V 15-deoxy Δ^12,14-Prostaglandin J₂
　　PGD₂ was non-enzymatically metabolized to prostaglandin J₂ (PGJ₂), Δ¹²-PGJ₂ and 15d-PGJ₂ (Figure 7). Among PGD₂ metabolites, 15d-PGJ₂ exhibited neurotoxicity most potently (Figure 8).
15d-PGJ₂ induced neuronal cell death via apoptosis more potently than PGD₂ (Figure 9). 15d-PGJ₂ is believed to be actively transported into the cytosol and covalently binds to Cys²⁸⁵ of its nuclear receptor, peroxysome-proliferator activated receptorγ (PPARγ) (Figure 10). The neurotoxicity of
15d-PGJ₂ was the most potent among PGD₂ and its metabolites (Figure 8), whereas neurotoxicities of other eicosanoids besides PGA₂ (Figure 11) and PPAR agonists (Figure 12) were not detected. Chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2) is identified as a type 2 receptor for PGD₂ (DP2), and reported to be a membrane receptor for 15d-PGJ₂ (Figure 10). The apoptotic effect of 15d-PGJ₂-related compounds was correlated to their affinities for neither DP1 nor DP2. According to LD₅₀ and LT₅₀, the apoptotic effect of 15d-PGJ₂-related compounds was
15d-PGJ₂ > Δ12-PGJ₂ > PGJ₂ > PGA₂ >> PGD₂ > 15d-PGD₂ in sequence (Table 3). In the view of IC₅₀, the affinity of 15d-PGJ₂–related compounds for DP1 was PGJ₂ > PGD₂ >> Δ¹²-PGJ₂> 15d-PGJ₂ > PGA₂ in sequence (Table 3). On the other hand, the affinity of 15d-PGJ₂–related compounds for CRTH2/DP2 was PGD₂ > 15d-PGD₂ >15d-PGJ₂ > PGJ₂ > Δ¹²-PGJ₂ >> PGA₂ in sequence (Table 3). Thus, neuronal apoptosis is suggested to be mediated independently of PPARγ and CRTH2 (Figure 10).