Involvement of Caspase-Dependent and Independent Pathway in Apoptotic Action of Extrinsic β-Hydroxybutyrate in Liver Tissue of Mice

β-hydroxybutyric acid (β-HB) is generated by degradation of fatty acids in the liver. β-HB level in serum increases significantly in a variety of metabolic disorder diseases, such as hyperketonemia and diabetic ketoacidosis, in which hepatocyte apoptosis have an important role. To investigate the effect of exogenous β-HB on the liver, mice were injected intraperitoneally with β-HB (7.5 mmol/kg) one time, three times and five times at 24 h intervals, respectively. Compared to the distilled water injection group, β-HB level in liver tissue increased significantly, while the triglycerides, high density lipoprotein cholesferol (HDL), low density lipoprotein cholestorol (LDL), alkaline phosphatase (ALP) in serum have not changed in the three β-HB injection groups. β-HB promoted the activation of caspase-12, caspase- 9, caspase-3 and EndoG, up-regulated Bax and down-regulated of Bcl-2.