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. Author manuscript; available in PMC: 2020 Oct 1.
Published in final edited form as: J Neurochem. 2019 Jul 28;151(1):50–63. doi: 10.1111/jnc.14813

Figure 4. Aspirin increases SOCS3 protein in cultured astrocytes and in vivo in the cortex via PPARα.

Figure 4.

WT (A), PPARα (−/−) (B) and PPARβ (−/−) (C) astrocytes were treated with different concentrations of aspirin under serum-free condition for 2 h followed by monitoring the protein level of SOCS3 by Western blot. Actin was run as a loading control. Bands were scanned and values (SOCS3/Actin) presented as relative to control [D, WT; E, PPARα (−/−); F, PPARβ (−/−)]. Results are mean ± SD of three independent cell preparations. *p < 0.05; ***p < 0.001 vs control. Significance of mean between control and aspirin-treated groups was analyzed by a two-tailed paired t-test. WT, PPARα (−/−) and PPARβ (−/−) mice (n=6 in each group; 8–10 week old) were treated with aspirin (2 mg/kg/day) orally for 7 days via gavage (G) followed by monitoring the protein level of SOCS3 in the cortex by Western blot (H). Actin was run as a loading control. Bands were scanned and values (SOCS3/Actin) presented as relative to untreated control in each group (I). Results are mean ± SEM of six mice per group. ***p < 0.001 vs control. Significance of mean between control and aspirin-treated groups was analyzed with a two-tailed paired t-test.