中华生物医学工程杂志
中華生物醫學工程雜誌
중화생물의학공정잡지
CHINESE JOURNAL OF BIOMEDICAL ENGINEERING
2013年
2期
106-109
,共4页
李运泉%林约瑟%李轩狄%方榕%李淑娟%朱玲%王慧深
李運泉%林約瑟%李軒狄%方榕%李淑娟%硃玲%王慧深
리운천%림약슬%리헌적%방용%리숙연%주령%왕혜심
硫化氢%高血压,肺性%环氧化酶2%依前列醇
硫化氫%高血壓,肺性%環氧化酶2%依前列醇
류화경%고혈압,폐성%배양화매2%의전렬순
Hydrogen sulfide%Hypertension,pulmonary%Cyclooxygenase-2%Epoprostenol
目的 观察硫化氢(H2S)对化学性缺氧诱导的人肺动脉平滑肌细胞(HPASMC)增殖的改善作用并探讨环氧化酶-2(COX-2)在其中的作用.方法 用化学性缺氧模拟剂氯化钴(CoCl2)处理HPASMC,建立缺氧性肺动脉高压的细胞模型.在CoCl2处理前,用硫氢化钠(NaHS,H2S的供体)预处理30 min,检测细胞存活率、胞内COX-2蛋白的表达以及培养基中前列环素(PGI2)的含量.结果 HPASMC经25,50和100 μmol/L的CoCl2处理24h诱导了明显的增殖反应,使细胞增殖率分别提高至(112.7±4.6)％,(116.2±3.3)％和(113.3±4.7)％,与对照组差异有统计学意义(依次P＜0.05,0.01和0.05).用50μmol/L CoCl2处理18～24 h,时间依赖性地诱导HPASMC增殖(R为0.99).50 μmol/LCoCl2处理HPASMC 24 h可明显下调胞内COX-2蛋白的表达(P＜0.05)并抑制细胞释放PGI2 (P＜0.05).外源性地给予PGI2可使CoCl2诱导的细胞增殖率约降低9％,二者差异有统计学意义(P＜0.05).在用50 μmol/L CoCl2处理HPASMC前,给予400 μmol/L NaHS预处理30 min,也可使CoCl2的致增殖效应明显减弱(P＜0.05),另外,NaHS预处理还使胞内COX-2的蛋白表达从0.17±0.08提高至0.59±0.21,并将细胞释放PGI2能力提高2倍.结论 H2S可改善缺氧诱导的HPASMC过度增殖,其分子机制与上调COX-2-PGI2通路的表达有关.
目的 觀察硫化氫(H2S)對化學性缺氧誘導的人肺動脈平滑肌細胞(HPASMC)增殖的改善作用併探討環氧化酶-2(COX-2)在其中的作用.方法 用化學性缺氧模擬劑氯化鈷(CoCl2)處理HPASMC,建立缺氧性肺動脈高壓的細胞模型.在CoCl2處理前,用硫氫化鈉(NaHS,H2S的供體)預處理30 min,檢測細胞存活率、胞內COX-2蛋白的錶達以及培養基中前列環素(PGI2)的含量.結果 HPASMC經25,50和100 μmol/L的CoCl2處理24h誘導瞭明顯的增殖反應,使細胞增殖率分彆提高至(112.7±4.6)％,(116.2±3.3)％和(113.3±4.7)％,與對照組差異有統計學意義(依次P＜0.05,0.01和0.05).用50μmol/L CoCl2處理18～24 h,時間依賴性地誘導HPASMC增殖(R為0.99).50 μmol/LCoCl2處理HPASMC 24 h可明顯下調胞內COX-2蛋白的錶達(P＜0.05)併抑製細胞釋放PGI2 (P＜0.05).外源性地給予PGI2可使CoCl2誘導的細胞增殖率約降低9％,二者差異有統計學意義(P＜0.05).在用50 μmol/L CoCl2處理HPASMC前,給予400 μmol/L NaHS預處理30 min,也可使CoCl2的緻增殖效應明顯減弱(P＜0.05),另外,NaHS預處理還使胞內COX-2的蛋白錶達從0.17±0.08提高至0.59±0.21,併將細胞釋放PGI2能力提高2倍.結論 H2S可改善缺氧誘導的HPASMC過度增殖,其分子機製與上調COX-2-PGI2通路的錶達有關.
