Fig 1: mRNA expression levels of ERK1/2 and p38 in human periodontal ligament cells following exposure to centrifugal force for different time points, as determined by reverse transcription-quantitative polymerase chain reaction. *P<0.05 vs. the control group. ERK1/2, extracellular signal-regulated kinase 1/2.
Fig 2: Kaplan-Meier survival plots comparing DFS for HCC patients stratified by low and high expression levels. (A) The DFS of patients with high IL-6 expression levels was worse than that of patients with low IL-6 expression levels (P=0.0065). (B) The DFS of patients with high IL-6R expression levels was worse than that of patients with low IL-6R expression levels (P=0.029). (C) The DFS of patients with high IL-1ß expression levels was better than that of patients with low IL-1ß expression levels (P=0.014). (D) The DFS of patients with high IKKß expression levels was better than that of patients with low IKKß expression levels (P=0.038). (E) The DFS of patients with high P38MAPK expression levels was better than that of patients with low P38MAPK expression levels (P=0.0033).Abbreviations: DFS, disease-free survival; HCC, hepatocellular carcinoma; IL-6, interleukin-6; IL-6R, interleukin-6 receptor; IL-1ß, interleukin-1 beta; IKKß, inhibitor kappa B kinase beta; P38MAPK, p38 mitogen-activated protein kinase.
Fig 3: TNF-a and p38MAPK expression levels detected using immunohistochemistry. (A) Low expression and (B) high expression of TNF-a in the hepatocellular carcinoma microenvironment (magnification, ×100 and ×400). (C) Low expression and (D) high expression of p38MAPK in the hepatocellular carcinoma microenvironment (magnification, ×100 and ×400). TNF-a, tumour necrosis factor-a; p38MAPK, p38 mitogen-activated protein kinase.
Fig 4: Immunohistochemical analysis of IL-6, IL-6R, IL-1ß, IKKß, and P38MAPK protein levels in HCC tissue specimens (A) IL-6 expression (×400), (B) IL-6R expression (×400), (C) IL-1ß expression (×400), (D) IKKß expression (×400), (E) P38MAPK expression (×400).Abbreviations: IL-6, interleukin-6; IL-6R, interleukin-6 receptor; IL-1ß, interleukin-1 beta; IKKß, inhibitor kappa B kinase beta; P38MAPK, p38 mitogen-activated protein kinase; HCC, hepatocellular carcinoma.
Fig 5: p-P38MAPK is a regulator of the GGT. To further understand how P38 regulates GGT, we treated cells with P38 inhibitors, SB203580 (20 µM), for 24 h. Western blot analysis results showed that the protein levels of p-p38 decreased significantly, while GGT increased after treatment with SB203580 (Panels 10A, B).
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