Abstract: Objective To investigate the role of hepatocye apoptosis and mitochondrial permeability transition pore (MPTP)
opening in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Methods Thirty male SD rats were randomized into
normal diet group and high-fat diet group. At 4, 8 and 12 week of feeding. The hepatocyte apoptosis index (AI) was measured
using flow cytometry, and MPTP opening was evaluated with ultraviolet spectrophotometry. Immunohistochemistry was
employed to detect hepatic expressions of Bcl-2 and Bax, and Western blotting was used to detect Bax protein expression
changes. Results High-fat feeding resulted in significantly increased hepatocyte AI at 4-12 weeks and gradually increased
MPTP opening. In the high-fat diet group, hepatic Bcl-2 expression was detected but the positive cell number remained stable,
whereas Bax-positive cell number increased steadily with time with progressively increased intensity of Bax protein
expression, resulting in gradually decreased Bcl-2/Bax ratio. Conclusion Hepatocyte apoptosis occurs in the rat model of
NAFLD in close correlation with mitochondrial damage. Increased MPTP opening as the result of increased Bax expression
and aberrant Bcl-2/Bax ratio is an important mechanism of hepatocye mitochondrial damage in NAFLD.