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Updated: Jun 30, 2026
Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
Hyperbaric Oxygen Treatment Decreases Cd36 Gene Expression Through HIF-1α/PPAR-γ and Reverses Non-Alcoholic Fatty
Marcos J Reyes Bocanegra1, Rodolfo Quintana Castro2, Luis Páez Martínez2
1Escuela de Posgrados de Sanidad Naval, Hospital Naval de Especialidades de Veracruz, Secretaría de Marina, Gral. Figueroa No. 151. Col. Faros Centro. Veracruz, Ver., 91700. México.
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.
Insights
Hyperbaric oxygen therapy (HBO₂) reduced key gene expressions linked to non-alcoholic fatty liver disease (NAFLD) in rats. This treatment shows promise for reversing NAFLD by downregulating Cd36 expression.
Area of Science:
- Hepatology
- Molecular Biology
- Biomedical Engineering
Background:
- Non-alcoholic fatty liver disease (NAFLD) is a progressive condition characterized by liver fat accumulation, potentially leading to NASH, cirrhosis, and cancer.
- NASH affects a significant global population, necessitating research into effective treatments.
- The molecular mechanisms of hyperbaric oxygen (HBO₂) therapy for NAFLD remain largely unexplored.
Purpose of the Study:
- To investigate the effects of hyperbaric oxygen (HBO₂) on non-alcoholic fatty liver disease (NAFLD) in a rat model.
- To evaluate the impact of HBO₂ on the expression of specific genes, including Cd36, HIF-1α, and PPAR-γ, in the context of NAFLD.
Main Methods:
- A rat model of NAFLD was established using sucrose consumption.
- Experimental groups included NAFLD rats with and without HBO₂ treatment, and a control group.
- Hepatic gene expression of HIF-1α, PPAR-γ, and Cd36 was quantified using real-time PCR.
Main Results:
- NAFLD rats exhibited increased expression of HIF-1α, PPAR-γ, and Cd36 mRNA compared to controls.
- HBO₂ treatment led to decreased expression of these genes in NAFLD rats, irrespective of sucrose intake.
- A significant reduction in Cd36 expression was observed, correlating with NAFLD reversal.
Conclusions:
- HBO₂ therapy effectively downregulates the expression of HIF-1α and PPAR-γ in NAFLD.
- These molecular changes induced by HBO₂ are associated with a significant decrease in Cd36 expression.
- The findings suggest that HBO₂ may reverse NAFLD through the modulation of these key regulatory genes.
