Table 2.
The effects of gliotoxin and C1-3-gliotoxin on parameters of liver fibrosis in a sustained carbon tetrachloride model of liver fibrosis [21]
Treatment | Number of myofibroblasts | Number of F4/80 cells | Fibrosis severity | MMP-13 levels |
---|---|---|---|---|
DMSO vehicle | +++++ | +++ | ++++ | ++++ |
Free gliotoxin | +++a | ++a | ++++ | +++a |
PBS | +++++ | +++ | ++++ | ++++ |
C1-3 | ||||
C1-3-gliotoxin | +b | +++ | ++b | ++++ |
CSBD9 | +++++ | +++ | ++++ | ++++ |
CSBD9-gliotoxin | +++++ | +++ | ++++ | ++++ |
Mice were administered CCl4 over a 8-week period as outlined [21] and the liver was examined for myofibroblasts via α-smooth muscle actin immunostaining [11]; Kupffer cells by immunostaining for F4/80 [21]; fibrosis severity through histochemical staining with Sirius red [11]; and MMP-13 levels by immunohistochemistry [21]. Note, gliotoxin was administered in DMSO at a dose of 0.6 mg/kg body weight. ScAbs were administered in phosphate-buffered saline (PBS) at a dose of 20 mg of protein/kg body weight. Mice received conjugates at an equivalent dose of 0.6 mg of gliotoxin/kg body weight. Data are blinded examination of staining intensity in liver sections from five animals per treatment group—significantly different (two tailed) from aDMSO control or bPBS control using Student’s T test (P > 95%) [21]