinogenesis. Bax had antagonistic effect to Bcl-2. Detections of Bcl-2 and Bax may be beneficial to the early diagnosis of gastric tumor and precancerous lesions.
文摘Objective: To investigate the apoptosis effect of TNF-α on HepG2 cells and its mechanism in vitro. Methods: HepG2 cells were treated with TNF-α (400 U/mL). HepG2 cells treated with TNF-α for 24 h and apoptosis was proved by DNA fragments on gel electrophoresis. Fluorescent quantitative real-time PCR was used to detect Fas and FasL expression. HepG2 cells treated by TNF-α were co-cultivated with normal HepG2 cells. Apoptosis of HepG2 cells was determined by the method of FACS. Results: After 24 h TNF-α treatment, DNA was collapsed into fragments to form DNA ladder in gel elec- trophoresis; FasL expression increases and induces HepG2 cells apoptosis. By FACS, 98.4% of the co-cultivated cells were apoptosis, but 16.5% cells in control group were apoptosis. Conclusion: TNF-α can induce apoptosis of HepG2 cells in vitro. FasL expression on TNF-α pre-treated HepG2 cells increased and these cells can lead normal HepG2 cells to apoptosis. This may attribute to the cure of virus hepatitis and hepatoma.
