CAJ | 학술논문

目的探讨线粒体通透性转换孔(mitochondrial permeability transition pore,mPTP)功能状态与心肌细胞缺氧/复氧损伤过程中炎症反应的关系.方法心肌细胞培养72 h后,采用随机数字表法将其随机分为4组:空白对照组(Sham 组)、缺氧/复氧损伤对照组(AR组)、mPTP开放抑制剂环孢素A(ciclosporin A,CSA)后处理组(CSA组)、mPTP开放剂苍术苷(atractyloside,ATR)后处理组(ATR组).实验结束后检测各组心肌细胞乳酸脱氢酶(lactate dehydrogenase,LDH)漏出率、心肌细胞凋亡、线粒体膜电位的变化和心肌细胞核转录因子-κB p65(nuclear factor-κB p65,NF-κB p65)与磷酸化核转录因子-κBp65 Ser536(p-NF-κB p65 Ser536)蛋白的表达量,并检测心肌细胞培养上清液白细胞介素-6(interleukin-6,IL-6)与肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的浓度.结果与AR组比较,CSA组LDH漏出率显著降低[(27.2±2.6)％,(19.0±2.3)％](P＜0.01),早期凋亡细胞百分比显著降低[(33.4±2.8)％,(15.4±2.3)％](P＜0.01),p-NF-κB p65 Ser536蛋白表达量显著降低(5.1±0.7,4.4±0.4)(P＜0.01),IL-6和TNF-α浓度均显著降低[IL-6 (190±10),(170±11) ng/L;TNF-α(129±9),(118±12) ng/L](P＜0.01).与AR组比较,ATR组LDH漏出率显著升高[(27.2±2.6)％,(32.1±3.6)％](P＜0.01),早期凋亡细胞百分比显著升高[(33.4±2.8)％,(43.0±3.3)％](P＜0.0l),p-NF-κB p65 Ser536蛋白表达量显著升高(5.1±0.7,5.8±0.6)(P＜0.01),IL-6和TNF-α浓度均显著升高[IL-6 (189±10),(205±9) ng/L;TNF-α(129±9),(144±10) ng/L] (P＜0.01).结论 mPTP开放状态能够通过调控心肌细胞缺氧/复氧过程中的炎症反应而显著影响缺氧/复氧心肌细胞损伤的程度.
목적 탐토선립체통투성전환공(mitochondrial permeability transition pore,mPTP)공능상태여심기세포결양/복양손상과정중염증반응적관계.방법 심기세포배양72 h후,채용수궤수자표법장기수궤분위4조:공백대조조(Sham 조)、결양/복양손상대조조(AR조)、mPTP개방억제제배포소A(ciclosporin A,CSA)후처리조(CSA조)、mPTP개방제창술감(atractyloside,ATR)후처리조(ATR조).실험결속후검측각조심기세포유산탈경매(lactate dehydrogenase,LDH)루출솔、심기세포조망、선립체막전위적변화화심기세포핵전록인자-κB p65(nuclear factor-κB p65,NF-κB p65)여린산화핵전록인자-κBp65 Ser536(p-NF-κB p65 Ser536)단백적표체량,병검측심기세포배양상청액백세포개소-6(interleukin-6,IL-6)여종류배사인자-α(tumor necrosis factor-α,TNF-α)적농도.결과 여AR조비교,CSA조LDH루출솔현저강저[(27.2±2.6)％,(19.0±2.3)％](P＜0.01),조기조망세포백분비현저강저[(33.4±2.8)％,(15.4±2.3)％](P＜0.01),p-NF-κB p65 Ser536단백표체량현저강저(5.1±0.7,4.4±0.4)(P＜0.01),IL-6화TNF-α농도균현저강저[IL-6 (190±10),(170±11) ng/L;TNF-α(129±9),(118±12) ng/L](P＜0.01).여AR조비교,ATR조LDH루출솔현저승고[(27.2±2.6)％,(32.1±3.6)％](P＜0.01),조기조망세포백분비현저승고[(33.4±2.8)％,(43.0±3.3)％](P＜0.0l),p-NF-κB p65 Ser536단백표체량현저승고(5.1±0.7,5.8±0.6)(P＜0.01),IL-6화TNF-α농도균현저승고[IL-6 (189±10),(205±9) ng/L;TNF-α(129±9),(144±10) ng/L] (P＜0.01).결론 mPTP개방상태능구통과조공심기세포결양/복양과정중적염증반응이현저영향결양/복양심기세포손상적정도.
Objective To explore the relation between mitochondrial permeability transition pore (mPTP) and inflammatory response in myocardial cells during anoxia/reoxygenation.Methods Myocardial cells,cultured for 72 h were divided into 4 groups by a random number method:Sham group,anoxia/reoxygenation injury group (AR group),ciclosporin A (mPTP opening inhibitor) postconditioning group (CSA group),atractyloside (mPTP opening activator) postconditioning group (ATR group).After these treatments,lactate dehydrogenase (LDH) release rate,apoptosis,mitochondrial membrane potential were detected in myocardial cells ofall groups,the protein levels of nuclear factor-κB p65 (NF-κB p65) and phosphorylated NF-κB p65 Ser536 were also detected,the concentrations of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were assayed in myocardial cell culture supernatant fluids.Results Compared to the AR group,the LDH release rate [(27.2±2.6)％ vs (19.0±2.3)％](P＜0.01),early apoptosis [(33.4±2.8)％ vs (15.4±2.3)％] (P＜0.01),phosphorylated NF-κB p65 Ser536 (5.1 ±0.7 vs 4.4±0.4)] (P＜0.01) and the supernatant concentrations of TNF-α and IL-6 [IL-6 (190±10) ng/L vs (170±11) ng/L,TNF-α (129±9) ng/L vs (118±12) ng/L] (P＜0.01) were significantly decreased in the CSA group.While in the ATR group,the LDH release rate [(27.2±2.6)％ vs (32.1± 3.6)％](P＜0.01),early apoptosis[(33.4±2.8)％ vs (43.0±3.3)％](P＜0.01),phosphorylated NF-κB p65 Ser536 (5.1±0.7 vs 5.8± 0.6)] (P＜0.01) and the supernatant concentrations of TNF-α and IL-6 [IL-6(189±10) ng/L vs(205±9) ng/L,TNF-α (129±9) ng/L vs (144±10) ng/L](P＜0.01) were higher than in the AR group.Conclusions mPTP opening can significant impact on the degree of myocardial cell injury during anoxia/reoxygenation by regulating the inflammatory response.