CAJ | 학술논문

目的观察细胞因子信号转导抑制因子3(SOCS3)基因对慢性排斥反应的影响.方法建立小鼠同种异体腹主动脉移植模型,分为对照组、Ad-GFP组和Ad-SOCS3组.分别于术后24h经尾静脉注射100μl无菌磷酸盐缓冲液(PBS)注射液、空白和编码SOCS3基因的腺病毒载体.术后分批获取动脉移植物、脾脏标本,用于组织学、逆转录-聚合酶链反应(RT-PCR)、混合淋巴细胞反应强度(MLR)检测.结果 SOCS3基因转染可明显增强移植动脉内SOCS3 mRNA表达(P＜0.05).Ad-SOCS3组移植动脉狭窄率明显降低[(19.62±2.91)％、(35.67±4.72)％和(38.21±3.59)％,P＜0.05].该组移植动脉内转录信号转导子与激活子3(STAT3) mRNA、干扰素(IFN)-γmRNA、白细胞介素(IL)-6 mRNA、血管细胞间黏附分子-1(VCAM-1)mRNA表达明显下调(P＜0.01),MLR明显减弱(P＜0.05).结论腺病毒载体介导的供体SOCS3基因转染能够抑制移植动脉慢性排斥反应.
목적 관찰세포인자신호전도억제인자3(SOCS3)기인대만성배척반응적영향.방법 건립소서동충이체복주동맥이식모형,분위대조조、Ad-GFP조화Ad-SOCS3조.분별우술후24h경미정맥주사100μl무균린산염완충액(PBS)주사액、공백화편마SOCS3기인적선병독재체.술후분비획취동맥이식물、비장표본,용우조직학、역전록-취합매련반응(RT-PCR)、혼합림파세포반응강도(MLR)검측.결과 SOCS3기인전염가명현증강이식동맥내SOCS3 mRNA표체(P＜0.05).Ad-SOCS3조이식동맥협착솔명현강저[(19.62±2.91)％、(35.67±4.72)％화(38.21±3.59)％,P＜0.05].해조이식동맥내전록신호전도자여격활자3(STAT3) mRNA、간우소(IFN)-γmRNA、백세포개소(IL)-6 mRNA、혈관세포간점부분자-1(VCAM-1)mRNA표체명현하조(P＜0.01),MLR명현감약(P＜0.05).결론 선병독재체개도적공체SOCS3기인전염능구억제이식동맥만성배척반응.
Objective To investigate the effect of suppressors of cytokine signaling 3 (SOCS3) on chronic rejection.Methods The mouse model of artery allograft was developed,which were randomly assigned to 3 groups:(1) The control group,(2) Ad-SOCS3 group,(3) Ad-GFP group.24 hours after operation,100 μl sterile phosphate buffer (PBS) injection,1 × 109 pfu the recombinant adenovirus vector carrying mouse SOCS3 gene and green fluorescent protein (GFP) reported gene were injected by tail vein,respectively.The mouse of each groups were sacrificed in batches.The grafts were used for reverse transcription-polymerase chain reaction (RT-PCR) and histological detected.And the spleens were used for mixed lymphocyte reaction (MLR).Results To transfect with Ad-SOCS3 can enhance the SOCS3 mRNA expression in the graft significantly,compared with the control and Ad-GFP groups.The stenosis rate of the graft were (19.62 ± 2.91) ％ in Ad-SOCS3 group,which were significantly down-regulated,compared with (35.67 ± 4.72) ％ and (38.21 ± 3.59) ％ in the control and Ad-GFP groups (P ＜ 0.05).The expression of mRNA of signa i transducers and activators of transcription 3 (STAT3),interferon (IFN)-γ,interleukin (IL)-6,VCAM-1 were significantly down-regulated in Ad-SOCS3 group,compared with the control and Ad-GFP groups (P ＜ 0.01).The MLR was significantly down-regulated in Ad-SOCS3 group,compared with the control and Ad-GFP groups (P ＜ 0.05).Conclusion To transfect SOCS3 gene by adenovirus vector can inhibit the chronic rejection of allograft in mice abdominal aorta transplantation model.