Koh Kyung Bong, Lee Youngjoon, Beyn Keyng Min, Chu Sang Hee, Kim Duck Man
Department of Psychiatry, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul 120-752, Republic of Korea.
Brain Behav Immun. 2008 Nov;22(8):1130-7. doi: 10.1016/j.bbi.2008.06.009. Epub 2008 Jun 27.
The counter-stress effects of relaxation on proinflammatory and anti-inflammatory cytokines were examined. From 36 medical students, 18 were randomly assigned to the relaxation group, and 18 were randomly assigned to the non-relaxation group. Relaxation lasted for four weeks. The levels of stimulated production of IL-6, TNF-alpha, and IL-10, and blood pressure were measured during the non-examination period (baseline period) and the pre-examination period (stress period). The levels of perceived stress were assessed by the Global Assessment of Recent Stress (GARS) scale, the Stress Response Inventory (SRI) and the Symptom Checklist-90-Revised (SCL-90-R) anxiety subscale. Repeat measure ANOVA revealed that the SRI total score, scores of the SCL-90-R anxiety subscale and diastolic blood pressure were significantly higher during the stress period than during the baseline period regardless of groups. The level of IL-6 production was significantly lower but the level of IL-10 production was significantly higher during the stress period than during the baseline period. Significant reduction in the delta (stress period value minus baseline period value) in the total GARS score, systolic and diastolic blood pressure, the levels of IL-6 and TNF-alpha production but significant enhancement in the delta in the level of the IL-10 production were found in the relaxation group compared with the non-relaxation group. These results suggest that relaxation is associated with reduction in stress-induced psychological or physiological responses and proinflammatory cytokine alterations but with enhancement in stress-induced anti-inflammatory cytokine alteration. Therefore, relaxation is more likely to have counter-stress effect on proinflammatory cytokines than on anti-inflammatory cytokine.
研究了放松对促炎和抗炎细胞因子的抗压作用。从36名医科学生中，随机将18人分配到放松组，18人分配到非放松组。放松持续四周。在非检查期（基线期）和检查前期（应激期）测量了IL-6、TNF-α和IL-10的刺激产生水平以及血压。通过近期应激综合评估（GARS）量表、应激反应量表（SRI）和症状自评量表90修订版（SCL-90-R）焦虑分量表评估感知应激水平。重复测量方差分析显示，无论组别如何，应激期的SRI总分、SCL-90-R焦虑分量表得分和舒张压均显著高于基线期。应激期IL-6的产生水平显著低于基线期，但IL-10的产生水平显著高于基线期。与非放松组相比，放松组的GARS总分、收缩压和舒张压、IL-6和TNF-α产生水平的差值（应激期值减去基线期值）显著降低，但IL-10产生水平的差值显著升高。这些结果表明，放松与应激诱导的心理或生理反应及促炎细胞因子改变的减少有关，但与应激诱导的抗炎细胞因子改变的增强有关。因此，放松对促炎细胞因子的抗压作用可能比对抗炎细胞因子的作用更强。
