中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2006年
4期
630-633
,共4页
涂胜豪%胡永红%翁庚民%陆付耳%张明敏%赖先阳%刘沛霖
塗勝豪%鬍永紅%翁庚民%陸付耳%張明敏%賴先暘%劉沛霖
도성호%호영홍%옹경민%륙부이%장명민%뢰선양%류패림
雷公藤甲素%滑膜%细胞凋亡%关节炎,实验性
雷公籐甲素%滑膜%細胞凋亡%關節炎,實驗性
뢰공등갑소%활막%세포조망%관절염,실험성
Triptolide%Synovial membrane%Apoptosis%Arthritis,experimental
目的:以胶原诱导的关节炎(CIA)为动物模型,探讨雷公藤甲素能否诱导CIA大鼠滑膜细胞凋亡.方法:选用雄性Wistar大鼠造模,将造模成功的大鼠随机分为模型组和雷公藤甲素组.雷公藤甲素按40μg/kg BW,肌注给药,每3 d 1次.凋亡检测:给药31 d后处死,取膝关节滑膜,作苏木素-伊红染色(HE)、电镜、缺口末端标记法(TUNEL)标记及流式细胞仪检测.结果:电镜下可见早期阶段的滑膜凋亡细胞.流式细胞仪检测结果显示:正常组、模型组、雷公藤甲素组的凋亡细胞分别为(0.87±0.24)%、(1.83±0.82)%和(3.98±1.16)%.正常组、模型组、雷公藤甲素组的S期细胞分别为(3.4±0.7)%、(8.0±1.4)%和(3.3±1.2)%.雷公藤甲素组与模型组比较差异均显著(P<0.01).TUNEL标记结果显示:正常组、模型组、雷公藤甲素组的凋亡细胞分别为(1.0±0.4)%、(2.2±1.0)%和(4.5±0.9)%,雷公藤甲素组与模型组的差异显著(P<0.01).结论:本实验首次阐明了雷公藤甲素可诱导CIA大鼠滑膜细胞的凋亡.
目的:以膠原誘導的關節炎(CIA)為動物模型,探討雷公籐甲素能否誘導CIA大鼠滑膜細胞凋亡.方法:選用雄性Wistar大鼠造模,將造模成功的大鼠隨機分為模型組和雷公籐甲素組.雷公籐甲素按40μg/kg BW,肌註給藥,每3 d 1次.凋亡檢測:給藥31 d後處死,取膝關節滑膜,作囌木素-伊紅染色(HE)、電鏡、缺口末耑標記法(TUNEL)標記及流式細胞儀檢測.結果:電鏡下可見早期階段的滑膜凋亡細胞.流式細胞儀檢測結果顯示:正常組、模型組、雷公籐甲素組的凋亡細胞分彆為(0.87±0.24)%、(1.83±0.82)%和(3.98±1.16)%.正常組、模型組、雷公籐甲素組的S期細胞分彆為(3.4±0.7)%、(8.0±1.4)%和(3.3±1.2)%.雷公籐甲素組與模型組比較差異均顯著(P<0.01).TUNEL標記結果顯示:正常組、模型組、雷公籐甲素組的凋亡細胞分彆為(1.0±0.4)%、(2.2±1.0)%和(4.5±0.9)%,雷公籐甲素組與模型組的差異顯著(P<0.01).結論:本實驗首次闡明瞭雷公籐甲素可誘導CIA大鼠滑膜細胞的凋亡.
목적:이효원유도적관절염(CIA)위동물모형,탐토뢰공등갑소능부유도CIA대서활막세포조망.방법:선용웅성Wistar대서조모,장조모성공적대서수궤분위모형조화뢰공등갑소조.뢰공등갑소안40μg/kg BW,기주급약,매3 d 1차.조망검측:급약31 d후처사,취슬관절활막,작소목소-이홍염색(HE)、전경、결구말단표기법(TUNEL)표기급류식세포의검측.결과:전경하가견조기계단적활막조망세포.류식세포의검측결과현시:정상조、모형조、뢰공등갑소조적조망세포분별위(0.87±0.24)%、(1.83±0.82)%화(3.98±1.16)%.정상조、모형조、뢰공등갑소조적S기세포분별위(3.4±0.7)%、(8.0±1.4)%화(3.3±1.2)%.뢰공등갑소조여모형조비교차이균현저(P<0.01).TUNEL표기결과현시:정상조、모형조、뢰공등갑소조적조망세포분별위(1.0±0.4)%、(2.2±1.0)%화(4.5±0.9)%,뢰공등갑소조여모형조적차이현저(P<0.01).결론:본실험수차천명료뢰공등갑소가유도CIA대서활막세포적조망.
AIM: To determine whether triptolide induce apoptosis of synovial cells in collagen - induced arthritis(CIA) in rats. METHODS: The male Wistar rats were used to make CIA models by immunized with Bovine collagen Ⅱ ( BC Ⅱ )in Freund's complete adjuvant (FCA). A total of 20 CIA rats were randomly divided into 2 groups, triptolide group (10 rats) and CIA control group (10 rats). Triptolide group were administered with triptolide at 40 μg/kg body weight intramuscularly every three days. CIA control group andanother 10 age - matched normal rats were given normal saline instead. The rats were sacrificed on the 31st day after the triptolide administration. The pieces of synovium of the rat knee joints were harvested. The synovium was examined by HE staining and electron microscope. The apoptosis was tested by TUNEL and flow cytometer. RESULTS: The earlier phase of apoptotic synoviocytes were observed under the electron microscope. The flow cytometry showed that the percentage of the apoptotic cells was (3.98 ± 1.16)% in the triptolide group, (1.83 ± 0.82)% in the CIA control group, and (0.87 ±0.24)% in the normal group (P<0.01: triptolide vs control group). While the percentage of the cells in DNA synthesis phase was (3.3± 1.2)% in the triptolide goup, (8.0± 1.4)% in the CIA control group, and (3.4 ± 0.7)% in the normal group.There is significantly different in the apoptosis changes between the triptolide group and the CIA control group ( P < 0.01: triptolide vs CIA control group). The TUNEL labeling demonstrated that the percentage of the apoptotic cells was (4.5 ± 1.0)% in the triptolide group, (2.2 ± 1.0) % in the CIA control group, and ( 1.0 ± 0.4) % in the normal group. The difference of apoptotic rate between the triptolide group and the CIA control group is significant ( P < 0.01). CONCLUSION: This study demonstrates that triptolide can induce apoptosis in CIA rats, which may be one of the mechanisms that triptolide treats the rheumatoid arthritis.