Baicalein inhibits neuroapoptosis via pathways in sevoflurane induced rats

Abstract

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. 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. Baicalein reduced neurodegeneration and improved learning and memory retention of rats and as well modulated PI3/Akt/GSK-3β and JNK/ERK signalling pathways.