中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
12期
2811-2813
,共3页
郝永壮%张宇明%高刚%卫小春
郝永壯%張宇明%高剛%衛小春
학영장%장우명%고강%위소춘
肩%肩周炎%糖尿病%病因%退变
肩%肩週炎%糖尿病%病因%退變
견%견주염%당뇨병%병인%퇴변
Shoulder%Periarthritis%Diabetes%Etiology%Degeneration
目的 探讨糖尿病大鼠肩关节病理改变及其形成机制.方法 选取体质量为240～260 g之间的SPF级雄性SD大鼠45只,随机分为两组,即对照组(20只)和模型组(25只).对照组采用维持饲料喂养.模型组持续高糖高脂饲料喂养1个月后,链脲佐菌素(STZ) 30 mg/kg注射诱导建立2型糖尿病模型(T2DM).造模成功后,留取各组大鼠双侧肩关节软骨、滑膜及周围肌肉(包括肌腱)等软组织,行苏木素-伊红(HE)染色,在光镜下观察各部位组织形态学变化;酶联免疫吸附法检测各组血浆及肌肉前列腺素E-2(PGE-2)、转化生长因子-β1(TGF-β1)的含量;样本碱水解法检测肌腱羟脯氨酸(HYP)的含量;逆转录-聚合酶链反应(RT-PCR)检测上述指标mRNA的相对表达量.结果 模型组和对照组肩关节出现病理改变的比例分别为76.19％和10.00％,差异有统计学意义(P＜0.05).两组出现病理改变的关节软骨、滑膜、肌腱的镜下特点基本相似,主要变现为关节软骨面粗糙,部分可见细胞外基质浅层裂开,软骨外观呈丝绒状;滑膜肥厚与纤维化,滑膜细胞肥大增生;肌腱中胶原纤维结构疏松而紊乱,部分断裂.模型组血浆及肌肉PGE-2的含量分别为(39.13±7.72)、(42.18±12.73) ng/L,较对照组(18.86±6.35)、(21.39±7.18)ng/L比较均升高(P＜0.05).模型组血浆及肌肉TGF-β1的含量分别为(23.44 ±7.28)、(29.14 ±7.33) μg/L,较对照组(10.58 ±3.52)、(12.43 ±4.56) μg/L比较均升高(P＜0.05).模型组与对照组肌腱HYP的含量分别为(119.42 ±27.18)、(64.19±10.45)μg/g,两者比较差异有统计学意义(P＜0.05).模型组软组织中TGF-β1、PGE-2及HYP mRNA的相对表达量分别为5.78±0.90、8.29±1.76、13.89±3.18,明显高于对照组的1.89±0.27、3.06 ±0.60、7.22±2.05,差异有统计学意义(P＜0.05).结论 T2DM可导致大鼠肩关节软骨、滑膜及周围肌肉等软组织出现炎性改变及纤维化,与肩周炎肩周软组织自然退变病理特点一致,可认为是肩周炎的成因之一.
目的 探討糖尿病大鼠肩關節病理改變及其形成機製.方法 選取體質量為240～260 g之間的SPF級雄性SD大鼠45隻,隨機分為兩組,即對照組(20隻)和模型組(25隻).對照組採用維持飼料餵養.模型組持續高糖高脂飼料餵養1箇月後,鏈脲佐菌素(STZ) 30 mg/kg註射誘導建立2型糖尿病模型(T2DM).造模成功後,留取各組大鼠雙側肩關節軟骨、滑膜及週圍肌肉(包括肌腱)等軟組織,行囌木素-伊紅(HE)染色,在光鏡下觀察各部位組織形態學變化;酶聯免疫吸附法檢測各組血漿及肌肉前列腺素E-2(PGE-2)、轉化生長因子-β1(TGF-β1)的含量;樣本堿水解法檢測肌腱羥脯氨痠(HYP)的含量;逆轉錄-聚閤酶鏈反應(RT-PCR)檢測上述指標mRNA的相對錶達量.結果 模型組和對照組肩關節齣現病理改變的比例分彆為76.19％和10.00％,差異有統計學意義(P＜0.05).兩組齣現病理改變的關節軟骨、滑膜、肌腱的鏡下特點基本相似,主要變現為關節軟骨麵粗糙,部分可見細胞外基質淺層裂開,軟骨外觀呈絲絨狀;滑膜肥厚與纖維化,滑膜細胞肥大增生;肌腱中膠原纖維結構疏鬆而紊亂,部分斷裂.模型組血漿及肌肉PGE-2的含量分彆為(39.13±7.72)、(42.18±12.73) ng/L,較對照組(18.86±6.35)、(21.39±7.18)ng/L比較均升高(P＜0.05).模型組血漿及肌肉TGF-β1的含量分彆為(23.44 ±7.28)、(29.14 ±7.33) μg/L,較對照組(10.58 ±3.52)、(12.43 ±4.56) μg/L比較均升高(P＜0.05).模型組與對照組肌腱HYP的含量分彆為(119.42 ±27.18)、(64.19±10.45)μg/g,兩者比較差異有統計學意義(P＜0.05).模型組軟組織中TGF-β1、PGE-2及HYP mRNA的相對錶達量分彆為5.78±0.90、8.29±1.76、13.89±3.18,明顯高于對照組的1.89±0.27、3.06 ±0.60、7.22±2.05,差異有統計學意義(P＜0.05).結論 T2DM可導緻大鼠肩關節軟骨、滑膜及週圍肌肉等軟組織齣現炎性改變及纖維化,與肩週炎肩週軟組織自然退變病理特點一緻,可認為是肩週炎的成因之一.
