miR‑155 mediates inflammatory injury of hippocampal neuronal cells via the activation of microglia.

MicroRNA (miR)‑155 has a crucial role in various cellular functions, including differentiation of hematopoietic cells, immunization, inflammation and cardiovascular diseases. The present study aimed to investigate the roles and mechanisms of miR‑155 in treatment‑resistant depression (TRD). A Cell Counting Kit‑8 assay and flow cytometry were performed to assess the cell viability and apoptosis of microglial cells, respectively. Western blotting and reverse transcription‑quantitative polymerase chain reaction assays were used to evaluate the associated protein and mRNA expression, respectively. The results revealed that miR‑155 reduced the cell viability of BV‑2 microglial cells, and miR‑155 enhanced the expression levels of pro‑inflammatory cytokines in BV‑2 microglial cells. Furthermore, conditioned medium from miR‑155‑treated microglia decreased the cell viability of HT22 hippocampal cells. miR‑155‑treated microglia increased the apoptosis of neuronal hippocampal cells by modulating the expression levels of apoptosis regulator Bax, apoptosis regulator Bcl‑2, pro‑caspase‑3 and cleaved‑caspase‑3. The cell cycle distribution was disrupted by miR‑155‑treated microglia through induction of S phase arrest. Furthermore, the overexpression of suppressor of cytokine signaling 1 reversed the pro‑apoptotic effect of activated microglia on hippocampal neuronal cells. In conclusion, the present results suggested that miR‑155 mediated the inflammatory injury in hippocampal neuronal cells by activating the microglial cells. The potential effects of miR‑155 on the activation of microglial cells suggest that miR‑155 may be an effective target for TRD therapies.