BackgroundH protons magnetic resonance spectroscopy (1H-MRS) has been used to detect the biochemical metabolism changes and the mechanism of executive dysfunction in major depressive disorder (MDD). While, finding information associated with non-suicidal self-injury (NSSI) among adolescents with MDD is challenging. The present study aimed to examine the executive function and biochemical metabolism alterations, as well as to elucidate their associations in depressed adolescents with NSSI. MethodsA total of 86 adolescents with MDD (40 with NSSI, and 46 without NSSI) and 28 healthy controls were recruited in the current study. The executive function was assessed by Digital symbol test (DST), Wisconsin Card Sorting Test (WCST), Trail Making Test, part B (TMT-B), and Verbal fluency (VF). Bilateral metabolite levels of the prefrontal cortex (PFC), anterior cingulated cortex (ACC), lenticular nucleus (LN) of basal ganglia and thalamus were obtained by 1H-MRS at 3.0 T, and then the ratios of N-acetyl aspartate (NAA) and choline-containing compounds (Cho) to creatine (Cr) were determined, respectively. Finally, association analysis was conducted to investigate their relationships. ResultsThe depressed adolescents with NSSI showed significantly lower VF scores than those without NSSI and healthy controls. We also found significantly higher NAA/Cr ratios in the right thalamus, while significantly lower Cho/Cr ratios in the right thalamus of NSSI group than the MDD without NSSI group and healthy controls. And NSSI group also showed lower NAA/Cr ratio in the right LN than the MDD without NSSI group. For MDD with NSSI, the NAA/Cr ratios of the left thalamus were positively correlated with the time of TMTB and the Cho/Cr ratios of the left ACC were positively correlated with the VF scores. ConclusionsDepressed adolescents with NSSI may have executive dysfunction and NAA and Cho metabolism abnormalities in the thalamus. And the NAA/Cr ratios of the right LN could distinguish NSSI from depressed adolescents. Further, the executive dysfunction may be associated with the abnormal NAA metabolism in the left thalamus and ACC.