목적 관찰류화경(H2S)대화학성결양유도적인폐동맥평활기세포(HPASMC)증식적개선작용병탐토배양화매-2(COX-2)재기중적작용.방법 용화학성결양모의제록화고(CoCl2)처리HPASMC,건립결양성폐동맥고압적세포모형.재CoCl2처리전,용류경화납(NaHS,H2S적공체)예처리30 min,검측세포존활솔、포내COX-2단백적표체이급배양기중전렬배소(PGI2)적함량.결과 HPASMC경25,50화100 μmol/L적CoCl2처리24h유도료명현적증식반응,사세포증식솔분별제고지(112.7±4.6)％,(116.2±3.3)％화(113.3±4.7)％,여대조조차이유통계학의의(의차P＜0.05,0.01화0.05).용50μmol/L CoCl2처리18～24 h,시간의뢰성지유도HPASMC증식(R위0.99).50 μmol/LCoCl2처리HPASMC 24 h가명현하조포내COX-2단백적표체(P＜0.05)병억제세포석방PGI2 (P＜0.05).외원성지급여PGI2가사CoCl2유도적세포증식솔약강저9％,이자차이유통계학의의(P＜0.05).재용50 μmol/L CoCl2처리HPASMC전,급여400 μmol/L NaHS예처리30 min,야가사CoCl2적치증식효응명현감약(P＜0.05),령외,NaHS예처리환사포내COX-2적단백표체종0.17±0.08제고지0.59±0.21,병장세포석방PGI2능력제고2배.결론 H2S가개선결양유도적HPASMC과도증식,기분자궤제여상조COX-2-PGI2통로적표체유관.
Objective To investigate the effects of hydrogen sulfide (H2S) on excessive proliferation of human pulmonary artery smooth muscle cells (HPASMC) induced by chemical hypoxia and to explore the role of cyclooxygenase-2 (COX-2).Methods HPASMCs were treated with CoCl2,a hypoxiamimicking agent,to establish a cellular model of hypoxic pulmonary arterial hypertension (PAH).Prior to the treatment with CoCl2,HPASMCs were preconditioned with sodium hydrosulfide (NaHS),a donor of H2S,for 30 minutes.Cell viability,intracellular expression of COX-2 and the level of PGI2 in culture medium were assayed.Results Exposure of HPASMCs to CoCl2 at the concentrations of 25,50 and 100 μmol/L for 24 hours markedly induced cellular proliferation,with the ratio of (112.7±4.6) ％ (P＜0.05),(116.2±3.3) ％ (P＜0.01) and (113.3±4.7)％ (P＜0.05) compared with control group.Treatment of HPASMC with 50 μ mol/L CoCl2 for 18 to 24 hours promoted cellular proliferation in a time-dependent manner (R=0.99).Treatment with 50 μmol/L CoCl2 for 24 hours significantly attenuated intracellular COX-2 expression and PGI2 secretion from HPASMCs(both P＜0.05),whilst exogenous administration of PGI2 considerably reduced CoCl2-induced cellular proliferation by 9％ (P＜0.05).Preconditioning of HPASMCs with 400 μ mol/L NaHS for 30 minutes markedly attenuated cellular proliferation induced by CoCl2 (P＜0.05),promoted COX-2 expression from 0.17±0.08 to 0.59±0.21 and resulted in a 2-fold increase in PGI2 secretion.Conclusion H2S can ameliorate hypoxia-induced cellular proliferation possibly related to the up-regulation of COX-2-PGI2 signaling pathway.
