Bin Liu1, Yanhong Zhang2, Ying Jiang2, Longling Li2, Changqing Li2, Jinfang Li2. 1. a Department of Neurology , Shandong Provincial Jiaotong Hospital , Jinan , Shandong , China. 2. b Department of Neurology , The Second Affiliated Hospital of Chongqing Medical University , Chongqing , China.
Abstract
OBJECTIVE: Cerebellar fastigial nucleus stimulation (FNS) has been shown to protect against cerebral ischemic injury. Peroxisome proliferator activator receptor gamma (PPARγ) has been reported to cause neuroprotection in animal models of stroke. The present study was performed to explore the neuroprotective mechanisms of FNS treatment in experimental stroke. METHODOLOGY: Adult male Sprague-Dawley (SD) rats preconditioned through transfection with either PPARγ-small hairpin RNA (shRNA) or lentiviral vector without shRNA and surgically subjected to middle cerebral artery occlusion and reperfusion subsequently received FNS treatment. The expression of PPARγ after FNS treatment was measured using western blotting and immunohistochemistry. Subsequently, the neuronal apoptosis, neurological deficits scores, and cerebral infarction were also evaluated. Additionally, the influence of FNS on the pro-inflammatory cytokines expression were determined by ELISA. RESULTS: We found that FNS significantly upregulated PPARγ expression, attenuated apoptosis and inflammatory response, and reduced infarct volume. The protective effect of FNS was abrogated by PPARγ-shRNA. CONCLUSION: Our results as described above suggested that FNS confers neuroprotection by upregulated PPARγ.
OBJECTIVE: Cerebellar fastigial nucleus stimulation (FNS) has been shown to protect against cerebral ischemic injury. Peroxisome proliferator activator receptor gamma (PPARγ) has been reported to cause neuroprotection in animal models of stroke. The present study was performed to explore the neuroprotective mechanisms of FNS treatment in experimental stroke. METHODOLOGY: Adult male Sprague-Dawley (SD) rats preconditioned through transfection with either PPARγ-small hairpin RNA (shRNA) or lentiviral vector without shRNA and surgically subjected to middle cerebral artery occlusion and reperfusion subsequently received FNS treatment. The expression of PPARγ after FNS treatment was measured using western blotting and immunohistochemistry. Subsequently, the neuronal apoptosis, neurological deficits scores, and cerebral infarction were also evaluated. Additionally, the influence of FNS on the pro-inflammatory cytokines expression were determined by ELISA. RESULTS: We found that FNS significantly upregulated PPARγ expression, attenuated apoptosis and inflammatory response, and reduced infarct volume. The protective effect of FNS was abrogated by PPARγ-shRNA. CONCLUSION: Our results as described above suggested that FNS confers neuroprotection by upregulated PPARγ.