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机构地区:[1]四川大学华西医院消化内科,四川省成都市610041 [2]四川大学华西公共卫生学院,四川省成都市610041
出 处:《世界华人消化杂志》2009年第30期3096-3100,共5页World Chinese Journal of Digestology
摘 要:目的:探讨人源乳酸杆菌对Hpylori诱导SGC7901细胞分泌IL-8及p38MAPK磷酸化水平的影响.方法:实验分为空白对照组、Hpylori刺激组、SB203580干预Hpylori刺激组和Lac15干预Hpylori刺激组.采用免疫细胞化学法观察该人源乳酸杆菌Lac15对Hpylori致SGC7901细胞p38MAPK磷酸化的影响.ELISA法观察该人源乳酸杆菌对Hpylori致SGC7901细胞分泌IL-8的影响.结果:Hpylori能诱导细胞的p38MAPK磷酸化水平增高(IA:1.90±0.36vs14.01±1.12,P<0.01)以及IL-8分泌量明显增高(27.2616±0.27ng/Lvs46.3691±0.33ng/L,P<0.01).预先使用一定浓度(3.0×1011cfu/L,3.0×1010cfu/L,3.0×109cfu/L)的人源乳酸杆菌Lac15干预后,p38MAPK磷酸化水平明显降低(IA:4.61±1.13,6.11±0.19,8.25±0.56vs14.01±1.12,均P<0.01),IL-8分泌量明显降低(42.3209±0.24ng/L,42.1046±0.23ng/L,43.4636±0.25ng/Lvs46.3691±0.33ng/L,均P<0.05或0.01),与Hpylori刺激组比较,具有统计学意义.结论:p38MAPK磷酸化参与Hpylori诱导的SGC7901细胞分泌IL-8,人源乳酸杆菌Lac15可能通过抑制p38MAPK磷酸化途径抑制IL-8的分泌,从而抑制炎症反应.AIM: To investigate the effects of human-derived lactobacillus Lac15 on p38 mitogen-activated protein kinase (MAPK) phosphorylation and interleukin-8 (IL-8) secretion in human gastric cancer SGC7901 cells infected with Helicobacter pylori (H pylori). METHODS: SGC7901 cells were divided into four groups: normal control group, H pylori infection group, SB203580 intervention group, and lactobacillus intervention group. The phos-phorylation level of p38 MAPK in SGC7901 cells infected with H pylori was evaluated by immunocytochemistry. The release of IL-8 in SGC7901 cells was detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: The phosphorylation level of p38 MAPK (IA: 1.90 ± 0.36 vs 14.01 ± 1.12, P〈0.01) and IL-8 secretion (27.2616 ± 0.27 ng/L vs 46.3691 ± 0.33 ng/L, P〈0.01) were signifi cantly higher in SGC7901 cells infected with H pylori than in normal control cells. After intervention with lactobacillus Lac15 at doses of 3×1011, 3× 1010 and 3×109 cfu/L, both the phosphorylation level of p38 MAPK (IA: 4.61 ± 1.13, 6.11 ± 0.19 and 8.25 ± 0.56 vs 14.01 ± 1.12, respectively; all P〈0.01) and IL-8 secretion (42.3209 ± 0.24 ng/L, 42.1046 ± 0.23 ng/L and 43.4636 ± 0.25 ng/L vs 46.3691 ± 0.33 ng/L, respectively; all P〈0.05 or P〈0.01) decreased signifi cantly in SGC7901 cells infected with H pylori. CONCLUSION: H pylori infection can induce IL-8 secretion perhaps via a mechanism associated with promoting p38MAPK phosphorylation. Human-derived lactobacillus Lac15 can inhibit p38MAPK phosphorylation and thus decrease IL-8 secretion.
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