ISSN 0439-755X
CN 11-1911/B

›› 2007, Vol. 39 ›› Issue (06): 1034-1040.

### Effects of Chronic Stress on Behavior and Heat Shock Protein 70

Wang Weiwen,Shao Feng,Liu Mei,Sun Meng,Lin Wenjuan

1. Key Lab of Mental Health, Chinese Academy of Sciences, Beijing 100101, China
• Received:2007-01-10 Revised:1900-01-01 Published:2007-11-30 Online:2007-11-30
• Contact: Lin Wenjuan

Abstract: Chronic stress can suppress organisms’ resistance to adverse stimuli in the environment. The stress responses occur at both the system and single-cell levels. Although many studies have investigated the neuroendocrine mechanisms underlying the effects of stress on health, the characteristics of cellular stress response are still poorly understood. One manner in which cells resist damage and/or death induced by stress is to synthesize a highly conserved set of intracellular proteins, termed heat shock protein (HSP). In particular, the 70-kDa HSP (HSP70) is essential for cellular recovery after stress as well as survival and maintenance of normal cellular function. It has been demonstrated that the expression of high levels of HSP70 is associated with an increased resistance of cells to challenges that would otherwise lead to cell injury and/or death. Therefore, the intensity of an HSP70 response to stress is an important biomarker of how the cell tolerates stress damage.
This study aimed to determine whether prior chronic stress inhibited the synthesis of HSP70 in immune cells in the peripheral blood and spleen of rats exposed to an acute hot water bath. Twenty-eight rats were randomly divided into 2 groups with 14 rats in each group: the control group (C) and the chronic stress group (CS). CS rats were exposed to chronic unpredictable stress for 4 weeks to induce depressive-like behavior. The controls were stress-free. Thereafter, 8 rats in each group were exposed to acute heat stress (C-heat shock and CS-heat shock) to induce whole-body hyperthermia (maintaining the core temperature at 41°C for 25 minutes).The other rats remained undisturbed in their home cages (C-no heat shock and CS-no heat shock). All rats were decapitated 6 hours after the completion of the treatments. The blood and spleen were collected and the level of HSP70 expression in the leukocytes was measured using flow cytometry.
It was found that CS rats showed a decreased cellular HSP70 expression following the heat treatment, while a significant increase in the synthesis of HSP70 was observed in all types of immune cells from C rats. However, in CS rats, such HSP70 changes were only detected in the monocytes and granulocytes. Further, the increasing degree of heat-induced cellular HSP70 expression in CS rats was less pronounced than that observed in C rats.
These results demonstrated that chronic stress decreased heat-induced HSP70 response in immune cells. Further, they suggested that the deficit of HSP70 might be involved in the suppressive modulation of the immune function induced by chronic stress.

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