Hypoxic-ischemic encephalopathy (HIE) is a cause of serious morbidity and mortality in newborns. Dexpanthenol, which is metabolized into D-pantothenic acid, has antioxidant and other potentially therapeutic properties. We examined some effects of dexpanthenol on the brains of week-old rat pups with HIE induced by obstruction of the right carotid artery followed by keeping in 8% O 2 for 2 hours. Dexpanthenol (500 mg/kg) was administered intraperitoneally to 16 of 32 pups with HIE. Protein, DNA, and lipid oxidation degradation products were assayed and hippocampal and cortical cell apoptosis and neuronal cell numbers were evaluated in stained sections. Dexpanthenol application reduced oxidative stress and inflammation. TNF-α and IL-6 cytokine levels in HIE also decreased with dexpanthenol treatment. The numbers of caspase-3 positive cells in the dentate gyrus and CA1/CA2/CA3 regions of the hippocampus was lower, and apoptosis was decreased in the dexpanthenol-treated animals. These findings suggest possible clinical applications of dexpanthenol in human HIE.
Keyphrases
- oxidative stress
- induced apoptosis
- cell cycle arrest
- cell death
- early onset
- endoplasmic reticulum stress
- dna damage
- rheumatoid arthritis
- ischemia reperfusion injury
- cell proliferation
- cerebral ischemia
- stem cells
- brain injury
- amino acid
- small molecule
- cognitive impairment
- fatty acid
- signaling pathway
- preterm birth
- combination therapy
- heat shock