تعامل بین استرس شغلی و پلی مورفیسم BDNF Val66Met موثر بر علائم افسردگی در کارکنان مراقبت های بهداشتی چینی Interaction between job stress and the BDNF Val66Met polymorphism affects depressive symptoms in Chinese healthcare workers

1. Introduction Job stress is usually defined as an adverse relationship of person and work environment in which work tasks exceed an individual’s knowledge, skills, or ability, inhibiting one’s behavior to cope and triggering a lot of psychological and physical issues (Lazarus and Folkman, 1984). Due to the nature of their jobs, the individuals working in healthcare professions are exposed to chronically high levels of stress, making them particularly susceptible to job stress-related mental health problems (McVicar, 2003; Chou et al., 2014). Many studies have shown that the long-term stressful work conditions lead to depressive symptoms (Ahola and Hakanen, 2007). Moreover, the researchers have used stress paradigms as the model of depression for a long time (Willner, 1997). Depression is a common mental disorder among healthcare workers with complex origins that is linked with considerable morbidity and mortality (Kiecolt-Glaser and Glaser, 2002; Cheung and Yip 2015; Wurm et al., 2016). For example, a study of 3474 nurses showed that 38% of nurses had depressive symptoms, and they reported tension in nurse–patient relationships and work load as the main reasons for those symptoms (Gong et al., 2014). A series of consequences may be caused by depression, including sleep problems, physical illness, and even impaired cognitive performance (Asarnow et al., 2013; Clarke et al., 2009; Rock et al., 2014). Further, depression not only endangers the health and well-being of occupational staff themselves, but also is associated with lower job performance and work productivity (Lerner and Henke, 2008). The projection for depression has become the second most common cause of disability by 2020 (Moussavi et al., 2007). Therefore, it is necessary to understand the relevant risk factors and susceptibility of depression. Although many risk factors for depression have been identified, the underlying mechanisms for depression are still unknown. Both environmental factors, such as stressful life events (SLEs), and genetic predisposition play an important role in the etiology of depression (Levinson, 2006), highlighting the importance of gene–environment interactions. Brain derived neurotrophic factor (BDNF), an important member of the neurotrophin family, is a protein with a broad range of activities in the central nervous system, such as the regulation of synaptic function, synaptic plasticity and the promotion of neuronal survival (Hyman et al., 1991;Kowianski et al., 2017), suggesting its implication for synaptogenesis and neurogenesis, especially for hippocampal neurogenesis (Kowianski et al., 2017). Many studies have shown that BDNF plays a central role in the neuropathology of depression by modulating the neuroplastic response (Brunoni et al., 2008; Jiang et al., 2013). The neurotrophin hypothesis of depression, one of leading hypotheses to explain the etiology and clinical course of this disorder, proposes that depression results from stress-induced reduction of BDNF expression levels while increases in BDNF levels could cause an antidepressant effect (Martinowich et al., 2007; Molendijk et al., 2014). Decreased brain levels of BDNF could contribute to cell loss and neuronal atrophy in the hippocampus and prefrontal cortex in depressed subjects (Duman and Monteggia, 2006). A meta-analyses study found reduced serum BDNF levels in major depression patients, indicating peripheral BDNF alteration in depression (Bocchio-Chiavetto et al., 2010).