Hyperbaric oxygen (HBO2) therapy decreases Cd36 gene expression through HIF-1α/PPAR-γ and reverses non-alcoholic fatty liver disease in rats
Hyperbaric oxygen (HBO2) therapy decreases Cd36 gene expression through HIF-1α/PPAR-γ and reverses non-alcoholic fatty liver disease in rats
Description
Marcos de J. Reyes Bocanegra, BS1; Rodolfo Quintana Castro, PhD3; Luis Páez Martínez3, BS; Beatriz Agame Lagunes, PhD3; Peter Grube Pagola3, PhD; Sandra Hernández Leyva2, PhD; Julio C. Ramírez Nava2*, MSc; Alfonso Alexander Aguilera, PhD2*
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.
2Instituo de Investigación en Ciencias de la Salud de la Secretaría de Marina (INICISEM), Centro de Estudios Navales en Ciencias de la Salud (CENCIS), Polígono Naval de San Pablo Tepetlapa, Calzada de la Vírgen 1800, Ciudad de México. 04800. México.
3Facultad de Bioanálisis e Instituto de Investigaciones Médico-Biológicas. Universidad Veracruzana, Carmen Serdán s/n. Col. Flores Magón, Veracruz, Ver., 91700. México.
Corresponding author: aalexander_2000@yahoo.com; smarnav@hotmail.com
Hyperbaric oxygen (HBO2) therapy decreases Cd36 gene expression through HIF-1α/PPAR-γ and reverses non-alcoholic fatty liver disease in rats
Running title
HBO2 and Cd36 expression associated with NAFLD
ABSTRACT
Background: Non-alcoholic fatty liver disease (NAFLD) is characterized by accumulation of liver fat (steatosis), which can progress to nonalcoholic steatohepatitis (NASH), cirrhosis, and cancer. NASH is estimated to affect up to 32% of the world population. Different treatments are being investigated, such as hyperbaric oxygen (HBO2) therapy, but the molecular mechanisms associated with this therapy are unknown. The effect of HBOT 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 StepOneTM 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. Conclusion: 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: Non-alcoholic fatty liver disease, Hyperbaric oxygen (HBO2) therapy, Cd36 gene expression.