Salvianolic acid A attenuates early brain injury after subarachnoid hemorrhage in rats by regulating ERK/P38/Nrf2 signaling.

Oxidative stress and inflammation play an important role in the pathogenesis of early brain injury (EBI) following subarachnoid hemorrhage (SAH). The present study aimed to evaluate the effect of salvianolic acid A (SalA) on EBI after SAH via its antioxidative, anti-inflammatory, and anti-apoptotic effects. The intraperitoneal administration of SalA (10 and 50 mg/kg/day) significantly alleviated EBI (including neurobehavioral deficits, brain edema, blood-brain barrier permeability, and cortical neuron apoptosis) after SAH in rats. SalA treatment also reduced the post-SAH elevated levels of reactive oxygen species level and malondialdehyde. Further, SalA increased glutathione peroxidase enzymatic activity and the concentrations of glutathione and brain-derived neurotrophic factor in brain cortex, at 24 h after SAH. In addition, SalA also decreased the release of inflammation cytokines (i.e., TNF-α, IL-1β, IL-6, and IL-8) in SAH rats. Expressions of cell apoptosis-related proteins were also regulated by SalA treatment in SAH rats. Meanwhile, SalA also modulated Nrf2 signaling, and the phosphorylation of ERK and P38 MAPK signaling in SAH rats. These results indicated that the administration of SalA may ameliorate EBI and provide neuroprotection after SAH in rat models.