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
ABSTRACTBackground: 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 ..