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. 2022 May 16;13:848957. doi: 10.3389/fphar.2022.848957

FIGURE 4.

FIGURE 4

PPARγ/AMPK pathway in astilbin-treated CD4+ T cells. Variations of LKB1/p-LKB1, AMPK/p-AMPK, and mTOR/p-mTOR in CD4+ T cells treated with various doses of astilbin (A) or at different time points (B). (C) Variations of proteins involved in glucose and lipid metabolism. CD36 of CD4+ T cells affected by astilbin (D, E). Mean ± SD; n = 3. (F) Effects of PPARγ inhibition on CD36 expression. Mean ± SD; n = 3. Effects of CPT inhibition (etomoxir) (G) or AMPK inhibition (dorsomorphin) (H) on IFN-γ, TNF-α, CD36, and CCR9 of astilbin-treated CD4+ T cells. Mean ± SD; n = 3. Effects of etomoxir (I) or dorsomorphin (J) on PTEN expression of astilbin-treated CD4+ T cells. (K) Effects of PPARγ inhibition on AMPK and CPT1a expression of astilbin-treated CD4+ T cells. (L) Diagram of PPAR/PTEN pathway on CD4+ T cells by astilbin. Each experiment was performed at least three times. The inhibitor of CPT, etomoxir, is abbreviated as CPTi. The inhibitor of AMPK, dorsomorphin, is abbreviated as AMPKi. p values (*p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ns, no significant difference) determined by one-way ANOVA (E–H).