Expression of p53, Bax and Bcl-2 proteins in hepatocytes in non-alcoholic fatty liver disease.
OBJECTIVE
To analyze the protein expression essential for apoptosis in liver steatosis.


METHODS
The expression of proapoptotic proteins p53, Bax, and antiapoptotic Bcl-2 in hepatocytes with steatosis (SH) and without steatosis (NSH) was evaluated in 84 patients at various stages of non-alcoholic fatty liver disease (NAFLD).


RESULTS
Immunohistochemical staining of liver tissue showed the activation of p53 protein in SH and NSH with increased liver steatosis, diminished Bcl-2 and slightly decreased Bax protein. Positive correlation was found between the stage of liver steatosis with p53 expression in SH (r = 0.54, P < 0.01) and NSH (r = 0.49, P < 0.01). The antiapoptotic protein Bcl-2 was diminished together with the advancement of liver steatosis, especially in non-steatosed hepatocytes (r = 0.43, P < 001).


CONCLUSIONS
Apoptosis is one of the most important mechanisms leading to hepatocyte elimination in NAFLD. The intensification of inflammation in NAFLD induces proapoptotic protein p53 with the inhibition of antiapoptotic Bcl-2.
Panasiuk
Anatol
A
Department of Infectious Diseases, Medical University of Bialystok, Zurawia Str. 14, Bialystok 15-540, Poland. anatol@panasiuk.pl
Dzieciol
Janusz
J
Panasiuk
Bozena
B
Prokopowicz
Danuta
D
D000328:Adult; D017209:Apoptosis / Q000502:physiology; D005234:Fatty Liver / Q000378:metabolism*; D005260:Female; D015870:Gene Expression; D022781:Hepatocytes / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D051028:bcl-2-Associated X Protein / Q000378:metabolism*
D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein