中国行为医学科学
中國行為醫學科學
중국행위의학과학
2008年
6期
525-527
,共3页
夏静%邵云%李艳辉%王旭梅%金魁和
夏靜%邵雲%李豔輝%王旭梅%金魁和
하정%소운%리염휘%왕욱매%금괴화
氟西汀%慢性应激%皮质醇%肿瘤坏死因子-α%细胞间黏附分子-1%胃黏膜
氟西汀%慢性應激%皮質醇%腫瘤壞死因子-α%細胞間黏附分子-1%胃黏膜
불서정%만성응격%피질순%종류배사인자-α%세포간점부분자-1%위점막
Fluoxetine%Chronic stress%Cortisol%TNF-α%ICAM-1%Gastric mucosa
目的 研究氟西汀对慢性应激大鼠血清皮质醇、肿瘤坏死因子-α(TNF-α)含量、胃黏膜细胞间黏附分子-1(ICAM-1)表达的影响.方法 将青年雄性Wistar大鼠24只随机分为对照组、应激组、氟西汀组各8只.应激组和氟西汀组大鼠每笼1只喂养,实验第1-21天,接受各种不同的应激.氟西汀组大鼠每天给予氟西汀水溶液灌胃.对照组大鼠群养不给任何刺激.实验第22天杀死所有大鼠,检测血清皮质醇、TNF-α浓度;用免疫组化法检测胃黏膜蛋白ICAM-1表达,进行图像分析,测定光密度平均值.结果 应激组大鼠与对照组比较,血清皮质醇含量[(77.12±9.76)μg/ml,(44.96±6.25)μg/ml,t=7.85,P<0.01]、TNF-α含量[(69.66±6.68)pg/ml,(39.21±3.57)pg/ml,t=11.37,P<0.01]、胃黏膜ICAM-1表达的光密度平均值[(53.87±6.84),(30.26±3.68),t=8.59,P<0.01]有明显增高;与应激组比较,氟西汀组大鼠血清皮质醇含量[(58.82±6.56)μg/ml,t=4.40,P<0.01]、TNF-α含量[(50.18±3.23)pg/ml,t=7.43.P<0.01]、胃黏膜ICAM-1表达的光密度平均值(36.61±4.39,t=6.00,P<0.01)明显下降.结论 慢性应激可引起大鼠血清皮质醇、TNF-α含量增高,胃黏膜ICAM-1过表达,而氟西汀可以部分的逆转这些改变.
目的 研究氟西汀對慢性應激大鼠血清皮質醇、腫瘤壞死因子-α(TNF-α)含量、胃黏膜細胞間黏附分子-1(ICAM-1)錶達的影響.方法 將青年雄性Wistar大鼠24隻隨機分為對照組、應激組、氟西汀組各8隻.應激組和氟西汀組大鼠每籠1隻餵養,實驗第1-21天,接受各種不同的應激.氟西汀組大鼠每天給予氟西汀水溶液灌胃.對照組大鼠群養不給任何刺激.實驗第22天殺死所有大鼠,檢測血清皮質醇、TNF-α濃度;用免疫組化法檢測胃黏膜蛋白ICAM-1錶達,進行圖像分析,測定光密度平均值.結果 應激組大鼠與對照組比較,血清皮質醇含量[(77.12±9.76)μg/ml,(44.96±6.25)μg/ml,t=7.85,P<0.01]、TNF-α含量[(69.66±6.68)pg/ml,(39.21±3.57)pg/ml,t=11.37,P<0.01]、胃黏膜ICAM-1錶達的光密度平均值[(53.87±6.84),(30.26±3.68),t=8.59,P<0.01]有明顯增高;與應激組比較,氟西汀組大鼠血清皮質醇含量[(58.82±6.56)μg/ml,t=4.40,P<0.01]、TNF-α含量[(50.18±3.23)pg/ml,t=7.43.P<0.01]、胃黏膜ICAM-1錶達的光密度平均值(36.61±4.39,t=6.00,P<0.01)明顯下降.結論 慢性應激可引起大鼠血清皮質醇、TNF-α含量增高,胃黏膜ICAM-1過錶達,而氟西汀可以部分的逆轉這些改變.
목적 연구불서정대만성응격대서혈청피질순、종류배사인자-α(TNF-α)함량、위점막세포간점부분자-1(ICAM-1)표체적영향.방법 장청년웅성Wistar대서24지수궤분위대조조、응격조、불서정조각8지.응격조화불서정조대서매롱1지위양,실험제1-21천,접수각충불동적응격.불서정조대서매천급여불서정수용액관위.대조조대서군양불급임하자격.실험제22천살사소유대서,검측혈청피질순、TNF-α농도;용면역조화법검측위점막단백ICAM-1표체,진행도상분석,측정광밀도평균치.결과 응격조대서여대조조비교,혈청피질순함량[(77.12±9.76)μg/ml,(44.96±6.25)μg/ml,t=7.85,P<0.01]、TNF-α함량[(69.66±6.68)pg/ml,(39.21±3.57)pg/ml,t=11.37,P<0.01]、위점막ICAM-1표체적광밀도평균치[(53.87±6.84),(30.26±3.68),t=8.59,P<0.01]유명현증고;여응격조비교,불서정조대서혈청피질순함량[(58.82±6.56)μg/ml,t=4.40,P<0.01]、TNF-α함량[(50.18±3.23)pg/ml,t=7.43.P<0.01]、위점막ICAM-1표체적광밀도평균치(36.61±4.39,t=6.00,P<0.01)명현하강.결론 만성응격가인기대서혈청피질순、TNF-α함량증고,위점막ICAM-1과표체,이불서정가이부분적역전저사개변.
Objective To study the effects of fluoxetine on serum cortisol, TNF-α and expression of ICAM-1 in gastric mucosa in chronic stress rats. Methods Male Wistar rats were divided into control group,stress group and fluoxetine group randomly, and 8 rats each group. Stress group and fluoxetine group were separated one rat in each box, from 1 ～ 21 days,and accepted various types of stresses. At the same time,fluoxetine group were given fluoxetine every day. The control group were fed in two boxes with no stress from 1 ～ 21 days. On 22nd day, all the rats were killed. The concentrations of cortisol and TNF-α in serum were measured. Immunohistochemistry method was used to measure the expression of ICAM-1 protein in gastric mucosa and analyze optical density (OD) average of ICAM-1. Results After 21 days stress,compared with control group, cortisol [ (77.12±9.76)μg/ml,(44.96±6.25)μg/ml, t=7.85, P<0.01] ,TNF-α[ (69.66±6.68)pg/ml, (39.21±3.57) pg/ml, t=11.37, P < 0.001 ] concentration and OD of ICAM-1 (53.87±6.84,30.26±3.68, t = 8.59, P < 0.01 ) increased significantly in stress group. Compared with stress group, cortisol [ ( 58.82±6.56)μg/ml, t = 4.40, P < 0. 01 ],TNF-α[ (50.18±3.23)pg/ml, t=7.43, P<0.01 ]concentration and OD of ICAM-1 (36.61±4.39, t=6.00, P< 0.01 ) decreased in fluoxetine group. Conclusion Chronic stress result in serum cortisol,TNF-α increase and overexpression of ICAM-1 in gastric mucosa. Those changes can be reversed by fluoxetine to some extent.
