中华行为医学与脑科学杂志
中華行為醫學與腦科學雜誌
중화행위의학여뇌과학잡지
CHINESE JOURNAL OF BEHAVIORAL MEDICINE AND BRAIN SCIENCE
2011年
6期
488-490
,共3页
吴高义%陈磊%朱国雄%彭玲燕%李东临
吳高義%陳磊%硃國雄%彭玲燕%李東臨
오고의%진뢰%주국웅%팽령연%리동림
心理应激%颞下颌关节%白介素-1%肿瘤坏死因子
心理應激%顳下頜關節%白介素-1%腫瘤壞死因子
심리응격%섭하합관절%백개소-1%종류배사인자
Emotional stress%Temporomandibular joint%Interlukin-1%Tumor necrosis factor- α
目的 通过观察心理干预后心理应激状态下大鼠颞下颌关节的相关变化,探讨心理干预在颞下颌关节疾病防治过程中的作用.方法 应用交流箱心理应激动物模型对大鼠进行心理应激.分别在应激前后应用抗焦虑药物和去除应激源.用ELISA法和RT-PCR检测各组大鼠颞下颌关节髁突软骨细胞内白细胞介素-1(IL-1)和肿瘤坏死因子(TNF-α)的表达变化.结果 PCR结果显示:IL-1βmRNA在应激后第1周表达最强,第3周时减弱,第5周时达到正常水平;TNF-αmRNA在应激后第1周表达最强,第3周后逐渐达到正常水平.Elisa结果显示:抗焦虑药物组IL-1OD值(分别为0.107 ±0.024,0.101±0.005,0.088±0.010)、去除应激源恢复组IL-1OD值(分别为0.090±0.016,0.088±0.005,0.089 ±0.011)和肿瘤坏死因子的OD值(分别为0.095 ±0.006,0.077±0.007,0.069.±0.009;0.079±0.010,0.075±0.009.0.079 ±0.012)与对照组(分别为0.087±0.004,0.090±0.009,0.089±0.010;0.074±0.008.0.069±0.015.0.068±0.011)差异不显著(P>0.05);抗焦虑药物组、去除应激源恢复组IL-1和TNF-α的OD值与心理应激组(分别为0.282±0.045,0.226 ±0.021,0.092±0.002;0.164±0.009,0.123±0.013,0.091±0.006)有显著差异(P<0.05).结论 应用抗焦虑药物和去除应激源能有效降低心理应激对大鼠颞下颌关节的影响.
目的 通過觀察心理榦預後心理應激狀態下大鼠顳下頜關節的相關變化,探討心理榦預在顳下頜關節疾病防治過程中的作用.方法 應用交流箱心理應激動物模型對大鼠進行心理應激.分彆在應激前後應用抗焦慮藥物和去除應激源.用ELISA法和RT-PCR檢測各組大鼠顳下頜關節髁突軟骨細胞內白細胞介素-1(IL-1)和腫瘤壞死因子(TNF-α)的錶達變化.結果 PCR結果顯示:IL-1βmRNA在應激後第1週錶達最彊,第3週時減弱,第5週時達到正常水平;TNF-αmRNA在應激後第1週錶達最彊,第3週後逐漸達到正常水平.Elisa結果顯示:抗焦慮藥物組IL-1OD值(分彆為0.107 ±0.024,0.101±0.005,0.088±0.010)、去除應激源恢複組IL-1OD值(分彆為0.090±0.016,0.088±0.005,0.089 ±0.011)和腫瘤壞死因子的OD值(分彆為0.095 ±0.006,0.077±0.007,0.069.±0.009;0.079±0.010,0.075±0.009.0.079 ±0.012)與對照組(分彆為0.087±0.004,0.090±0.009,0.089±0.010;0.074±0.008.0.069±0.015.0.068±0.011)差異不顯著(P>0.05);抗焦慮藥物組、去除應激源恢複組IL-1和TNF-α的OD值與心理應激組(分彆為0.282±0.045,0.226 ±0.021,0.092±0.002;0.164±0.009,0.123±0.013,0.091±0.006)有顯著差異(P<0.05).結論 應用抗焦慮藥物和去除應激源能有效降低心理應激對大鼠顳下頜關節的影響.
목적 통과관찰심리간예후심리응격상태하대서섭하합관절적상관변화,탐토심리간예재섭하합관절질병방치과정중적작용.방법 응용교류상심리응격동물모형대대서진행심리응격.분별재응격전후응용항초필약물화거제응격원.용ELISA법화RT-PCR검측각조대서섭하합관절과돌연골세포내백세포개소-1(IL-1)화종류배사인자(TNF-α)적표체변화.결과 PCR결과현시:IL-1βmRNA재응격후제1주표체최강,제3주시감약,제5주시체도정상수평;TNF-αmRNA재응격후제1주표체최강,제3주후축점체도정상수평.Elisa결과현시:항초필약물조IL-1OD치(분별위0.107 ±0.024,0.101±0.005,0.088±0.010)、거제응격원회복조IL-1OD치(분별위0.090±0.016,0.088±0.005,0.089 ±0.011)화종류배사인자적OD치(분별위0.095 ±0.006,0.077±0.007,0.069.±0.009;0.079±0.010,0.075±0.009.0.079 ±0.012)여대조조(분별위0.087±0.004,0.090±0.009,0.089±0.010;0.074±0.008.0.069±0.015.0.068±0.011)차이불현저(P>0.05);항초필약물조、거제응격원회복조IL-1화TNF-α적OD치여심리응격조(분별위0.282±0.045,0.226 ±0.021,0.092±0.002;0.164±0.009,0.123±0.013,0.091±0.006)유현저차이(P<0.05).결론 응용항초필약물화거제응격원능유효강저심리응격대대서섭하합관절적영향.
Objective To investigate the role of psychological intervention in the prevention of the temporomandibular joint disease (TMD) , through the observation of the relative changes in the rat TMJ under psychological stress after psychological intervention. Methods The rat model of communication box was built to exert the psychological stress. The antianxiety agent was applied before stress, and the stressor was removed after stress. The expression of the proinflammatory cytokines IL-1 and TNF-α in the mandibular condylar chondrocytes in rat TMJ was detected by ELISA and RT-PCR. Results The RT-PCR results showed that the expression of IL-1 mR-NA increased into the peak in the 1st week, weakened in the 3rd week, and returned to normal in the 5th week, while the TNF-αmRNA peaked in the 1st week, returned to normal in the 3rd week. The ELISA results showed that there was no significant difference of the OD value of the serum IL-1 and TNF-α(0. 095 ±0. 006,0. 077 ± 0.007,0.069 ±0.009 ;0.079 ±0.010,0.075 ±0. 009,0.079 ± 0.012) in the antianxiety agent group (0. 107 ± 0.024,0. 101 ±0.005,0.088 ±0.010)and the stressor removal group(0. 090 ±0.016,0. 088 ±0.005,0.089 ± 0.011) , compared with the control group(0.087 ±0.004,0.090 ±0.009,0.089 ±0.010;0.074 ±0.008,0.069 ±0.015,0.068 ±0.011) (P>0.05), while significant differences were observed when compared with the psychological stress group(0.282 ±0.045,0.226 ±0.021,0.092 ±0.002;0. 164 ±0.009,0.123 ±0.013,0.091 ± 0.006) (P<0.05 ). Conclusion Application of the antianxiety agent and stressor removal could effectively counter the influence of psychological stress to TMJ, which provides good experience for the clinical prevention of TMD.
