6-O-Galloylpaeoniflorin Attenuates Cerebral Ischemia Reperfusion-Induced Neuroinflammation and Oxidative Stress via PI3K/Akt/Nrf2 Activation

Figure 5

GPF mitigates the cerebral infarction volume and neurological impairment through the PI3K/Akt pathway in a rat CIRI model in vivo. Before being subjected to CIRI, rats were pretreated with different dose of GPF (2.5, 5, or 10 mg/kg/day) for 14 days. In some cases, Ly294002 (20 mM, 5 μL) was injected into the lateral ventricle daily for 7 days before CIRI model establishment. The infarct volume was remarkably decreased in the GPF treatment groups, compared with rats without GPF treatment. Yet, the infarct volume further increased after treatment with Ly294002 (a) and (b). The neurological score was reduced in the GPF treatment groups, compared with the CIRI rats without GPF treatment, indicating that GPF could protect nerve function and improve brain function in a dose-dependent manner. Nevertheless, the nerve-protecting and nerve-improving activities of GPF were diminished after treatment with Ly294002 (c). Each group contains at least six rats. versus 0 mg/kg GFP in the CIRI models; versus 0 mg/kg GFP in the CIRI models; versus 10 mg/kg GFP in the CIRI models.

(a)

(b)

(c)