polysaccharides attenuates the apoptosis of hippocampal neurons induced by sevoflurane.

Following the application of inhalational anesthetics, including sevoflurane, patients may suffer from neural injury. The present study was conducted to explore the mechanism involved in polysaccharides (LBP) treatment of sevoflurane injured hippocampal neurons. Primary hippocampal neurons were isolated from Sprague Dawley embryonic rats. The Cell Counting Kit-8 (CCK-8) assay was used to detect cell viability. Furthermore, flow cytometry (FCM) was used to determine cell proliferation and apoptosis rates. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were applied to detect the expression levels of apoptosis-related factors, including activated-Caspase-3, B-cell lymphoma/leukemia-2 (Bcl-2) and Bcl-2 associated X (Bax), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and total ERK1/2. The results showed that LBP promoted cell viability and cell proliferation but inhibited cell apoptosis in neurons injured with 3% sevoflurane, in dose-dependent manners (100, 200 and 400 µg/ml). LBP increased the expression levels of Bcl-2 and p-ERK1/2, and decreased levels of activated-Caspase-3 and Bax in a dose-dependent manner in hippocampal neurons that were injured with sevoflurane. In addition, ERK1/2 inhibitor reversed the above phenomenon in 400 µg/ml LBP and 3% sevoflurane-treated hippocampal neurons. Therefore, the present study indicated that LBP protected hippocampal neurons from sevoflurane injury, including aberrant cell apoptosis, via the ERK1/2 pathway.