乳酸杆菌对幽门螺旋杆菌脂多糖作用下的SGC-7901细胞p38MAPK磷酸化水平和凋亡率的影响
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周 超, 马洪升
乳酸杆菌;幽门螺旋杆菌;脂多糖;SGC7901细胞;p38丝裂原活化蛋白激酶;细胞凋亡周超,马洪升.乳酸杆菌对幽门螺旋杆菌脂多糖作用下的SGC-7901细胞p38MAPK磷酸化水平和凋亡率的影响. 世界华人消化杂志2007;15(8)807-812,乳酸杆菌对幽门螺旋杆菌脂多糖作用下的S
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周超, 马洪升, 四川大学华西医院消化内科 四川省成都市 610041
周超, 在读博士, 主要从事胃内微生态及胃肠多肽的研究.四川省科技厅应用基础研究项目, No.04JY029-090-1
通讯作者: 马洪升, 610041, 四川省成都市国学巷37号, 四川大学华西医院消化内科. mhswch@163.com
电话: 028-85422296
收稿日期: 2006-12-16 接受日期: 2007-01-10
Effects of lactobacillus on phosphorylated p38 mitogen-activated protein kinase and apoptosis in SGC-7901 cells treated with lipopolysaccharide of Helicobacter pylori
Chao Zhou, Hong-Sheng Ma
Chao Zhou, Hong-Sheng Ma, Department of Gastroenterology, West China Hospital of Sichuan University, Chengdu 610041, Sichuan Province, China
Supported by the Basic Research Project of Science and Technology Office of Sichuan Province, No. 04JY029-090-1
Correspondence to: Hong-Sheng Ma, Department of Gastroenterology, West China Hospital of Sichuan University, 37 Guoxue Alley, Chengdu 610041, Sichuan Province, China. mhswch@163.com
Received: 2006-12-16 Accepted: 2007-01-10
AbstractAIM:To investigate effects of lactobacillus bulgaricus (LBG) on the levels of phosphorylated p38 mitogen-activated protein kinase (P-p38MAPK) and apoptosis index (AI) in gastric cancer cell line SGC-7901 treated with lipopolysaccharide of H pylori Sydney strain 1 (H pyloriSS1-LPS).
METHODS:Human gastric cancer cell line SGC-7901 was treated withH pyloriSS1-LPS at the concentration of 2.5×103, 2.5×104, 2.5 ×105 EU/L, respectively, after pretreatment for 1 hour with 10 mmol/L SB203580 (blocker of p38MAPK) or 1×1013 CFU/L LBG. The level of P-p38MAPK was analyzed by immunocytochemistry after 2 hours of H pyloriSS1-LPS treatment. The cell activity was detected by MTT assay after 4, 5 and 6 hours of treatment, and the apoptosis was measured by flow cytometry at the 6th hour.
RESULTS: H pyloriSS1-LPS inhibited cell activity (0.164 ± 0.028 vs 0.622 ± 0.068, P < 0.05) and up-regulated the level of P-p38MAPK (79.771 ± 1.424 vs 4.075 ± 0. 135, P < 0.01) and AI value (10.000% ± 0.510% vs 4.175% ± 0.206%, P < 0.05) in a dose-dependent manner. The level of P-p38MAPK and AI value in SGC-7901 cells were not significantly different between LBG pretreatment group and the controls, and the cell activity and AI value were not markedly different between SB203580 pretreatment group and the controls.
CONCLUSION: H pyloriSS1-LPS may induce the apoptosis of SGC-7901 cells by activating the phosphorylation of p38MAPK, while LBG can prevent H pyloriSS1-LPS-induced apoptosis of SGC-7901 cells by inhibiting the phosphorylation of p38MAPK.
Key Words: Lactobacillus; Helicobacer pylori; Lipopolysaccharide; SGC-7901; p38 mitogen-activated protein kinase; Cell apoptosis
Zhou C, Ma HS. Effects of lactobacillus on of phosphorylated p38 mitogen-activated protein kinase and apoptosis index in SGC-7901 cells treated with lipopolysaccharide of Helicobacer pylori ......
周超, 马洪升, 四川大学华西医院消化内科 四川省成都市 610041
周超, 在读博士, 主要从事胃内微生态及胃肠多肽的研究.四川省科技厅应用基础研究项目, No.04JY029-090-1
通讯作者: 马洪升, 610041, 四川省成都市国学巷37号, 四川大学华西医院消化内科. mhswch@163.com
电话: 028-85422296
收稿日期: 2006-12-16 接受日期: 2007-01-10
Effects of lactobacillus on phosphorylated p38 mitogen-activated protein kinase and apoptosis in SGC-7901 cells treated with lipopolysaccharide of Helicobacter pylori
Chao Zhou, Hong-Sheng Ma
Chao Zhou, Hong-Sheng Ma, Department of Gastroenterology, West China Hospital of Sichuan University, Chengdu 610041, Sichuan Province, China
Supported by the Basic Research Project of Science and Technology Office of Sichuan Province, No. 04JY029-090-1
Correspondence to: Hong-Sheng Ma, Department of Gastroenterology, West China Hospital of Sichuan University, 37 Guoxue Alley, Chengdu 610041, Sichuan Province, China. mhswch@163.com
Received: 2006-12-16 Accepted: 2007-01-10
AbstractAIM:To investigate effects of lactobacillus bulgaricus (LBG) on the levels of phosphorylated p38 mitogen-activated protein kinase (P-p38MAPK) and apoptosis index (AI) in gastric cancer cell line SGC-7901 treated with lipopolysaccharide of H pylori Sydney strain 1 (H pyloriSS1-LPS).
METHODS:Human gastric cancer cell line SGC-7901 was treated withH pyloriSS1-LPS at the concentration of 2.5×103, 2.5×104, 2.5 ×105 EU/L, respectively, after pretreatment for 1 hour with 10 mmol/L SB203580 (blocker of p38MAPK) or 1×1013 CFU/L LBG. The level of P-p38MAPK was analyzed by immunocytochemistry after 2 hours of H pyloriSS1-LPS treatment. The cell activity was detected by MTT assay after 4, 5 and 6 hours of treatment, and the apoptosis was measured by flow cytometry at the 6th hour.
RESULTS: H pyloriSS1-LPS inhibited cell activity (0.164 ± 0.028 vs 0.622 ± 0.068, P < 0.05) and up-regulated the level of P-p38MAPK (79.771 ± 1.424 vs 4.075 ± 0. 135, P < 0.01) and AI value (10.000% ± 0.510% vs 4.175% ± 0.206%, P < 0.05) in a dose-dependent manner. The level of P-p38MAPK and AI value in SGC-7901 cells were not significantly different between LBG pretreatment group and the controls, and the cell activity and AI value were not markedly different between SB203580 pretreatment group and the controls.
CONCLUSION: H pyloriSS1-LPS may induce the apoptosis of SGC-7901 cells by activating the phosphorylation of p38MAPK, while LBG can prevent H pyloriSS1-LPS-induced apoptosis of SGC-7901 cells by inhibiting the phosphorylation of p38MAPK.
Key Words: Lactobacillus; Helicobacer pylori; Lipopolysaccharide; SGC-7901; p38 mitogen-activated protein kinase; Cell apoptosis
Zhou C, Ma HS. Effects of lactobacillus on of phosphorylated p38 mitogen-activated protein kinase and apoptosis index in SGC-7901 cells treated with lipopolysaccharide of Helicobacer pylori ......
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