*3.5. Liver Integrity was Ameliorated by Fibrocyte Depletion*

Cell death is a key event in the pathogenesis of liver fibrosis. Significantly reduced serum levels of alanine amino transferase (ALT) demonstrated a mitigation of liver-specific cellular damage in the fibrocyte-ablated group (−20.9%; 95% CI: 0.4–36.9%; *p* = 0.049; Figure 5a). High-throughput gene expression analysis indicated a decrease of the extracellular death ligand FAS (Figure S3), providing a possible explanation in the differential regulation of apoptosis. Subsequently performed quantitative real-time PCR, however, did not support a regulation of *Fasl* (fold-change 1.04; 95% CI: 0.83–1.34; *p* = 0.666; Figure 5b). Even more, further analyses displayed a subtle downregulation of the antiapoptotic factor Bcl-2 as a consequence of the depletion of fibrocytes (Figure 5c). Neither the transcriptional analysis of *Bcl2* (fold-change 0.97; 95% CI: 0.83–1.13; *p* = 0.661; Figure 5d), nor western blotting (Figure 5e) and quantitative real-time PCR of the Bcl-2 associated factor Bax (fold-change 0.99; 95% CI: 0.86–1.15; *p* = 0.921; Figure 5f) corroborated a general regulation regarding the Bcl-2 family.
