This study assesses the role of inhibitory receptor FcγRIIB in the occurrence and development of HCC,which lays the foundation for exploring the regulatory mechanism of hepatic inflammation-induced carcinogene-sis.FcγRIIB(129Sv)gene knockout mice were hybridized with C57BL/6 mice,and the genotype of the offspring mice was identified by PCR.The chemical carcinogen DEN was used to induce the mice HCC,the survival time,number of liver tumors,and liver weight index were compared between FcγRIIB-/-mice and WT mice.The mor-phology of hepatocytes in the two groups of mice was observed by H&E staining.The levels of CIC in the serum of two groups of mice were compared by PEG precipitation turbidimetry.The homozygous mice with FcγRIIB dele-tion of C57BL/6 strain(FcγRIIB-/-mice)were successfully obtained.In the DEN-induced mice HCC model,the survival rate of FcγRIIB-/-mice was significantly lower than that of WT mice,and the number of liver tumors and liver weight index in FcγRIIB-/-mice were significantly higher than those in WT mice.The results of H&E staining showed that the hepatocytes of FcγRIIB-/-mice were arranged in disorder with obvious heteromor-phism,and multinuclear tumor cells and inflammatory cell infiltration were observed.The results of PEG precipi-tation turbidimetry showed that the levels of CIC in the serum of FcγRIIB-/-mice were significantly higher than that of WT mice.This study suggests that FcγRIIB deletion can promote the development of DEN-induced HCC in mice and FcγRIIB may play an important role in the hepatic inflammation-induced carcinogenesis.
维普
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