Liver fibrosis is an inevitable stage in the development of chronic liver disease to cirrhosis. Nonetheless, the interventional treatment and achieving control over the disease at this stage can substantially reduce the incidence of liver cirrhosis. To demonstrate these aspects, liver pathological sections of 18 patients with chronic liver disease are collected for research according to the degree of fibrosis. Further, the expressions of related proteins in each group are studied by the Western blot method. The cell proliferation and apoptosis are detected by CKK-8 and flow cytometry analyses. Further, a rat model with carbon tetrachloride (CCl4)-induced liver fibrosis is employed to verify the effect and mechanism of VDR on the process of liver fibrosis in vivo. The expression of VDR in liver tissues of patients with liver fibrosis is negatively correlated with α-smooth muscle actin (α-SMA), Col-1, and liver fibrosis stages. Moreover, the tumor necrosis factor (TNF)-α stimulation could increase the proliferation of LX-2, up-regulate the expression of α-SMA, Col-1, NF-κB, p-IκBα, p-IKKβ, p-p65m, and some fibrosis factors, as well as down-regulate the expressions of VDR and matrix metalloproteinase-1 (MMP-1). Considering the protective actions of VDR, calcipotriol, a VDR agonist, effectively reduced the degree of liver fibrosis in a rat model of liver fibrosis by inhibiting the deposition of extracellular (ECM) and activation of hepatic stellate cells (HSCs), which is negatively correlated with the degree of liver fibrosis. Together, these shreds of evidence demonstrated that the calcipotriol showed great potential in effectively attenuating liver fibrosis.
Keywords: NF-κB; Vitamin D receptor; calcipotriol; hepatic stellate cells; liver fibrosis.