Lycium�barbarum polysaccharides attenuates the apoptosis of hippocampal neurons induced by sevoflurane

Abstract

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 Lycium barbarum 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.

Compound Porcine Cerebroside and Ganglioside Injection (CPCGI) Attenuates Sevoflurane-Induced Nerve Cell Injury by Regulating the Phosphorylation of p38 MAP Kinase (p38MAPK)/Nuclear Factor kappa B (NF-κB) Pathway

“…However, 3% sevoflurane is quite high and this level is rarely used in clinical practice, which is a limitation of the present study. MTT and FCM analysis were carried out to measure the effects of 3% sevoflurane on neuronal cell growth and apoptosis at 0, 2, 4, and 6 h. Consistent with a previous study [20], we found that 3% sevoflurane inhibited neuronal cell viability and promoted cell apoptosis in a time-dependent manner, so we chose to treat neuronal cells with 3% sevoflurane for 6 h in subsequent experiments. Abnormal apoptosis can also suppress cell growth, and sevoflurane neurotoxicity is associated with increased apoptosis, such as abnormal regulation of Bcl-2 family members and caspases [25,26].…”

“…In this study, we separated hippocampal neurons from Sprague-Dawley embryonic rats, and used 3% sevoflurane to induce a neuronal cell injury model [20]. We used 3% sevoflurane to stimulate the nerve injury, as previously described [20]. However, 3% sevoflurane is quite high and this level is rarely used in clinical practice, which is a limitation of the present study.…”

“…We used 3% sevoflurane to induce the nerve damage model [20]. Cells were first cultured in phosphate-buffered saline (PBS) or CPCGI for 6 h, then the cells were stimulated with 3% sevoflurane (Sigma-Aldrich, USA) for 6 h and assigned into 1 of 4 groups: control, sevoflurane, sevoflurane+PBS (vehicle), and sevoflurane+CPCGI.…”

Role of NR2B/ERK signaling in the neuroprotective effect of dexmedetomidine against sevoflurane induced neurological dysfunction in the developing rat brain

“…Sevo urane is an inhalational anesthetics, which is commonly used in cesarean delivery and pediatric clinical application [2]. Previous evidence has suggested that sevo urane exposure has certain harm on learning and cognitive functions, especially for children [5,11].…”

“…Sevo urane is one of the most comment used inhalational anesthetics, which is characterized by rapid induction and recovery properities [1]. It is widely used in cesarean delivery and pediatric clinical application [2]. Sevo urane has some neurotoxicity for the nervous system, especially for developing brain [3][4][5].…”