Abstract
<title>Abstract</title> <p>Objectives Infantile acute encephalopathy (AE) is characterized by impaired consciousness, fever, status epilepticus (SE), and a high frequency of cognitive dysfunction and mortality, without established treatment. We generated an infant AE mouse model and treated it with human umbilical cord-derived mesenchymal stromal cells (UC-MSCs). Methods The infant AE model mice demonstrated SE by peritoneal injection of poly(I:C) and kainic acid (KA) on day 15 after birth (SE group), followed by the injection of UC-MSCs intravenously (SE + MSCs group). Results Mice in the SE group showed hyperactivity-like abnormal behavior, which was attenuated by UC-MSCs injection. FjC-positive neurogenic degeneration in the hippocampal CA1 and LSN regions was increased in the SE group and attenuated in the SE + MSC group. Iba1 + microglia increased in both the SE and SE + MSC groups compared to those in the control group. RT-PCR analysis revealed that the inflammatory cytokines of the hippocampus, including IL-6, TNF-α, and iNOS, were elevated in the SE group, while these were significantly suppressed in the SE + MSCs group. In vitro analysis showed that the poly (I:C) induced the fetal brain-derived microglia to express ameboid change with increased inflammatory cytokines such as iNOS, IL-1β, TNF-α, and IL-6, while the co-cultured with UC-MSCs subsided them with increased Arg-1. Conclusions These results might suggest that UC-MSCs may exert neuroprotective effects against infant AE by suppressing inflammation and improving the microenvironment at the site of neurological damage.</p>