Abstract
Inflammatory injury and neuronal apoptosis participate in the period of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Suppression of inflammation has recently been shown to reduce neuronal death and neurobehavioral dysfunction post SAH. Biochanin A (BCA), a natural bioactive isoflavonoid, has been confirmed to emerge the anti-inflammatory pharmacological function. This original study was aimed at evaluating and identifying the neuroprotective role of BCA and the underlying molecular mechanism in an experimental Sprague-Dawley rat SAH model. Neurobehavioral function was evaluated via the modified water maze test and modified Garcia neurologic score system. Thus, we confirmed that BCA markedly decreased the activated level of TLRs/TIRAP/MyD88/NF-κB pathway and the production of cytokines. BCA also significantly ameliorated neuronal apoptosis which correlated with the improvement of neurobehavioral dysfunction post SAH. These results indicated that BCA may provide neuroprotection against EBI through the inhibition of inflammatory injury and neuronal apoptosis partially via the TLRs/TIRAP/MyD88/NF-κB signal pathway.
Highlights
Subarachnoid hemorrhage (SAH) is known as an acute catastrophic neurological disease with a high rate of perioperative mortality and permanent morbidity worldwide
Recent basic and clinical studies have focused on the pathologic mechanism that occurs in the period from 0 h to 72 h post SAH, often known as early brain injury (EBI), the most crucial and etiological factor of poor clinical prognosis among SAH cases [2]
The degree of secondary inflammatory injury and severe neuronal apoptosis correlates with the progress of SAH, and many previous studies implicated that the uncontrolled inflammatory response and neuronal apoptosis may aggravate EBI post SAH [4]
Summary
Subarachnoid hemorrhage (SAH) is known as an acute catastrophic neurological disease with a high rate of perioperative mortality and permanent morbidity worldwide. Recent basic and clinical studies have focused on the pathologic mechanism that occurs in the period from 0 h to 72 h post SAH, often known as early brain injury (EBI), the most crucial and etiological factor of poor clinical prognosis among SAH cases [2]. The degree of secondary inflammatory injury and severe neuronal apoptosis correlates with the progress of SAH, and many previous studies implicated that the uncontrolled inflammatory response and neuronal apoptosis may aggravate EBI post SAH [4]. Biochanin A (BCA), an organic isoflavone derived from natural plant sources, has been classified as a special phytoestrogen [5,6,7]. BCA has exhibited various beneficial bioactivities, such as antidiabetic, anticancer, antiallergic, and
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