Purpose: This quasi-experimental single group study aimed to confirm the effects of discharge education using a systematic discharge education program on anxiety and parenting confidence in mothers of premature babies. Methods: This study conducted discharge education for 3 to 5 days prior to the discharge of 29 mothers of premature babies born in the neonatal intensive care unit. Data were collected between April 1, 2021, to June 30, 2021, and were examined. The hypotheses were analyzed using the Wilcoxon signed-rank test. Results: Discharge education using a systematic discharge education program was effective in increasing the parenting confidence of mothers with premature babies (z=-3.839, p<0.001). However, it was not effective in reducing anxiety (z=-1.712, p=0.087). Conclusion The effects of the systematic discharge education program development and discharge education systematized discharge nursing education, reduced mothers’ anxiety in raising premature babies at home after discharge, and contributed to improving parenting confidence.

Sirtuin 3 (SIRT3), a well-known mitochondrial deacetylase, is involved in mitochondrial function and metabolism under various stress conditions. In this study, we found that the expression of SIRT3 was markedly increased by oxidative stress in dopaminergic neuronal cells. In addition, SIRT3 overexpression enhanced mitochondrial activity in differentiated SH-SY5Y cells. We also showed that SIRT3 overexpression attenuated rotenoneor H2 O2 -induced toxicity in differentiated SH-SY5Y cells (human dopaminergic cell line). We further found that knockdown of SIRT3 enhanced rotenone- or H2 O2 -induced toxicity in differentiated SH-SY5Y cells. Moreover, overexpression of SIRT3 mitigated cell death caused by LPS/IFN-γ stimulation in astrocytes. We also found that the rotenone treatment increases the level of SIRT3 in Drosophila brain. We observed that downregulation of sirt2 (Drosophila homologue of SIRT3) significantly accelerated the rotenone-induced toxicity in flies. Taken together, these findings suggest that the overexpression of SIRT3 mitigates oxidative stress-induced cell death and mitochondrial dysfunction in dopaminergic neurons and astrocytes.