Purpose. Red blood cell distribution width (RDW) is increased in a variety of inflammatory-related diseases. However, there is no report of its clinical significance in poststroke depression (PSD). This study explores the clinical significance of RDW in PSD patients. Methods. A total of 185 patients with first-ever acute ischaemic stroke (AIS) in the Second Hospital of Anhui Medical University were chosen as subjects. A retrospective observational study was conducted from February 2019 to February 2020. PSD patients were diagnosed at 6 months after stroke based on the Diagnostic and Statistical Manual of Mental Disorders-IV criteria. Clinical and laboratory data were obtained from all patients. Coefficient of Variation (RDW-CV) and standard deviation (RDW-SD) were used to statistically report the performance of red blood cell distribution width. Results. At the 6-month follow-up, 46 patients were diagnosed with PSD. Compared with non-PSD patients, PSD patients exhibited an increase in RDW-CV and RDW-SD, which positively correlated with serum interleukin 6 (IL-6) concentrations. In PSD patients, only RDW-SD demonstrated a consistent positive association with the Hamilton Rating Scale for Depression (HAM-D) scores at 6 months after admission. RDW-CV, RDW-SD, and IL-6 were recognized as independent predictors of PSD. The area under the receiver operating characteristic (ROC) curve (AUC) of RDW-SD was 0.796 (95% CI: 0.731-0.852) for the prediction of PSD, which was superior to that of RDW-CV. The specificity for predicting PSD was 60.43%, and the sensitivity was 91.30% if RDW-SD was higher than 43.80 fL. Conclusions. RDW-SD is a simple, inexpensive, rapid, and easily accessible parameter that can be used to predict PSD in patients with stroke.

Introduction Previous studies have shown that gestational inflammation can accelerate age‐associated cognitive decline (AACD) in maternal mice; enriched environments (EEs) have been reported to protect normally aging mice from AACD and improve mitochondrial function. However, it is unclear whether the nitrosative stress‐related proteins tet methylcytosine dioxygenase 1 (TET1) and S‐nitrosoglutathione reductase (GSNOR) are involved in the accelerated aging process of gestational inflammation and whether EEs can slow this process. Methods In this study, CD‐1 female mice on the 15th day of pregnancy were injected with bacterial lipopolysaccharide (50 μg/kg; LPS group) or an equivalent amount of normal saline (CON group) from the abdominal cavity for 4 consecutive days. Twenty‐one days after delivery, half of the LPS‐treated mice were randomly selected for EE until the end of the behavioral experiment (LPS‐E group). When the female rats were raised to 6 months and 18 months of age, the Morris water maze (MWM) was used to detect spatial learning and memory ability; RT‐PCR and Western blots were used to measure the mRNA and protein levels of hippocampal TET1 and GSNOR. Results As for the control group, compared with 6‐month‐old mice, the spatial learning and memory ability of 18‐month‐old mice decreased, and the hippocampal TET1 and GSNOR mRNA and protein levels were decreased. Gestational inflammation exacerbated these age‐related changes, but an EE alleviated the effects. Pearson's correlation analysis indicated that performance during the learning and memory periods in the MWM correlated with the levels of hippocampal TET1 and GSNOR. Conclusions Our findings suggest that gestational inflammation accelerates age‐related learning and memory impairments and that postpartum EE exposure could alleviate these changes. These effects may be related to hippocampal TET1 and GSNOR expression.