15-Deoxy-γ12,14-prostaglandin J2 Reduces Liver Impairment in a Model of ConA-Induced Acute Hepatic Inflammation by Activation of PPARγ and Reduction in NF-κB Activity

Figure 3

15d-PGJ2 activated PPARγ, blocked IκBα degradation, and reduced the NF-κB activation in ConA-induced hepatitis. (a) The western blot and qRT-PCR analysis of PPARγ, IκBα, and NF-κB at 6 h, 12 h, and 24 h after ConA injection in mice and effects of both low (10 μg) and high (25 μg) dose 15d-PGJ2 pretreatment groups at the same time. The phosphorylation status of NF-κB and IκBα (P-NF-κB and P-IκBα) were also detected by using western blot. The results were analyzed using Quantity One (𝑛=3, ^∗𝑃<0.05 for NC versus ConA, ^#𝑃<0.05 for ConA versus ConA + 10 μg 15d-PGJ2, and ⁺𝑃<0.05 for ConA versus ConA + 25 μg 15d-PGJ2). (b) Immunohistochemistry used to detect the expression level of PPARγ at 24 h in all four groups. The result was analyzed using Image-Pro Plus 6.0 (𝑛=3, ^#𝑃<0.05 for ConA versus ConA + 10 μg 15d-PGJ2, ⁺𝑃<0.05 for ConA versus ConA + 25 μg 15d-PGJ2, and black bar for 200 μM). (c) The different expression of NF-κB evaluated by immunohistochemistry. Image-Pro Plus 6.0 was used to analyze whether there exists statistical significance among different groups (𝑛=3, ^∗𝑃<0.05 for NC versus ConA, ^#𝑃<0.05 for ConA versus ConA + 10 μg 15d-PGJ2, ⁺𝑃<0.05 for ConA versus ConA + 25 μg 15d-PGJ2, black bar for 200 μM, and small black arrow for positive cells).

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