Fisetin Alleviates Neointimal Hyperplasia via PPARγ/PON2 Antioxidative Pathway in SHR Rat Artery Injury Model

Figure 5

Fisetin regulates PON2 expression through PPARγ pathway in VSMCs. (a, b) Effects of fisetin with incremental doses or incremental incubation times on PON2 protein expression in the absence of AngII. Protein level was determined by Western blotting after A10 cells were incubated with incremental concentrations (0.1~100 μM) of fisetin alone for 24 h or with a fixed concentration of fisetin (100 μM) for incremental times (3~24 h). (c, d) Role of PPARγ in fisetin’s upregulation of PON2 expression in VSMCs. A10 cells were treated with 100 μM of fisetin for 24 hours in the presence of either PPARγ inhibitor GW9662 (10 mM) or MAPK inhibitor PD98059 (10 mM) or JNK inhibitor SP600125 (1 mM). The expression of PON2 was detected by (c) Western blotting and (d) q-PCR. (e) Effect of PPARγ agonist rosiglitazone on protein expression of PON2. A10 cells were treated with incremental concentrations of rosiglitazone (10~30 μM) for 24 hours before PON2 protein immunoblotting ( vs. control and ^# vs. fisetin only).

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