中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2001年
6期
510-514
,共5页
何贤辉%曾耀英%李振%徐丽慧%孙荭%曾洁铭
何賢輝%曾耀英%李振%徐麗慧%孫葒%曾潔銘
하현휘%증요영%리진%서려혜%손홍%증길명
棉酚%T淋巴细胞%流式细胞术
棉酚%T淋巴細胞%流式細胞術
면분%T림파세포%류식세포술
目的:以体外培养的人外周血单个核细胞为材料,研究多酚类抗生育药物棉酚对正常人外周血T淋巴细胞体外活化作用的影响。方法:利用双荧光染色流式细胞术分析棉酚对人T淋巴细胞在丝裂原或佛波醇酯刺激下早期活化抗原CD69表达的影响。结果: 100 μmol/L的棉酚预先与T细胞温育,能完全抑制10 mg/L植物血凝素(PHA)刺激的CD3+T细胞活化抗原CD69的表达,又可阻断10-7 mol/L佛波醇酯(PDB)对T细胞的活化作用。这种抑制作用呈剂量依赖性,棉酚对PDB及PHA抑制作用的IC50分别为(35.7±2.9) μmol/L和(32.8±1.5) μmol/L。此外,棉酚对CD3-的淋巴细胞CD69表达也有类似的抑制作用。然而,它对多克隆激活剂引起的T细胞表面分子CD3的下调无明显影响。结论:在体外活化模型中,棉酚能够同时抑制多克隆激活剂PHA和PDB对T细胞的活化作用,提示其作用部位可能位于PKC或下游,并提示棉酚具有潜在的免疫调节作用。
目的:以體外培養的人外週血單箇覈細胞為材料,研究多酚類抗生育藥物棉酚對正常人外週血T淋巴細胞體外活化作用的影響。方法:利用雙熒光染色流式細胞術分析棉酚對人T淋巴細胞在絲裂原或彿波醇酯刺激下早期活化抗原CD69錶達的影響。結果: 100 μmol/L的棉酚預先與T細胞溫育,能完全抑製10 mg/L植物血凝素(PHA)刺激的CD3+T細胞活化抗原CD69的錶達,又可阻斷10-7 mol/L彿波醇酯(PDB)對T細胞的活化作用。這種抑製作用呈劑量依賴性,棉酚對PDB及PHA抑製作用的IC50分彆為(35.7±2.9) μmol/L和(32.8±1.5) μmol/L。此外,棉酚對CD3-的淋巴細胞CD69錶達也有類似的抑製作用。然而,它對多剋隆激活劑引起的T細胞錶麵分子CD3的下調無明顯影響。結論:在體外活化模型中,棉酚能夠同時抑製多剋隆激活劑PHA和PDB對T細胞的活化作用,提示其作用部位可能位于PKC或下遊,併提示棉酚具有潛在的免疫調節作用。
목적:이체외배양적인외주혈단개핵세포위재료,연구다분류항생육약물면분대정상인외주혈T림파세포체외활화작용적영향。방법:이용쌍형광염색류식세포술분석면분대인T림파세포재사렬원혹불파순지자격하조기활화항원CD69표체적영향。결과: 100 μmol/L적면분예선여T세포온육,능완전억제10 mg/L식물혈응소(PHA)자격적CD3+T세포활화항원CD69적표체,우가조단10-7 mol/L불파순지(PDB)대T세포적활화작용。저충억제작용정제량의뢰성,면분대PDB급PHA억제작용적IC50분별위(35.7±2.9) μmol/L화(32.8±1.5) μmol/L。차외,면분대CD3-적림파세포CD69표체야유유사적억제작용。연이,타대다극륭격활제인기적T세포표면분자CD3적하조무명현영향。결론:재체외활화모형중,면분능구동시억제다극륭격활제PHA화PDB대T세포적활화작용,제시기작용부위가능위우PKC혹하유,병제시면분구유잠재적면역조절작용。
AIM: Peripheral blood mononuclear cells (PBMC) were cultured in vitro to study the effect of gossypol, a polyphenolic antifertility agent, on the activation of normal human T cells. METHODS: Double fluorescent staining together with flow cytometry was adopted to analyze the influence of gossypol on expression of the early activation antigen CD69 on T-lymphocytes under stimulation of mitogen or phorbol ester. RESULTS: Analysis of T cell activation in vitro revealed that preincubation of PBMC with 100 μmol/L gossypol could completely inhibit the expression of early activation marker CD69 on CD3+ T cells in response to 10 mg/L PHA, and block T cell activation by 10-7 mol/L PDB as well. The suppression of CD69 expression was dose-dependent and IC50 of gossypol on PDB and PHA were (35.7±2.9) μmol/L and (32.8±1.5) μmol/L(眘), respectively. Besides, gossypol had similar inhibitory effect on CD69 expression of CD3- lymphocytes. However, it did not have any significant effect on T cell surface molecule CD3 down-regulation. CONCLUSION: Gossypol could inhibit T cell activation in vitro in response to polyclonal activators, both PHA and PDB, suggesting that its action site may be at PKC or its downstream and that gossypol possessed potential immuno-regulatory effect.