- Atorvastatin protects BV‑2 mouse microglia and hippocampal neurons against oxygen‑glucose deprivation‑induced neuronal inflammatory injury by suppressing the TLR4/TRAF6/NF‑κB pathway.
Atorvastatin protects BV‑2 mouse microglia and hippocampal neurons against oxygen‑glucose deprivation‑induced neuronal inflammatory injury by suppressing the TLR4/TRAF6/NF‑κB pathway.
Atorvastatin is a member of the statin class of drugs, which competitively inhibit the activity of 5‑hydroxy‑3‑methylglutaryl‑coenzyme A reductase. The aim of the present study was to assess whether atorvastatin may protect BV‑2 microglia and hippocampal neurons against oxygen‑glucose deprivation (OGD)‑induced neuronal inflammatory injury and to determine the underlying mechanisms by which its effects are produced. Cell viability and apoptotic ability were assessed using an MTT assay and annexin V‑fluorescein isothiocyanate/propidium iodide double staining followed by flow cytometry, respectively. The expression of inflammation and apoptosis‑associated mRNAs and proteins were assessed using reverse transcription‑quantitative polymerase chain reaction and western blotting, and the expression of inflammatory factors was determined using ELISA. The results of the current study revealed that atorvastatin treatment suppressed the viability of OGD BV‑2 microglia and hippocampal neurons. Furthermore, atorvastatin treatment reduced the expression of proinflammatory factors in OGD BV‑2 microglia. Additionally, it was demonstrated to downregulate the toll‑like receptor 4 (TLR4)/tumor necrosis factor receptor‑associated factor 6 (TRAF6)/nuclear factor‑κB (NF‑κB) pathway in OGD BV‑2 microglia. Atorvastatin also inhibited the apoptosis of OGD hippocampal neurons by regulating the expression of apoptosis‑associated proteins. It was concluded that atorvastatin treatment may protect BV‑2 microglia and hippocampal neurons from OGD‑induced neuronal inflammatory injury by suppressing the TLR4/TRAF6/NF‑κB pathway. This may provide a potential strategy for the treatment of neuronal injury.