Effects of Buyanghuanwu decoction on the protein expression of PI3K, Akt, Bcl-2 and BAX in brain tissue of a rat model of cerebral hemorrhage / 中国组织工程研究

ABSTRACT

BACKGROUND:Buyanghuanwu decoction has excel ent neuroprotective effect and can efficiently suppress nerve cel apoptosis caused by cerebral ischemia-reperfusion injury. OBJECTIVE:To investigate the effect and mechanisms of Buyanghuanwu decoction on neuronal apoptosis around hematoma in cerebral hemorrhage rats. METHODS:Seventy-two adult Sprague-Dawley rats were randomly divided into sham operation group, model group, Buyanghuanwu decoction group, and Ginkgo biloba group. Except the sham operation group, rat models of cerebral hemorrhage were established in other three groups. At 2 days after modeling, rats in the Buyanghuanwu group and Ginkgo biloba group were given Buyanghuanwu decoction 26 g/(kg?d)and Ginkgo biloba 3.5 mg/(kg?d) daily by gavage, for 14 consecutive days. Rats in the sham operation group and model group received an equal volume of saline for 14 consecutive days. After the last administration, brain tissue was obtained. TUNEL assay was utilized to detect neuronal apoptosis. Immunohistochemistry was used to detect PI3K, Akt, Bcl-2, and BAX protein expression. Wet and dry weight method was used to detect brain water content. Evans Blue assay was utilized to determine blood-brain barrier permeability. RESULTS AND CONCLUSION:(1) Compared with the sham operation group, the number of apoptotic neurons, brain water content, Evans blue content and PI3K, Akt, Bcl-2, BAX protein expression increased in the model group (P<0.05). (2) Compared with the model group, the number of apoptotic neurons, BAX protein expression, brain water content and Evans blue content were significantly reduced in the Buyanghuanwu group and Ginkgo biloba group (P<0.05), but PI3K, Akt and Bcl-2 protein expression was significantly increased (P<0.05). (3) Results suggested that Buyanghuanwu decoction inhibited neuronal apoptosis and protected brain tissue by reducing blood-brain barrier permeability, cerebral edema, and by activating PI3K/Akt signaling pathway, regulating Bcl-2 and BAX protein expression ratio.