Fig. 4
From: Elevated Kallistatin promotes the occurrence and progression of non-alcoholic fatty liver disease
KAL causes hepatic steatosis by down-regulating both CGI-58 and ATGL, and inflammation mainly by CGI-58. a Representative immunoblot and quantification of ATGL and CGI-58 in liver tissues from 6-month-old mice. b, c Representative immunoblot and quantification of protein levels, mRNA levels of ATGL and CGI-58 in primary hepatocytes cultured from WT or KAL-Tg mice. d Oil red O staining of primary hepatocytes cultured from WT and KAL-Tg mice and transfected with ATGL and/or CGI-58 plasmids for 48 h. Scale bar: 50 μm. e, f The levels of ATGL and CGI-58 in liver tissues from rats fed with MCD for 10 weeks (e) or HFruD for 16 weeks(f). g Representative immunoblot of ATGL and CGI-58 in liver tissues from 3-month-old mice. h mRNA levels of ABHD5 in liver tissue from patients with hepatic steatosis or NASH (Control, n = 24; steatosis, n = 20; NASH, n = 19 for GEO accession number GSE89632). i Correlation analysis of mRNA levels of ABHD5 and SERPINA4. j–l Representative immunoblot and quantification of TNFα, mRNA levels of TNFα, and supernatant TNFα levels in primary hepatocytes treated with Ad-KAL or Ad-RFP for 48 h. m–o Representative immunoblot and quantification of TNFα, mRNA levels of TNFα in primary hepatocytes transfected with Ad-KAL and ATGL or CGI-58 plasmid for 48 h. p, q Protein levels and mRNA levels of CGI-58 in Raw macrophagocytes. Data represent the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001
