Fibroblast Growth Factor Type 1 Ameliorates High-Glucose-Induced Oxidative Stress and Neuroinflammation in Retinal Pigment Epithelial Cells and a Streptozotocin-Induced Diabetic Rat Model.
Hsin-Wei HuangChung-May YangChang-Hao YangPublished in: International journal of molecular sciences (2021)
Diabetic retinopathy (DR) is a common complication of diabetes that causes severe visual impairment globally. The pathogenesis of DR is related to oxidative stress and chronic inflammation. The fibroblast growth factor type 1 (FGF-1) mitogen plays crucial roles in cell function, development, and metabolism. FGF-1 is involved in blood sugar regulation and exerts beneficial antioxidative and anti-inflammatory effects on various organ systems. This study investigated the antioxidative and anti-inflammatory neuroprotective effects of FGF-1 on high-glucose-induced retinal damage. The results revealed that FGF-1 treatment significantly reversed the harmful effects of oxidative stress and inflammatory mediators in retinal tissue in a streptozotocin-induced diabetic rat model. These protective effects were also observed in the in vitro model of retinal ARPE-19 cells exposed to a high-glucose condition. We demonstrated that FGF-1 attenuated p38 mitogen-activated protein kinase and nuclear factor-κB pathway activation under the high-glucose condition. Our results indicated that FGF-1 could effectively prevent retinal injury in diabetes. The findings of this study could be used to develop novel treatments for DR that aim to reduce the cascade of oxidative stress and inflammatory signals in neuroretinal tissue.
Keyphrases
- high glucose
- oxidative stress
- diabetic retinopathy
- diabetic rats
- endothelial cells
- anti inflammatory
- optical coherence tomography
- induced apoptosis
- nuclear factor
- type diabetes
- dna damage
- ischemia reperfusion injury
- cardiovascular disease
- optic nerve
- toll like receptor
- glycemic control
- protein kinase
- early onset
- editorial comment
- heat shock
- inflammatory response
- nitric oxide
- skeletal muscle
- cognitive impairment
- insulin resistance
- single cell
- hydrogen peroxide
- metabolic syndrome
- cerebral ischemia
- mouse model
- pi k akt
- brain injury
- smoking cessation
- immune response
- mass spectrometry
- cell cycle arrest