中华地方病学杂志
中華地方病學雜誌
중화지방병학잡지
Chinese Journal of Endemiology
2014年
4期
363-366
,共4页
陈晨%陈静宏%曹峻岭%王伟%张增铁%杨占田%于伯泉%马天有
陳晨%陳靜宏%曹峻嶺%王偉%張增鐵%楊佔田%于伯泉%馬天有
진신%진정굉%조준령%왕위%장증철%양점전%우백천%마천유
大骨节病%软骨%白细胞介素-1β%白细胞介素-6%肿瘤坏死因子-α
大骨節病%軟骨%白細胞介素-1β%白細胞介素-6%腫瘤壞死因子-α
대골절병%연골%백세포개소-1β%백세포개소-6%종류배사인자-α
Kashin-Beck disease%Cartilage%Interleukin-1β%Interleukin-6%Tumor necrosis factor alpha
目的:通过检测大骨节病儿童软骨细胞中白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)的表达,探讨细胞因子与大骨节病(KBD)之间的关系。方法5例KBD儿童(KBD组)手指软骨组织来自西安交通大学医学院地方病研究所保存的大骨节病患儿尸检样本;5例正常儿童(对照组)手指软骨组织来自陕西省西安市非KBD病区,其中3例来自车祸死亡儿童,2例为先天6指畸形手术标本。采用免疫组织化学染色的方法,分别检测软骨中IL-1β、IL-6、TNF-α的表达;并将关节软骨细胞分层(表层、中层、深层),分析软骨各层中IL-1β、IL-6、TNF-α的表达。结果 KBD组关节软骨表层、中层、深层IL-1β阳性软骨细胞密度(63.50±7.19、54.75±5.50、66.20±9.91)均高于对照组(5.75±1.26、0.00±0.00、0.00±0.00,P均<0.05);KBD组关节软骨表层IL-6阳性软骨细胞密度(55.25±6.24)高于对照组(0.00±0.00,P<0.05);KBD组关节软骨表层、中层、深层TNF-α阳性软骨细胞密度(33.25±6.50、3.75±0.96、29.80±1.92)均高于对照组(3.74±0.82、0.00±0.00、0.00±0.00,P均<0.05)。结论 KBD儿童软骨细胞中IL-1β,IL-6和TNF-α表达显著升高,细胞因子的过量表达可能参与KBD软骨细胞死亡与软骨破坏过程。
目的:通過檢測大骨節病兒童軟骨細胞中白細胞介素-1β(IL-1β)、白細胞介素-6(IL-6)、腫瘤壞死因子-α(TNF-α)的錶達,探討細胞因子與大骨節病(KBD)之間的關繫。方法5例KBD兒童(KBD組)手指軟骨組織來自西安交通大學醫學院地方病研究所保存的大骨節病患兒尸檢樣本;5例正常兒童(對照組)手指軟骨組織來自陝西省西安市非KBD病區,其中3例來自車禍死亡兒童,2例為先天6指畸形手術標本。採用免疫組織化學染色的方法,分彆檢測軟骨中IL-1β、IL-6、TNF-α的錶達;併將關節軟骨細胞分層(錶層、中層、深層),分析軟骨各層中IL-1β、IL-6、TNF-α的錶達。結果 KBD組關節軟骨錶層、中層、深層IL-1β暘性軟骨細胞密度(63.50±7.19、54.75±5.50、66.20±9.91)均高于對照組(5.75±1.26、0.00±0.00、0.00±0.00,P均<0.05);KBD組關節軟骨錶層IL-6暘性軟骨細胞密度(55.25±6.24)高于對照組(0.00±0.00,P<0.05);KBD組關節軟骨錶層、中層、深層TNF-α暘性軟骨細胞密度(33.25±6.50、3.75±0.96、29.80±1.92)均高于對照組(3.74±0.82、0.00±0.00、0.00±0.00,P均<0.05)。結論 KBD兒童軟骨細胞中IL-1β,IL-6和TNF-α錶達顯著升高,細胞因子的過量錶達可能參與KBD軟骨細胞死亡與軟骨破壞過程。
목적:통과검측대골절병인동연골세포중백세포개소-1β(IL-1β)、백세포개소-6(IL-6)、종류배사인자-α(TNF-α)적표체,탐토세포인자여대골절병(KBD)지간적관계。방법5례KBD인동(KBD조)수지연골조직래자서안교통대학의학원지방병연구소보존적대골절병환인시검양본;5례정상인동(대조조)수지연골조직래자합서성서안시비KBD병구,기중3례래자차화사망인동,2례위선천6지기형수술표본。채용면역조직화학염색적방법,분별검측연골중IL-1β、IL-6、TNF-α적표체;병장관절연골세포분층(표층、중층、심층),분석연골각층중IL-1β、IL-6、TNF-α적표체。결과 KBD조관절연골표층、중층、심층IL-1β양성연골세포밀도(63.50±7.19、54.75±5.50、66.20±9.91)균고우대조조(5.75±1.26、0.00±0.00、0.00±0.00,P균<0.05);KBD조관절연골표층IL-6양성연골세포밀도(55.25±6.24)고우대조조(0.00±0.00,P<0.05);KBD조관절연골표층、중층、심층TNF-α양성연골세포밀도(33.25±6.50、3.75±0.96、29.80±1.92)균고우대조조(3.74±0.82、0.00±0.00、0.00±0.00,P균<0.05)。결론 KBD인동연골세포중IL-1β,IL-6화TNF-α표체현저승고,세포인자적과량표체가능삼여KBD연골세포사망여연골파배과정。
Objective To investigate the expressions of interleukin-1β(IL-1β), interleukin-6(IL-6) and tumor necrosis factor alpha(TNF-α) in cartilage of children with Kashin-Beck disease(KBD) in order to provide a possible mechanism of the disease. Methods Articular cartilage tissues of 5 KBD children(KBD group) were selected from KBD children autopsy samples keeping in Institute of Endemic Diseases, Medical School of Xi’an Jiaotong University; articular cartilage tissues of 5 normal children ( control group ) were selected from non-KBD areas of Shaanxi Province, three cases were from accident death children, two cases were the samples of congential malformation of six finger. Expressions of IL-1β, IL-6 and TNF-α in the cartilage were detected using immunohistochemistry; the cells of articular cartilage were divided into three areas (superficial zone, middle zone and deep zone) to analyze the expressions of IL-1β, IL-6 and TNF-α. Results The expressions of IL-1β in superficial zone , middle zone and deep zone of articular cartilage of KBD group (63.50 ± 7.19, 54.75 ± 5.50, 66.20 ± 9.91) were significantly higher than those of control group(5.75 ± 1.26, 0.00 ± 0.00, 0.00 ± 0.00, all P<0.05). The expression of IL-6 in superficial zone of articular cartilage in KBD group(55.25 ± 6.24) was significantly higher than that of control group(0.00 ± 0.00, P<0.05). The expressions of TNF-αin all zone of articular cartilage of KBD group(33.25 ± 6.50, 3.75 ± 0.96, 29.80 ± 1.92) were significantly higher than those of control group (3.74 ± 0.82, 0.00 ± 0.00, 0.00 ± 0.00, all P < 0.05). Conclusion The levels of IL-1β, IL-6 and TNF-α are up-regulated in articular cartilage of KBD children, suggesting that cytokines may play an important role in matrix degradation in KBD children cartilage.