HBOT Research

  1. Home
  2. HBOT Research

Explore our database on Hyperbaric Oxygen Therapy (HBOT) Research below.

Extivita maintains an extensive research & publication database for various diseases and therapies such as Hyperbaric Oxygen Therapy, Neurofeedback, Nutritional IV Therapy, Infrared Sauna, and Pulsed Electromagnetic Field Therapy.

For a complete list of indications treated at Extivita, explore the conditions we treat.

 

Hyperbaric oxygen protects mandibular condylar chondrocytes from interleukin-1ฮฒ-induced apoptosis via the PI3K/AKT signaling pathway

Hyperbaric oxygen protects mandibular condylar chondrocytes from interleukin-1ฮฒ-induced apoptosis via the PI3K/AKT signaling pathway

Objectives: Mandibular condylar chondrocyte apoptosis is mainly responsible for the development and progression of temporomandibular joint osteoarthritis (TMJ-OA). Interleukin-1ฮฒ (IL-1ฮฒ) generally serves an agent that induces chondrocyte apoptosis. Hyperbaric oxygen (HBO) treatment increases proteoglycan synthesis in vivo. We explore the protective effect of HBO on IL-1ฮฒ-induced mandibular condylar chondrocyte apoptosis in rats and the potential molecular mechanisms. Methods: Chondrocytes were isolated from the TMJ of 3-4-week old Sprague-Dawley rats. The Cell Counting Kit-8 (CCK-8) assay was used to determine cell viability. The phosphorylated phosphoinositide-3 kinase (p-PI3K), phosphorylated AKT (p-Akt), type II collagen (COL2), and aggrecan (AGG) content was detected by immunofluorescence, immunocytochemistry and western blotting. The expression of Pi3k, Akt, Col2 and Agg mRNA was measured using real-time quantitative polymerase chain reaction (RT-qPCR). Results: HBO inhibited the cytotoxicity and apoptosis induced by IL-1ฮฒ (10 ng/mL) in the mandibular condylar chondrocytes. HBO also decreased the IL-1ฮฒ activity that decreased p-PI3K and p-AKT levels, and increased COL2 and AGG expression, with the net effect of suppressing extracellular matrix degradation. Conclusions: These data suggest that HBO may protect mandibular condylar chondrocytes against IL-1ฮฒ-induced apoptosis via the PI3K/AKT signaling pathway, and that it may promote the expression of mandibular condylar chondrocyte extracellular matrix through the PI3K/AKT signaling pathway.

read more