Immunological Regulation of Hepatocyte Apoptosis During Toxic Damage

An experimental model of toxic hepatitis caused by intraperitoneal administration of carbon tetrachloride (CCl
4
) at a dose of 50mg/100g body weight was used to show that the use of the immunomodulator sodium aminophthalhydrazide (APH), whose corrective effect is based on the stimulation of macrophage activity, has an apoptotic protective effect on hepatocytes and helps to reduce the degree of liver damage, which is manifested in the decreasing the number of TUNEL-positive hepatocytes and lowering the index of alteration. Damage to the liver parenchyma during CCl
4
intoxication leads to a change in the expression of heat shock proteins in hepatocytes. Toxic liver damage by CCl
4
does not affect the quantitative content of HSP70, however, leads to a decrease in the number of hepatocytes with HSP60 granules on days 3 and 14 and prevents its release in into the extracellular space. On the early stage of toxic damage using APH allows you to maintain an increased number of hepatocytes with a heat shock protein content of mass of 60 kDa (HSP60), which is likely inhibits the activity of proteins responsible for apoptosis, and reduces the level of HSP70.