Hydroxysafflor Yellow A Shows Protection against PPARγ Inactivation in Nitrosative Neurons

Figure 3

Additional protection against SIN-1-induced neuronal injury by HSYA combined with PPARγ agonist. (a) PPARγ-mediated protection of neurons from SIN-1-induced cytotoxicity. The neurons were pretreated for 24 h with the PPARγ agonist 15d-PGJ2 (PGJ2) (5 μM) or rosiglitazone (Ros) (1 μM), antagonist GW9662 (GW) (5 μM), or their combination as described in Materials and methods. Cultures were then incubated with or without 1 mM SIN-1 (SIN) for further 24 h. LDH release to the media was employed as neuronal damage index. Data are presented as mean ± SEM (). compared to non-SIN-1-treated groups and compared to SIN-1 alone. (b, c) Additional protection against SIN-1-induced neuronal injury by HSYA combined with PPARγ agonist. The PPARγ agonist (5 μM 15d-PGJ2 or 1 μM rosiglitazone) with or without HSYA (0.1 mM) was added to the cultures 10 min prior to SIN-1 (1 mM) exposure. Activated PPARγ (b) and neuronal insult (c) were evaluated by PPARγ DNA-binding activity at 6 h and LDH release assay at 24 h, respectively, after the coincubation with SIN-1. Data are presented as mean ± SEM (). compared to SIN-1 alone and compared to SIN-1 plus HSYA alone.

(a)

(b)

(c)