To study the effects of sevoflurane anesthesia on JAK/STAT signaling pathway and cerebral nerve injury in the rats with lung cancer.

Twenty-four healthy male SD rats were randomly divided into four groups (n=6 each): model group, sevoflurane group A, sevoflurane group B and sevoflurane group C. All the rats received tail vein injection of Walker-256 cancer cell suspension to establish lung cancer models. Then the rats in sevoflurane group A, B and C inhaled 3% sevoflurane+ 2 ml/min oxygen for 4 h, 6 h and 8 h, respectively. The model group inhaled air for 6 h. And 24 hours after anesthesia, the levels of serum tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β were measured, the learning and memory abilities of the rats were measured by Morris water maze, and the levels of caspase-3 and caspase-12 mRNA in the hippocampus were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The levels of JAK2, STAT3, p-JAK2 and p-STAT3 in the lung tissues of the rats were detected by Western blotting.

Compared with the model group, after continuous inhalation of sevoflurane, the levels of serum TNF-α, IL-6 and IL-1β were significantly higher (P<0.05), the number of rats crossing the platform within 90 s was significantly decreased (P<0.05), the levels of caspase-3 and caspase-12 mRNA in the hippocampus were significantly increased (P<0.05), the escape latency and the first crossing time were significantly prolonged (P<0.05), the levels of JAK2 and STAT3 in the lung tissues were significantly increased, and the phosphorylation of JAK2 and STAT3 were significantly increased in the sevoflurane-anesthesized rats (P<0.05).

Sevoflurane anesthesia can activate the JAK/STAT signaling pathway in the lung cancer rats, and may induce cerebral nerve injury and affect the learning and memory abilities of lung cancer rats through promoting the expression of apoptotic genes in the hippocampus.