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. 2018 Apr 12;15(6):4599–4614. doi: 10.3892/etm.2018.6053

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Copyright: © Feng et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 7. — Protective effects of Sal on ConA-induced liver injury may be reversed by LY294002, a PI3K inhibitor. (A) Serum liver enzyme levels. (B) Relative mRNA levels of TNF-α, IL-6, Bcl-2, Bax, beclin-1 and LC3. (C and D) Protein expression of p-Akt, TNF-α, IL-6, Bcl-2, Bax, beclin-1, LC3 and β-actin. β-actin was used as the internal control. Data are presented as the mean + standard deviation (n=6). *P<0.05 vs. NC; ^ξP<0.05 vs. ConA; ^∞P<0.05 vs. ConA + Sal. Sal, salidroside; ConA, concanavalin A; NC, negative control; ALT, alanine aminotransferase; AST, aspartate aminotransferase; IL, interleukin; TNF-α, tumor necrosis factor-α; Bcl-2, B-cell lymphoma-2; Bax, Bcl-2-associated X protein; LC3, microtubule-associated protein 1A/1B-light chain 3; p-, phosphorylated.