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作 者:刘红[1] 方丹[1] 岳惠芬 邓宏明[3] 蒙碧辉[1] 温中薇[1] 孙晓菲[1]
机构地区:[1]广西医科大学第一附属医院老年内分泌科,南宁530021 [2]广西肿瘤研究所 [3]广西医科大学第一附属医院代谢糖尿病中心,南宁530021
出 处:《中华内科杂志》2010年第5期426-428,共3页Chinese Journal of Internal Medicine
基 金:广西自然科学基金(桂科自0832137)
摘 要:目的 探讨吸烟和戒烟对2型糖尿病大鼠IKK-β磷酸化的影响.方法 6周龄Wistar大鼠42只,随机分为4组:正常对照组(NC,7只)、糖尿病对照组(DC,7只)、糖尿病吸烟组(DS,14只)、糖尿病戒烟组(SC,14只).糖尿病吸烟组分为吸烟8周组(DS8,7只)和12周组(DS12,7只),糖尿病戒烟组分为吸烟8周戒烟组(SC8,7只)和吸烟12周戒烟组(SC12,7只).吸烟组进行8周或12周被动吸烟,戒烟组在8周或12周的被动吸烟后停止吸烟4周.Western blot方法检测各组大鼠骨骼肌中IKK-β磷酸化的程度.结果 与NC组比较,DC组IKK-β磷酸化程度增强(0.16±0.05 vs 0.30±0.08,P〈0.01);与DC组和SC8组比较,DS8组IKK-β磷酸化程度有增强趋势,但差异无统计学意义(0.30±0.08,0.36±0.10 vs 0.40±0.09,P〉0.05);DS12组IKK-β磷酸化程度明显增强,显著高于DC组和SC12组(0.74±0.11 vs 0.30±0.08,0.35±0.07,P〈0.01).结论 随吸烟时间延长2型糖尿病大鼠IKK-β磷酸化程度增强,戒烟后IKK-β磷酸化程度减弱,提示IKK-β磷酸化水平与吸烟致2型糖尿病的发生发展机制有关.Objective To investigate the effect of smoking and smoking cessation on the phosphorylation of IKK-β in type 2 diabetic rats. Methods Forty-two six-week-old Wistar rats were randomly divided into 4 groups: normal control( NC, n = 7), diabetes control (DC, n = 7), diabetes with smoking (DS, n = 14) and diabetes with smoking cessation(SC, n = 14). Rats in DS and SC groups were further assigned randomly into 8w and 12w subgroups. DS group was given passive smoking twice a day for 8 or 12 weeks, while SC group ceased passive smoking for 4 weeks after 8 or 12 weeks of smoking . Western blot method was used to detect the level of IKK-I3 phospholTlation in skeletal muscle. Results Compared with the NC group,the phosphorylation of IKK-I3 protein in DC group was increased (0. 16 ±0. 05 vs 0. 30 ± 0. 08, P 〈 0.01 ). There was an increasing trend with the phosphorylation level of IKK-β in the DS(8w) subgroup, but there was no statistical difference between the DC group and SC(8w) subgroup (0. 40 ±0. 09 vs 0. 30 ±0. 08,0. 36 ±0. 10, P 〉0. 05). The phosphorylation level of IKK-β in DS(12w) group increased obviously, being significantly higher than that in the DC group and SC (12w) subgroup(0. 74 ± 0. 11 vs 0.30±0.08,0.35 ±0.07,P 〈0.01). Conclusion With the prolongation of smoking duration, the phosphorylation of IKK-β in type 2 diabetic rats increased. After smoking cessation, the phosphorylation of IKK-β decreased. The phosphorylation of IKK-β may be involved in the mechanism by which smoking causes type 2 diabetes.
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