CTRP6 deficiency alleviates CCl4-induced liver fibrosis progression in mice

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.