Abstracto
Effects of puerarin on brain cell apoptosis, expression of transforming growth factor-β, vascular endothelial growth factor in hyperoxia-exposed neonatal rats
Tao Liu, Na Li, Hui Li, Liping Chu, Hongbo Gao, Qinzeng Qiao, Weikun Han, Junhui Zhang
Aims: To investigate effects of puerarin on apoptosis of microvascular endothelial cell, expression of transforming growth factor-β and vascular endothelial growth factor in the brain of hyperoxia-exposed neonatal rats, and to explore the molecular mechanism of the protective effects of puerarin on brain.
Methods: Thirty Spraque-Dawley (SD) neonatal male rats were randomly divided into three groups: normal group, model group, and puerarin group. Each group had 10 rats. Hyperoxia brain injury model was established by exposing newborn male rats to ≥ 90% hyperoxia continuously for 14 days. Brain cell apoptosis was detected by deoxyribonucleotidyl transferase-mediated apoptosis (TUNEL). Levels of TGF-β and were measured by double antibody sandwich enzyme-linked immunosorbent assay (ELISA). Expression of TGF-β and VEGF-B protein in rat brain tissue was measured using Western blot.
Results: The apoptotic index of model group was significantly higher than that of normal group and puerarin group (p<0.05). The apoptotic index of puerarin group was significantly lower than that of model group (p<0.05). Compared with model group, TGF-β1 level was significantly decreased and VEGF-B was significantly increased in brain tissue of puerarin group (p<0.05). Western blot showed that expression level of TGF-β1 protein was significantly higher in model group than in normal group p<0.05). Puerarin down-regulated the expression level of TGF-β. Expression level of VEGF-B protein in model group and puerarin group was significantly higher than that in normal group (p<0.05), and highest expression level of VEGF-B was observed in puerarin group.
Conclusion: Puerarin may inhibit apoptosis and maintain the integrity of cerebral microvascular endothelial cells by down-regulating TGF-β expression and up-regulating VEGF expression, so as to promote angiogenesis after hyperoxia injury.