CAJ | 학술논문

探讨鼠3型肝炎病毒（MHV-3）诱导的慢性病毒性肝炎C3H/Hej小鼠肝组织白细胞介素-22（IL-22）和细胞因子信号抑制因子3（SOCS3）mRNA水平的变化。方法给C3H/Hej小鼠腹腔注射MHV-3（100 pfu），诱导慢性病毒性肝炎模型，采用实时荧光定量PCR 法检测MHV-3感染后0、5、10、15和20 d时小鼠肝组织IL-22和SOCS3 mRNA水平的变化。结果模型鼠肝组织IL-22和SOC3 mRNA水平在0 d时分别为（0.26±0.15）%和（6.35±2.21）%，在感染后10、15和20 d后IL-22水平分别为（6.28±2.79）%、（2.50±1.24）%和（2.73±0.85）%，SOC3水平分别为（16.92±4.39）%、（14.06±4.09）%和（13.36±1.89）%，均较0 d时显著增高（P<0.05），且在第10 d达到最高峰。结论 IL-22和SOCS3可能参与了MHV-3诱导的小鼠慢性病毒性肝炎的发生发展过程。
탐토서3형간염병독（MHV-3）유도적만성병독성간염C3H/Hej소서간조직백세포개소-22（IL-22）화세포인자신호억제인자3（SOCS3）mRNA수평적변화。방법급C3H/Hej소서복강주사MHV-3（100 pfu），유도만성병독성간염모형，채용실시형광정량PCR 법검측MHV-3감염후0、5、10、15화20 d시소서간조직IL-22화SOCS3 mRNA수평적변화。결과모형서간조직IL-22화SOC3 mRNA수평재0 d시분별위（0.26±0.15）%화（6.35±2.21）%，재감염후10、15화20 d후IL-22수평분별위（6.28±2.79）%、（2.50±1.24）%화（2.73±0.85）%，SOC3수평분별위（16.92±4.39）%、（14.06±4.09）%화（13.36±1.89）%，균교0 d시현저증고（P<0.05），차재제10 d체도최고봉。결론 IL-22화SOCS3가능삼여료MHV-3유도적소서만성병독성간염적발생발전과정。
Objective To investigate the changes of interleukin-22 (IL-22) and suppressor of cytokine signaling 3(SOCS3) mRNA in murine hepatitis virus 3(MHV-3) induced chronic viral hepatitis in C3H/Hej mice. Methods Chronic viral hepatitis in C3H/Hej mice was induced by intra-peritoneal injection of MHV-3 virus at dose of 100pfu. At day 0,5,10,15 and 20 post-infection,IL-22 and SOCS3 mRNA in the liver tissues were detected by real-time PCR. Results IL-22 and SOCS3 mRNA level in livers of model mice at day 0 were (0.26±0.15)%and(6.35±2.21)%,respectively. At day 10,15 and 20,IL-22 mRNA levels in the liver tissues were (6.28±2.79)%, (2.50±1.24)% and (2.73±0.85)%,respectively,and SOCS3 mRNA levels were (16.92±4.39)%,(14.06±4.09)% and (13.36±1.89)%,respectively,all of which were markedly increased than baseline (P﹤0.05). The mRNA levels of IL-22 and SOCS3 both peaked at day 10 post MHV-3 infection. Conclusions IL-22 and SOCS3 may play an important role in the pathogenesis of MHV-3-induced chronic viral hepatitis in mice.