Abstract: Objective To explore the role and underlying mechanism of C1q/TNF-related protein 6 (CTRP6) in the development process of liver disease. Methods The histopathological examination and biochemical indexes of injured livers from wild-type (CTRP6^+/+) and knockout (CTRP6^-/-) mice induced by intragastric administration of CCl₄ were analyzed. RT-qPCR was used to detect the expression of the fibrosis marker genes (Acta2, Col1al, Mmp2 and TGF-β) and cell proliferation marker genes (Cyclin D, Cyclin E and CDK6). Results Compared with CTRP6^+/+ mice, the hepatocytes in CTRP6^-/- mice showed mild necrosis, looseness and swelling. The high SOD activity and low MDA level were also observed in CTRP6^-/- mice liver. Meanwhile, the expression of fibrosis and cell proliferation markers in CTRP6^-/- mice were significantly lower than those in CTRP6^+/+ mice. Conclusions CTRP6 gene is closely related to liver disease development, and the liver fibrosis progression induced by CCl₄ is alleviated by its deletion. The mechanism may be explained as that CTRP6 knockout affects the proliferative capacity of hepatocytes.

Key words: C1q/TNF-related protein 6 (CTRP6), liver fibrosis, carbon tetrachloride (CCl₄), gene expression