Establishment And Evaluation On The Model Of Radiation-Induced Hepatic Ifbrosis Of Rat Caused By Once Dose Radiation

Objective：To evaluate the feasibility, rationality and practicability about the model ofradiation-induced liver injury of rat caused by single30Gy dose radiation. And toinvestigate the related cell factors and TGF-β₁/Smads signaling pathways in the role ofradioactive liver fibrosis in rat model.Methods:60SD rats were randomly divided into control group （A group,n=10） and irradiationgroup （B group,n=50）. B group was irradiated fractionally by VARIN21-EX linearacceleratorat at right liver （dose30Gy once）, eight of which were killed on2nd、4th、8th、12thand26thweek after radiation. And A group were sacrificed on4thweekend. Thenwe observed the living appearance of rats, general sample of radiated liver. The bloodand liver of all rats were collected for further examinations. The level of Hyp in livertissue and the serum activities of ALT and AST were detected. The level of TGF-β₁，HA，PC-Ⅲ and LN of blood serum were measured by ELISA, histological change oflivers was observed with hematoxylin-eosin（HE） staining and Masson’s trichromestaining by optical microscopy. Meanwhile, the expression of TGF-beta1、Smad3/4、Smad7、PDGF-BB、TIMP-1and MMP-13proteins was detected by immunohistoch-emistry.Results：Compared with the control group （A group）, Display of radiating hepatitis and liver fibrosis were observed in radiated liver histology of the B group rats. The activities ofAST, ALT and the level of TGF-β₁in serum of the A group rats showed an increasefrom4thweek after the first radiation （P <0.05or P <0.01）, reaching the highest level at8thand12thweek, respectively. The content of HA，PC-Ⅲ and LN in blood serum andHyp in liver tissue of the B group rats have significantly increased from4thweek afterthe first radiation （P <0.05or P <0.01）. Histological change of livers was chronicprogressive liver fibrosis by light microscopy. The expression of TGF-beta1，Smad3/4，PDGF，and TIMP-1protein in liver tissue of the B group rats has significantlyincreased from2ndweek （P <0.05）. The expressions of Smad7and MMP-13in modelgroup were lower er than those of normal control group （P <0.01）.Conclusion：1. The model of radiation-induced liver injury of rat caused once dose radiation is stableand reliable, has lower death rate （15%）, conform to the practice of clinical radiationtherapy.2. Radioactive liver fibrosis and TGF-β₁/Smads signaling pathways exist inner link. Itsone of important mechanism that TGF-β₁/Smads signaling change may causeradioactive hepatic fibrosis.