Moscatilin inhibits sevoflurane-induced inflammatory and oxidative stress injury in hippocampal neuronal HT22 cells

In order to analyze the effect and mechanism of Moscatilin on sevoflurane-induced HT22 hippocampal neuron cell (HT22) injury, sevoflurane was applied to HT22 cells to create an in vitro model of nerve damage, and Moscatilin was given to observe its effect on indicators of nerve injury. The effect of Moscatilin on sevoflurane-induced cell injury was measured based on cell viability (Cell Counting Kit-8), the expression of inflammatory factors interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in the cells was detected by Enzyme-Linked Immunosorbent Assay (ELISA) and Polymerase Chain Reaction (PCR). Reactive oxygen species (ROS) production in the neuronal cells was detected by oxidative stress measurements based on the 2′,7′-Dichlorofluorescein (DCF) assay. Using flow cytometry, the rate of apoptosis was determined, and the expression of apoptosis-related markers cleaved-caspase3 and cleaved-Poly Adp Ribose Polymerase (cleaved-PARP), and nuclear factor-k-gene binding (NF-κB)-related proteins were detected by western-blot analysis. The results showed that sevoflurane caused a significant decrease in HT22 cell viability, an increase in inflammatory factors TNF-α, IL-6 and IL-1β, ROS and apoptosis, an increase in apoptosis-related markers, cleaved-caspase3 and cleaved-PARP, as well as in the p-p65/p65 ratio of NF-κB-related proteins, and a decrease in the expression of inhibitor of NF-κBα (IκBα) protein. Moscatilin treatment counteracted sevoflurane-induced reduction in cell viability, decreased inflammatory factors and ROS production, inhibited sevoflurane-induced apoptosis, suppressed p-p65/p65 ratio, and increased IκBα protein expression. In conclusion, Moscatilin inhibits the NF-κB pathway and ameliorates sevoflurane-induced inflammatory responses, ROS production and apoptosis in HT22 hippocampal neuronal cells.

Sevoflurane; Moscatilin; NF-κB; ROS; Apoptosis

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