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

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

Description

ABSTRACT

Reyes Bocanegra MdJ, Quintana Castro R, Páez Martínez L, Agame Lagunes B, Grube Pagola

P, Hernández Leyva S, Ramírez Nava JC, Alexander Aguilera A. Hyperbaric Oxygen Treatment

Decreases Cd36 Gene Expression Through HIF-1α/PPAR-γ and Reverses Non-Alcoholic Fatty Liver

Disease in Rats. Undersea Hyperb Med. 2026 Second Quarter; 53(2):215-226.

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 StepOne™ 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.

Keywords: Cd36 gene expression; HBO2 and Cd 36 expression; HBO2 regulates NAFLD; hyperbaric oxygen

(HBO2) treatment; non-alcoholic fatty liver disease

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