Paeonol Alleviates Brain Injury and Neurological Deficits Caused by Intracerebral Hemorrhage in Rats

Abstract

Aim: This study aimed to explore the effect and related mechanisms of paeonol (PAE) in intracerebral hemorrhage (ICH) in rats. Methods: The severity of neurological deficits in rats were assessed using Neurological deficits scores (NDA), righting reflex test, and foot stepping fault test, followed by measurements of water content and cell apoptosis level in rat brain tissues. Next, enzyme linked immunosorbent assay (ELISA) was used to evaluate the inflammatory cytokines and brain-specific biomarkers in the rat brain tissues. Oxidative stress levels in serum and phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B (PI3K/Akt) pathway-associated protein expression in rat brain tissues were assessed using different biochemical detection kit and Western blot analysis, respectively. Results: Rats with ICH presented severer brain injury, brain edema and neurological deficits than those only receiving sham operation (p < 0.01). In addition, the inflammation, oxidative stress and apoptosis levels were significantly up-regulated in ICH rats (p < 0.01). However, PAE treatment not only alleviated ICH-caused brain injury, neurological deficits and brain edema, but also inhibited inflammatory (down-regulation of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and IL-18 levels, p < 0.01) and oxidative stress responses (SOD (superoxide dismutase) and GSH (glutathione) levels increased, and MDA (malondialdehyde) levels were down-regulated, p < 0.01). Moreover, both Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling (TUNEL) staining and Western blot analysis indicated that PAE inhibited ICH induced apoptosis (p < 0.01). Additionally, PAE was able to activate the PI3K/Akt signaling pathway. Conclusions: Overall, PAE mitigates neurological deficits, brain edema and brain injury via ICH induced apoptosis, oxidative stress and inflammation suppression. This effect might be related to the PI3K/Akt signaling pathway activation. In a sentence, PAE is likely to be an effective therapeutic agent for ICH.