PI3K/AKT signaling pathway activation in a rat model of migraine
- Yun‑Yong Liu
- Zi‑Yao Jiao
- Wei Li
- Qian Tian
Published online on: August 8, 2017
The present study aimed to investigate phosphatidylinositol 4,5-bisphosphate 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathway activation in a rat model of migraine. A total of 60 male Sprague‑Dawley rats were randomly divided into three groups: Blank control; suspension control; and migraine model. The model group was subcutaneously injected with a glyceryl trinitrate suspension, using an optimized Tassorelli method to establish a rat model of migraine. The activation status of the PI3K/AKT signaling pathway was assessed via measurement of the phosphorylated (p)‑AKT level. The level of serum 5‑hydroxytryptamine was detected using an ELISA. The mRNA and protein expression levels of PI3K and AKT, and protein levels of p‑AKT were detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. Expression of the PI3K gene was significantly increased (P<0.01) 6‑24 h following the glyceryl trinitrate injection. There was no significant difference in the expression of AKT between any of the groups at any time. Expression of p‑AKT (S473) was significantly increased in the migraine model group (P<0.01) compared with the controls groups. Immunohistochemical analysis indicated that phosphatase and tensin homolog (PTEN) continuously decreased in the migraine model group during 1‑12 h, however this was only significant in the 12 h group. Levels of PTEN had increased again by 24 h. Glycogen synthase kinase (GSK)‑3β expression exhibited a similar expression pattern to PTEN. The results indicated that the PI3K/AKT signal pathway may be activated in the brain tissue of the rat migraine models. The inhibition of PTEN, which is an upstream modulator of the PI3K/AKT signaling pathway, may enhance the activation of phosphatidylinositol‑3,4,5‑triphosphate, thus inhibiting the expression of GSK-3β.