Fig 1.
Chronic calcitriol treatment ameliorates hepatic steatosis and improved inflammatory profiles of monocytes.
H-E (a) and O-red oil staining (b) for hepatic steatosis. (c) hepatic triglyceride content and (d) cytokines levels in the cell lysates of various rat monocytes. (e) A representative flow cytometric histogram/dot plots of the cytokines/cytokine receptors of NASH-V-rat monocytes. (f) A bar graph of the flow cytometry-assessed cytokines/cytokine receptors of monocytes from various rats. †P<0.05, †† P<0.01 vs. lean-V group; *P< 0.05, **P<0.01 vs. NASH-V group.
Table 1.
Basal characteristics of all rats.
Table 2.
Various pathogenic markers in all rats.
Fig 2.
Chronic calcitriol treatment normalizes intestinal VDR expression and improves intestinal hyper-permeability in NASH rats.
DX-4000 FITC-based (a) and fecal albumin-based (b) assessment of intestinal permeability. The expression of various proteins (c) and mRNAs (d) in intestines from different groups of rat; AUC: area under curves; †P<0.05, †† P<0.01 vs. lean-V group; *P< 0.05, **P<0.01 vs. NASH-V group.
Fig 3.
Chronic calcitriol treatment improved intestinal inflammation in NASH rats.
The expression of various proteins (a) in the intestines from various different groups of rat and the flow-cytometry-based analysis of macrophage infiltration in the same rat (b) small intestine. †P<0.05, †† P<0.01 vs. lean-V group; *P< 0.05, **P<0.01 vs. NASH-V group.
Table 3.
Qantification of total number of bacterial cells of the intestinal flora in cecal content.
Fig 4.
Chronic calcitriol treatment suppresses mesenteric adipose tissue (MAT) inflammation of NASH rats.
(a) A flow-cytometry-based analysis of macrophage infiltration in rat MAT. (b) The cytokines levels in the supernatant of MAT-derived adipocytes collected from different groups of rats. (c) The expression levels of mRNAs in the cell lysates of lean-V rat adipocytes after various treatments. (d) The peak levels of cytokine releases in the supernatant of NASH-V rat adipocytes after various treatments; †P<0.05, †† P<0.01 vs. lean-V/buffer group; *P< 0.05, **P<0.01 vs. NASH-V-CM/TNFα group.
Fig 5.
In vitro effects of calcitriol on the NASH-V-CM and TNFα-induced mucosal dysfunction in caco-2 cells.
(a,b) The in vitro effects of various treatments on caco-2 monolayer mucosal dysfunction and IF-stained ZO-1 expression. (c,d) protein and mRNA levels in the cell lysates of caco-2 monolayer cells after various treatments. †P<0.05, †† P<0.01 vs. lean-V group; *P< 0.05, **P<0.01 vs. NASH-V-CM group.
Fig 6.
In vitro effects of calcitriol on the NASH-V-CM and TNFα-induced lipogenesis in lean-V rat hepatocytes.
(a) representative micrographs of intracellular lipogenesis in lean-V rat hepatocytes after various different treatments. (b,c) The cytokines levels, lipogenic protein/mRNA levels in the cell lysates of lean-V rat hepatocytes after various treatments. †P<0.05, †† P<0.01 vs. buffer-group; *P< 0.05, **P<0.01 vs. NASH-V-CM-group/TNFα-group.