Search

The impact of cystatin A expression in bile salt-induced apoptosis in a rat hepatoma cell line was analyzed. Results showed that expression of cystatin A in the cell line reduced cathepsin B activity and apoptosis and inhibition of cathepsin B by expression of cystatin A does not prevent activation of hydrolytic activity. These suggested that cathepsin B contributes to bile salt-induced apoptosis.

Research suggests that gastrointestinal epithelial cell death, known as apoptosis, impacts cellular function. Contrastingly, apoptosis inhibition causes hyperplasia and malignancy. A definition of apoptosis is given. Apoptosis in the gastrointestinal tract, liver and pancreas is assessed. Apoptosis inhibitors include biochemicals eicosanoids and human growth factor.

The role of protein kinase C (PKC) in the induction of apoptosis by toxic hydrophobic bile salt glycochenodeoxycholate (GCDC) was analyzed in isolated and primary cultures of rat hepatocytes. Analysis of apoptosis in primary cultures of rat hepatocytes after incubation with GCDC indicated the role of PKC activation in mediating the pro- and antiapoptotic cellular signaling cascades that regulated apoptosis. The activation of PKC was also mediated by the retention and accumulation of toxic bile salts within the hepatocytes during cholestasis.