Non-suicidal self-injury (NSSI) refers to the deliberate, direct, and socially unacceptable destruction of one’s own body tissue without conscious suicidal intent , has consistently been reported to be associated with a variety of emotional or borderline personality disorders and increased risks for suicide [2, 3]. The onset and prevalence of NSSI are especially common in adolescence. A recent meta-analysis showed a NSSI lifetime prevalence of 17.2%, 13.4% and 5.5% in adolescents, young adults, and adults respectively . The high rate of NSSI behavior in Chinese adolescent is even up to 22.4%-29% [5, 6]. Clearly, adolescent NSSI is a serious public health concern worldwide , and it is important to identify the potential mechanisms and etiology of NSSI during this period.
Harsh parenting refers to a wide range of aversive parenting behaviors, includes physical (e.g., spanking, slapping, or hitting) and verbal punishment (e.g., yelling and cursing) at children who have done something wrong [8, 9]. According to Linehan , exposure to harsh parenting may influence the likelihood of engaging in NSSI behaviors. Victor et al.  also emphasized harsh parenting such as shouting, swearing, spanking, predicted increased odds of subsequent adolescent NSSI onset in a longitudinal design. Although previous research has investigated the linkage between harsh parenting and NSSI in Western countries [12, 13], research into this issue is still rare in China. As a Chinese proverb, “Beating and scolding is the emblem of love”, in the traditional Chinese culture context, harsh parenting behaviors were generally considered as an indication of parental involvement, concern, and love, therefore, harsh punishment is still adopted by approximately 50% parents in China [14–16]. Considering the cultural differences, it is necessary to further investigate the relationship between harsh parenting and NSSI in China.
Depressive symptoms have been frequently identified as a mediator of interpersonal risk factors and NSSI. On the one hand, NSSI is often considered to be an emotion-regulation strategy to decrease youth’s emotional distress by distracting from intense emotion through the sight of blood, the sensation of pain, or a focus on the injury itself [1, 17]. Experiential avoidance model (EAM) proposed that NSSI is maintained by negative reinforcement in the form of escape from unwanted emotional experiences . Consistent with the model, individuals who experience higher levels of anhedonia and depression, are more likely to report a history of NSSI [19, 20]. On the other hand, ample empirical studies have revealed the mediating role of depression between interpersonal stressors and NSSI among adolescents. Recent findings from a longitudinal study showed that depressive symptoms play a mediating role in the association between peer bullying and NSSI . Meanwhile, Madjar et al.  also found that sense of loneliness in school could increase the risk of NSSI by increases in severity of depressive symptoms. Although previous studies have indicated correlations of harsh parenting and depressive symptoms with NSSI [20, 23, 24], no research has explicitly addressed the mechanisms underlying harsh parenting, depression, and NSSI, especially lack of evidence from longitudinal studies. To bridge the research gaps, we conducted a three-waves longitudinal study to evaluate the longitudinal associations among harsh parenting, depressive symptoms, and NSSI in a community sample of Chinese adolescents.
Not all individuals who experience harsh parenting and depression engage in NSSI, Maciejewski et al.  indicted that NSSI was influenced by both environment and genetic. Brodsky  proposed a diathesis-stress models for suicide and NSSI by combined the findings from the fields of biology, neurology, and genetics, which provides a specific framework to understand how gene–environment (G × E) interactions correlated with suicidal or NSSI behaviors directly. However, through this framework previous studies mostly considering the genetic factor of suicide, only a few studies have identified the genetic factors related to NSSI such as serotonin transporter gene (5-HTTLPR) and brain-derived neurotrophic factor (BDNF Val66Met) gene [27, 28]. Catechol-O-methyltransferase (COMT) located on chromosome 22q11.1-q11.2 , and plays an important role in regulating an individual’s processing of emotion and cognition by inactivating catecholamine neurotransmitters. The activity of the COMT enzyme is influenced mainly by a functional single nucleotide polymorphism (rs4680; G to A) in the COMT coding region causes Val158Met aminoacid substitution in the corresponding protein, with Val allele exhibiting a 3- to 4-fold increase in enzyme activity compared to Met allele [30, 31]. Considering COMT Val158Met gene is associated with several traits related to NSSI behaviors, including emotion regulation [32, 33] and borderline personality disorders [34, 35] and suicidal behaviors [36, 37]. Thus, we speculate that the COMT Val158Met gene might moderate the relationship between harsh parenting and NSSI directly.
According to Brodsky , diathesis-stress model for suicide and NSSI also highlighted the complex interaction between environment and genetics factors could impact the expression of neurological and phenotypes (e.g., emotional dysregulation) that predispose to suicide and NSSI, thereby increasing the diathesis for the propensity to react to stressors for NSSI. That means, Phenotypes bridge the gap between the distal risk genes and the elusive disease process . Namely, phenotypes would play a meditator role in the relationship between G × E interactions and behavior outcomes. As we mentioned before, depression symptoms as a mediator may be useful for elucidating the role of biological mechanisms in the risk for NSSI. There are numerous genetic association studies implicating the COMT Val158Met polymorphism in the incidence of major depression disorder [38–40]. In the context of G × E, COMT Val158Met has been found to interact with environmental variations to predict outcomes related to depression symptoms. For example, a longitudinal study has shown that the Val-allele children were more likely to develop depression after exposure to high-risk nurturing environment . Cao et al.  also found that adolescents with Val/Val genotype were more sensitive to depression under negative peer relationships. Based on the theoretical and empirical evidence, it is plausible to assume that the interaction between COMT Val158Met polymorphism and harsh parenting would lead to NSSI through depressive symptoms.
To examined the potential mechanisms of NSSI, the current study constructs a moderated mediation model (see Fig. 1). Specifically, we proposed the following hypotheses:(1) harsh parenting would be positively associated with NSSI among adolescent; (2) depressive symptoms would mediate the relation between harsh parenting and NSSI; (3) COMT rs4680 would moderates the link between harsh parenting and NSSI, and the link between harsh parenting and depressive symptoms in the mediation model of the relationship between harsh parenting and NSSI.