목적 탐토당뇨병대서견관절병리개변급기형성궤제.방법 선취체질량위240～260 g지간적SPF급웅성SD대서45지,수궤분위량조,즉대조조(20지)화모형조(25지).대조조채용유지사료위양.모형조지속고당고지사료위양1개월후,련뇨좌균소(STZ) 30 mg/kg주사유도건립2형당뇨병모형(T2DM).조모성공후,류취각조대서쌍측견관절연골、활막급주위기육(포괄기건)등연조직,행소목소-이홍(HE)염색,재광경하관찰각부위조직형태학변화;매련면역흡부법검측각조혈장급기육전렬선소E-2(PGE-2)、전화생장인자-β1(TGF-β1)적함량;양본감수해법검측기건간포안산(HYP)적함량;역전록-취합매련반응(RT-PCR)검측상술지표mRNA적상대표체량.결과 모형조화대조조견관절출현병리개변적비례분별위76.19％화10.00％,차이유통계학의의(P＜0.05).량조출현병리개변적관절연골、활막、기건적경하특점기본상사,주요변현위관절연골면조조,부분가견세포외기질천층렬개,연골외관정사융상;활막비후여섬유화,활막세포비대증생;기건중효원섬유결구소송이문란,부분단렬.모형조혈장급기육PGE-2적함량분별위(39.13±7.72)、(42.18±12.73) ng/L,교대조조(18.86±6.35)、(21.39±7.18)ng/L비교균승고(P＜0.05).모형조혈장급기육TGF-β1적함량분별위(23.44 ±7.28)、(29.14 ±7.33) μg/L,교대조조(10.58 ±3.52)、(12.43 ±4.56) μg/L비교균승고(P＜0.05).모형조여대조조기건HYP적함량분별위(119.42 ±27.18)、(64.19±10.45)μg/g,량자비교차이유통계학의의(P＜0.05).모형조연조직중TGF-β1、PGE-2급HYP mRNA적상대표체량분별위5.78±0.90、8.29±1.76、13.89±3.18,명현고우대조조적1.89±0.27、3.06 ±0.60、7.22±2.05,차이유통계학의의(P＜0.05).결론 T2DM가도치대서견관절연골、활막급주위기육등연조직출현염성개변급섬유화,여견주염견주연조직자연퇴변병리특점일치,가인위시견주염적성인지일.
Objective To explore the pathological changes and its formation mechanism in the shoulder joint of diabetic rats.Methods The 45 SPF male SD rats that weighing between 240 and 260 gram were randomly divided into two groups namely the control group (20) and the model group (25).The control group maintained by general diet.The model group fed with high sugar and high fat diet for 1 month,after that streptozocin (STZ) 30 mg/kg were injected into rats aiming to induce the model of type 2 diabetes (T2DM).After the success of modeling,take specimens from each rat group with bilateral shoulder cartilage,synovial membrane,surrounding muscles (including tendons),and other soft tissues,observe morphologic-al changes of specimens under light microscopy after HE staining.Enzyme-linked immunosorbent assay was used to detect the prostaglandin E-2 (PGE-2) of plasma and muscle,and also transforming growth factor-beta 1 (TGF-β1) levels; sample based hydrolysis to detect tendon hydroxyproline (HYP) content; the expression of the above indicators relative mRNA were detected by reverse transcriptase-polymerase chain reaction (RT-PCR).Results The shoulder pathological changes of model group and control group were 76.19％ and 10.00％ respectively,the difference was statistically significant (P ＜ 0.05).The pathological changes of articular cartilage,synovial membrane and tendons observed under microscope are similar,the main features are articular cartilage surface roughness,partly visible shallow crack of the extracellular matrix,velvet-like appearance of cartilage ; Synovial hypertrophy and fibrosis,synovial cell hypertrophy and the structure of tendon collagen fiber is loose,disorder and partial rupture.The PGE-2 content of plasma and muscle in model group were (39.13 ± 7.72),(42.18 ± 12.73) ng/L respectively,compared with the control group (18.86 ±6.35),(21.39 ±7.18) ng/L respectively,were increased (P ＜0.05).The TGF-β1 level of plasma and muscle in model group were (23.44 ± 7.28),(29.14 ± 7.33) μg/L respectively,compared with the control group (10.58 ± 3.52),(12.43 ± 4.56) μg/L respectively,were elevated (P ＜0.05).The HYP content of model group and control group were (119.42 ± 27.18),(64.19 ± 10.45) μg/g respectively,the difference was statistically significant (P ＜ 0.05).TGF-β1,PGE-2 and HYP mRNA expression of soft tissue in model group were 5.78 ± 0.90,8.29 ± 1.76,13.89 ±3.18 respectively,significantly higher than the control group (1.89 ±0.27,3.06 ± 0.60,7.22 ± 2.05),the difference was statistically significant (P ＜ 0.05).Conclusion Type 2 diabetes can result in inflammatory changes and fibrosis of rat shoulder cartilage,synovial membrane,surrounding muscles and other soft tissues.The above pathological features are consistent with the natural degeneration of shoulder soft tissue and periarthritis.Therefore,type 2 diabetes can be considered as one of the causes of periarthritis.
