Our recent study demonstrated that pinocembrin （PB）, the most abundant flavonoid in propolis, has neuroprotective effect against 1-methyl4-phenylpyridinium （ MPP^＋ ）-induced SH-SY5Y neurotoxicity. However, the me...Our recent study demonstrated that pinocembrin （PB）, the most abundant flavonoid in propolis, has neuroprotective effect against 1-methyl4-phenylpyridinium （ MPP^＋ ）-induced SH-SY5Y neurotoxicity. However, the mechanism as how PB can induce neuroprotection is not known. In the present study, we demonstrate here that PB increased heme oxygenase-1 （HO-1） expression, which conferred protection against MPP^＋ -induced cytotoxici- ty, because the inhibitor of HO-1 zinc protoporphyrin-IX attenuated the neuroprotection of PB. PB induced the phosphorylation of ERK1/2, and its cytoprotective effect was abolished by ERK1/2 inhibitors. Meanwhile, we have shown that MPP ＋ induce the expression in a concentration-dependent manner in SH-SY5Y cells, which was further enhanced by PB. Taken together, the results suggest that PB enhances HO-1 expression to suppress MPP^＋ -induced oxidative damage via ERK1/2 signaling pathways. These results revealed the mechanisms of PB enhances HO-1 ex- pression , and contribute to shed some light on the mechanisms whereby PB inhibit the MPP^＋ -induced neurotoxici- ty. These data indicated that PB might provide a valuable therapeutic strategy for the treatment of PD.展开更多
文摘Our recent study demonstrated that pinocembrin （PB）, the most abundant flavonoid in propolis, has neuroprotective effect against 1-methyl4-phenylpyridinium （ MPP^＋ ）-induced SH-SY5Y neurotoxicity. However, the mechanism as how PB can induce neuroprotection is not known. In the present study, we demonstrate here that PB increased heme oxygenase-1 （HO-1） expression, which conferred protection against MPP^＋ -induced cytotoxici- ty, because the inhibitor of HO-1 zinc protoporphyrin-IX attenuated the neuroprotection of PB. PB induced the phosphorylation of ERK1/2, and its cytoprotective effect was abolished by ERK1/2 inhibitors. Meanwhile, we have shown that MPP ＋ induce the expression in a concentration-dependent manner in SH-SY5Y cells, which was further enhanced by PB. Taken together, the results suggest that PB enhances HO-1 expression to suppress MPP^＋ -induced oxidative damage via ERK1/2 signaling pathways. These results revealed the mechanisms of PB enhances HO-1 ex- pression , and contribute to shed some light on the mechanisms whereby PB inhibit the MPP^＋ -induced neurotoxici- ty. These data indicated that PB might provide a valuable therapeutic strategy for the treatment of PD.
