Evidence for injurious effect of cocaethylene in human microvascular endothelial cells.
Evidence for injurious effect of cocaethylene in human microvascular endothelial cells.
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可卡乙烯对人微血管内皮细胞有害作用的证据。
DOI：
10.1016/j.cccn.2004.02.031
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Okorodudu,AnthonyO
中科院分区：
文献类型：
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作者：
Tacker,DanyelHermes;Okorodudu,AnthonyO
研究背景可卡因乙烯（Cocaethylene，CE）是可卡因和乙醇的结合物，可能参与全身性血管疾病的发病机制。本研究进行了调查CE对人微血管内皮细胞（HMEC-1）在culture. Methodsdischarating和汇合单层的HMEC-1的影响，用于评估生长动力学，活力，细胞毒性，和形态/屏障改变后CE治疗（0-1 mmol/L）长达7天。台盼蓝拒染法、乳酸脱氢酶（LDH）释放法、手工细胞计数法和硝酸银银染色法测定HMEC-1细胞的倍增时间。结果0.5和1.0 mmol/l CE处理的HMEC-1细胞倍增时间分别为30.0和31.4 h，显著长于对照组的28.6 h（p<0.05）。台盼蓝排除染色实验的存活率为90.4±3.8%（对照）和93.1±1.9%（CE处理），表明CE无致死性。LDH活性为173±33 U/l（对照）和157±43 U/l（CE处理），证实不存在CE细胞毒性。银染色结果表明增加单层渗透性所证明的形成后，1小时的exposation.ConclusionsHMEC-1暴露于CE诱导的细胞损伤，可以影响小血管的渗透性。这些细胞变化可能部分是研究的关键点，以解释暴露于CE的个体周围组织的水肿和炎症。
BackgroundCocaethylene (CE) is a conjugate of cocaine and ethanol that may contribute to the pathogenesis of systemic vascular diseases. This study was conducted to investigate the effect of CE on human microvascular endothelial cells (HMEC-1) in culture.MethodsProliferating and confluent monolayers of HMEC-1 were used for assessing growth kinetics, viability, cytotoxicity, and morphologic/barrier alterations after CE treatment (0–1 mmol/l) for up to 7 days. The Trypan blue exclusion, lactate dehydrogenase (LDH) release assay, manual cell counts, and silver nitrate staining technique were used.ResultsThe doubling times of 30.0 and 31.4 h for the 0.5 and 1.0 mmol/l CE-treated HMEC-1, respectively, were significantly longer than the 28.6 h for the control group (p<0.05). The viabilities of 90.4±3.8% (control) and 93.1±1.9% (CE-treated) from the Trypan blue exclusion-staining experiments indicated non-lethality of CE. LDH activities of 173±33 U/l (control) and 157±43 U/l (CE-treated) confirmed the absence of CE cytotoxicity. Silver staining results indicated increased monolayer permeability as demonstrated by the formation of intercellular gaps after 1 h of exposure.ConclusionsHMEC-1 exposure to CE induced cellular injury that could affect the permeability of small blood vessels. These cellular changes could in part be the pivotal point for studies to explain the edema and inflammation in surrounding tissues of individuals exposed to CE.