中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2014年
18期
2806-2811
,共6页
宗少晖%方晔%彭金珍%高太行
宗少暉%方曄%彭金珍%高太行
종소휘%방엽%팽금진%고태행
实验动物%组织构建%白细胞介素1β%白细胞介素6%白细胞介素17%p-STAT3%脊髓损伤
實驗動物%組織構建%白細胞介素1β%白細胞介素6%白細胞介素17%p-STAT3%脊髓損傷
실험동물%조직구건%백세포개소1β%백세포개소6%백세포개소17%p-STAT3%척수손상
spinal cord injuries%interleukin-1 beta%interleukin-6%interleukin-17
背景:研究提示脊髓损伤早期神经元和神经胶质细胞分泌产生的细胞因子可能是造成损伤后继发免疫损伤的重要因素。<br> 目的:分析白细胞介素1β、白细胞介素6、白细胞介素17等炎症因子在急性脊髓损伤后炎症反应过程中的作用。<br> 方法:雄性成年SD大鼠75只,随机分为对照组和脊髓损伤1,6,24和72 h组。采用改良Al en氏法建立脊髓不完全损伤模型,对照组仅行椎板全切除。在建模之后相应的时间点获取损伤段脊髓、脾脏组织,免疫组织化学染色法检测白细胞介素6和白细胞介素17在损伤段脊髓组织中的分布及表达情况,蛋白免疫印迹法检测p-STAT3在损伤段脊髓组织中的表达变化,采用RT-PCR法检测白细胞介素1β mRNA、白细胞介素6 mRNA和白细胞介素17A mRNA在脾脏组织中的表达情况。<br> 结果与结论:脊髓损伤后p-STAT3、白细胞介素1β、白细胞介素6和白细胞介素17的表达明显高于对照组(P <0.05)。损伤后炎症因子表达量立即升高,白细胞介素1β和白细胞介素6在损伤后6 h到达高峰,随后开始下降;p-STAT3和白细胞介素17在损伤后24 h到达高峰,随后开始下降,至损伤后72 h表达量仍高于对照组。结果表明损伤早期p-STAT3介导的促炎因子白细胞介素1β和白细胞介素6表达增加,提示可能导致损伤区域炎症级联放大,诱导继发性脊髓损伤;促炎因子白细胞介素17的异常升高,提示可能在继发性损伤炎症反应中起着重要作用。
揹景:研究提示脊髓損傷早期神經元和神經膠質細胞分泌產生的細胞因子可能是造成損傷後繼髮免疫損傷的重要因素。<br> 目的:分析白細胞介素1β、白細胞介素6、白細胞介素17等炎癥因子在急性脊髓損傷後炎癥反應過程中的作用。<br> 方法:雄性成年SD大鼠75隻,隨機分為對照組和脊髓損傷1,6,24和72 h組。採用改良Al en氏法建立脊髓不完全損傷模型,對照組僅行椎闆全切除。在建模之後相應的時間點穫取損傷段脊髓、脾髒組織,免疫組織化學染色法檢測白細胞介素6和白細胞介素17在損傷段脊髓組織中的分佈及錶達情況,蛋白免疫印跡法檢測p-STAT3在損傷段脊髓組織中的錶達變化,採用RT-PCR法檢測白細胞介素1β mRNA、白細胞介素6 mRNA和白細胞介素17A mRNA在脾髒組織中的錶達情況。<br> 結果與結論:脊髓損傷後p-STAT3、白細胞介素1β、白細胞介素6和白細胞介素17的錶達明顯高于對照組(P <0.05)。損傷後炎癥因子錶達量立即升高,白細胞介素1β和白細胞介素6在損傷後6 h到達高峰,隨後開始下降;p-STAT3和白細胞介素17在損傷後24 h到達高峰,隨後開始下降,至損傷後72 h錶達量仍高于對照組。結果錶明損傷早期p-STAT3介導的促炎因子白細胞介素1β和白細胞介素6錶達增加,提示可能導緻損傷區域炎癥級聯放大,誘導繼髮性脊髓損傷;促炎因子白細胞介素17的異常升高,提示可能在繼髮性損傷炎癥反應中起著重要作用。
배경:연구제시척수손상조기신경원화신경효질세포분비산생적세포인자가능시조성손상후계발면역손상적중요인소。<br> 목적:분석백세포개소1β、백세포개소6、백세포개소17등염증인자재급성척수손상후염증반응과정중적작용。<br> 방법:웅성성년SD대서75지,수궤분위대조조화척수손상1,6,24화72 h조。채용개량Al en씨법건립척수불완전손상모형,대조조부행추판전절제。재건모지후상응적시간점획취손상단척수、비장조직,면역조직화학염색법검측백세포개소6화백세포개소17재손상단척수조직중적분포급표체정황,단백면역인적법검측p-STAT3재손상단척수조직중적표체변화,채용RT-PCR법검측백세포개소1β mRNA、백세포개소6 mRNA화백세포개소17A mRNA재비장조직중적표체정황。<br> 결과여결론:척수손상후p-STAT3、백세포개소1β、백세포개소6화백세포개소17적표체명현고우대조조(P <0.05)。손상후염증인자표체량립즉승고,백세포개소1β화백세포개소6재손상후6 h도체고봉,수후개시하강;p-STAT3화백세포개소17재손상후24 h도체고봉,수후개시하강,지손상후72 h표체량잉고우대조조。결과표명손상조기p-STAT3개도적촉염인자백세포개소1β화백세포개소6표체증가,제시가능도치손상구역염증급련방대,유도계발성척수손상;촉염인자백세포개소17적이상승고,제시가능재계발성손상염증반응중기착중요작용。
BACKGROUND:Cytokines secreted from neurons and glial cel s in early stage of spinal cord injury probably are essential factors for inducing secondary immunologic injury. <br> OBJECTIVE:To investigate the effects of interleukin-1β, interleukin-6 and interleukin-17 on inflammatory reaction after acute spinal cord injury. <br> METHODS:A total of 75 adult male Sprague-Dawley rats were randomly divided into control group and the spinal cord injury groups:1, 6, 24 and 72 hours. A rat model of incomplete spinal cord injury was established by the modified Al en weight drop method. The control group just underwent laminectomy. Injured spinal cord and spleen tissues were col ected at corresponding time points after model induction. Immunohistochemical staining was used to detect the distribution and expressions of interleukin-6 and interleukin-17 in spinal cord tissue. Western blot assay was utilized to detect the changes in p-STAT3 expression in injured spinal cord. RT-PCR was applied to measure the mRNA expression of interleukin-1β, interleukin-6 and interleukin-17 in the spleen. <br> RESULTS AND CONCLUSION:The expression levels of p-STAT3, interleukin-1β, interleukin-6, and interleukin-17 were significantly higher in the spinal cord injury groups than those in the control group (P<0.05). The expression of inflammatory cytokines increased immediately after injury. Interleukin-1βand interleukin-6 levels peaked at 6 hours, and then decreased. p-STAT3 and interleukin-17 levels peaked at 24 hours, and then decreased. The expression was stil higher at 72 hours than that in the control group. Results suggested that the expression of p-STAT3-mediated pro-inflammatory cytokines interleukin-1βand interleukin-6 in early stage increased. Inflammatory cascade would enlarge in the injured area, which probably induced secondary spinal cord injury and increased interleukin-17 levels. These possibly played a key role in secondary inflammatory reaction.