Baicalin is one of the major compounds in the traditional Chinese medicinal herb 
from Scutellaria baicalensis Georgi. We investigated the molecular mechanisms of 
cell autophagy induced by baicalin in human bladder cancer T24 cells. Baicalin 
inhibited cell survival as shown by MTT assay and increased cell death by trypan 
blue exclusion assay in a concentration-dependent manner. Baicalin did not 
induce apoptotic cell death in T24 cells by TUNEL and caspase-3 activity assay. 
Baicalin induced the acidic vesicular organelle cell autophagy marker, 
manifested by acridine orange (AO) and monodansylcadaverine (MDC) staining and 
cleavage of microtubule-associated protein 1 light chain 3 (LC3). The protein 
expression levels of the Atg 5, Atg 7, Atg 12, Beclin-1 and LC3-II were 
upregulated in T24 cells after baicalin treatment. Inhibition of autophagy by 
3-methyl-adenine (an inhibitor of class III phosphatidylinositol-3 kinase; 3-MA) 
reduced the cleavage of LC3 in T24 cells after baicalin treatment. Furthermore, 
protein expression levels of phospho-AKT (Ser473) and enzyme activity of AKT 
were downregulated in T24 cells after baicalin treatment. In conclusion, 
baicalin triggered cell autophagy through the AKT signaling pathway in T24 
cells.