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. 2016 Sep 16;6:33453. doi: 10.1038/srep33453

Figure 3. Hepatic levels of HSC activation marker α-SMA and cytokines involved in fibrogenesis, fibrinolysis, inflammation, proliferation and apoptosis.

Figure 3

(A) In the therapeutic study arm, the hepatic protein levels of α-SMA, assessed by Western blot, are clearly decreased following OCA treatment indicative of decreased HSC activation (n = 4 per group). (B) RT-PCR data showing decreased expression of pro-fibrotic (CTFG, PDGF-R, TGF-β1), anti-fibrinolytic (TIMP-1) as well as pro-inflammatory cytokines in either the therapeutic study arm alone or both upon OCA treatment (n = 6–8 per group). (C) Western blot data showing decreased levels of proliferation marker PCNA in OCA treated rats from the therapeutic study arm. (D) Western blot data showing a decrease in the small degradation fragment (24 kD) of PARP-1 in OCA treated rats from the therapeutic study arm, indicative of decreased capase-3 activity. (E) Immunohistochemical staining for caspase-3 showing decreased caspase-3 positivity in both the prophylactic and therapeutic study arm. HSC, hepatic stellate cell; α-SMA, alpha-smooth muscle actin; OCA, obeticholic acid; RT-PCR, reverse-transcriptase polymerase chain reaction; CTGF, connective tissue growth factor; PDGF-R, platelet-derived growth factor-beta receptor; TGF-β1, Transforming growth factor-β1; TIMP-1, tissue inhibitor of metallopeptidase-1; MCP, monocyte chemo-attractant protein-1; iNOS, inducible nitric oxide synthase; IFN-γ, interferon-gamma; PCNA, proliferating cell nuclear antigen; PARP-1, poly ADP ribose polymerase-1.