Hyperbaric Oxygen Treatment Decreases Cd36 Gene Expression Through HIF-1α/PPAR-γ and Reverses Non-Alcoholic Fatty Liver Disease in Rats.

INTRODUCTION

Non-alcoholic fatty liver disease (NAFLD) is characterized by the accumulation of liver fat (steatosis), which can progress to non-alcoholic steatohepatitis (NASH), cirrhosis, and cancer. NASH is estimated to affect up to 32% of the world's population. Different treatments, such as hyperbaric oxygen (HBO₂), are being investigated, but the molecular mechanisms associated with this treatment are unknown. The effect of HBO₂ on NAFLD associated with Cd36 expression was evaluated.

METHODS

Rats were divided into the following groups: rats that developed steatosis and consumed sucrose but did not receive HBO₂, rats with steatosis that consumed sucrose and received HBO₂, rats that developed steatosis and received HBO₂ but did not receive sucrose, and a control group. The HBO₂ groups underwent the procedure for 20 days (2.4 ATA pressure 60 min). An IYOCA hyperbaric chamber model for rats was used. The expression of HIF-1α, PPAR-γ, and Cd36 mRNA from hepatic tissue was measured with the StepOn™ real-time polymerase chain reaction (PCR) system.

RESULTS

The expression levels of hepatic HIF-1α, PPAR-γ, and Cd36 genes increased in NAFLD rats that consumed sucrose but did not receive HBO₂ compared to the control group (p <0.05). The rats that received HBO₂ with and without sucrose ingestion showed decreased expression levels of these genes compared to those with NAFLD that consumed sucrose.

DISCUSSION: HBO₂ decreased expression levels of HIF-1α and PPRA-γ, which independently or coordinately regulate Cd36 expression. Cd36 expression was significantly decreased in association with the reversal of NAFLD in rats.