Hyperbaric oxygen therapy suppresses hypoxia and reoxygenation injury to retinal pigment epithelial cells through activating peroxisome proliferator activator receptor-alpha signalling.
Tzong-Bor SunKuo-Feng HuangKo-Chi NiuCheng-Hsien LinWen-Pin LiuChao-Hung YehShu-Chun KuoChing-Ping ChangPublished in: Journal of cellular and molecular medicine (2023)
Retinal ischemia followed by reperfusion (IR) is a common cause of many ocular disorders, such as age-related macular degeneration (AMD), which leads to blindness in the elderly population, and proper therapies remain unavailable. Retinal pigment epithelial (RPE) cell death is a hallmark of AMD. Hyperbaric oxygen (HBO) therapy can improve IR tissue survival by inducing ischemic preconditioning responses. We conducted an in vitro study to examine the effects of HBO preconditioning on oxygen-glucose deprivation (OGD)-induced IR-injured RPE cells. RPE cells were treated with HBO (100% O 2 at 3 atmospheres absolute for 90 min) once a day for three consecutive days before retinal IR onset. Compared with normal cells, the IR-injured RPE cells had lower cell viability, lower peroxisome proliferator activator receptor-alpha (PPAR-α) expression, more severe oxidation status, higher blood-retinal barrier disruption and more elevated apoptosis and autophagy rates. HBO preconditioning increased PPAR-α expression, improved cell viability, decreased oxidative stress, blood-retinal barrier disruption and cellular apoptosis and autophagy. A specific PPAR-α antagonist, GW6471, antagonized all the protective effects of HBO preconditioning in IR-injured RPE cells. Combining these observations, HBO therapy can reverse OGD-induced RPE cell injury by activating PPAR-α signalling.
Keyphrases
- cell cycle arrest
- induced apoptosis
- cell death
- oxidative stress
- endoplasmic reticulum stress
- signaling pathway
- ischemia reperfusion injury
- optical coherence tomography
- pi k akt
- poor prognosis
- diabetic rats
- diabetic retinopathy
- type diabetes
- insulin resistance
- dna damage
- optic nerve
- fatty acid
- drug induced
- nitric oxide
- early onset
- blood pressure
- binding protein
- left ventricular