Baicalein inhibits neuroapoptosis via pathways in sevoflurane induced rats

Background: Baicalein, a bioactive flavonoid was explored for its capability to attenuate sevoflurane induced neuronal apoptosis and to improve behavioural and cognitive impairments. Sevoflurane is a frequently used inhalation anesthetic in neonates and children. Neonatal sevoflurane exposure causes widespread neurodegeneration and cognitive impairments. Development of compounds that could effectively prevent/reduce the adverse effects is of tremendous medical value. Methods: Isolated groups of neonatal rats were regulated with baicalein (25, 50 or 100 mg/kg b.wt) from postnatal day 3 (P3) to P21 and were exposed to sevoflurane (3%; 6 h) on P7. Results: Baicalein inhibited sevoflurane induced neuroapoptosis significantly as assessed by TUNEL assay. The raised levels of cleaved caspase-3, Bad and Bax were down-regulated by baicalein with enhanced Bcl-2, Bcl-xL, xIAP, c-IAP-1, c-IAP-2 and survivin expression. Baicalein regulated JNK/ERK signalling and also activated the PI3K/Akt pathway effectively as evident from the increased Akt, phospho-Akt, GSK-3β, phospho-GSK-3β levels. Baicalein, also improved the behaviour of animals in open filed and olfactory tests. The freezing responses and the performance in Morris Water Maze tests were enhanced. Conclusion: Baicalein reduced neurodegeneration and improved learning and memory retention of rats and as well modulated PI3/Akt/GSK-3β and JNK/ERK signalling pathways.