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首页> 外文期刊>Journal of applied toxicology >Exposure to mono (2-ethylhexyl) phthalate facilitates apoptosis and pyroptosis of human endometrial microvascular endothelial cells through NLRP3 inflammasome
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Exposure to mono (2-ethylhexyl) phthalate facilitates apoptosis and pyroptosis of human endometrial microvascular endothelial cells through NLRP3 inflammasome

机译：暴露于单邻（2-乙基己基）邻苯二甲酸酯促进人子宫内膜微血管内皮细胞通过NLRP3炎性凋亡和糊化酶

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Mono (2-ethylhexyl) phthalate (MEHP) is a major metabolite of di (2-ethylhexyl) phthalate (DEHP). This study aimed to observe the toxic effect of MEHP on human endometrial microvascular endothelial cells (HEMECs) and its potential molecular mechanism. HEMECs were exposed to different concentrations of MEHP (0, 50, 100, and 200 nM). Cell viability and apoptosis were assessed by cell counting kit-8 (CCK-8) and flow cytometry assays. Western blot was performed to examine the expression of apoptosis-related proteins (Bcl-2, Bax, and Caspase-3). Moreover, the expression of pyroptosis-related Caspase-1 was detected by western blot and immunofluorescence assays. Lactate dehydrogenase (LDH) release levels were evaluated in HEMECs treated with MEHP and/or Caspase-1 inhibitor Ac-YVAD-CHO. After exposure to MEHP, NLRP3 expression was examined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot. LDH release and apoptosis levels were tested in HEMECs induced by MEHP and/or siNLRP3. MEHP significantly induced cell viability and inhibited apoptosis for HEMECs, with a concentration-dependent manner. Furthermore, Bcl-2/Bax ratio was distinctly reduced and Caspase-3 expression was increased in HEMECs after exposure to MEHP. Western blot and immunofluorescence results confirmed that MEHP markedly augmented Caspase-1 expression in HEMECs. Furthermore, LDH release levels were fortified in HEMECs treated with MEHP, which were improved following cotreatment with Ac-YVAD-CHO. At the mRNA and protein levels, NLRP3 expression was prominently increased in HEMECs exposed to MEHP. NLRP3 knockdown markedly ameliorated the increase in LDH release and apoptosis induced by MEHP exposure in HEMECs. Our findings suggested that exposure to MEHP facilitates apoptosis and pyroptosis of HEMECs through NLRP3 inflammasome.
机译：邻苯二甲酸单（2-乙基己基）酯（MEHP）是邻苯二甲酸二（2-乙基己基）酯（DEHP）的主要代谢产物。本研究旨在观察MEHP对人子宫内膜微血管内皮细胞（HEMEC）的毒性作用及其可能的分子机制。HEMEC暴露于不同浓度的MEHP（0、50、100和200 nM）。通过细胞计数试剂盒-8（CCK-8）和流式细胞术检测细胞活力和凋亡。westernblot检测凋亡相关蛋白（Bcl-2、Bax和Caspase-3）的表达。此外，通过westernblot和免疫荧光检测热下垂相关的Caspase-1的表达。用MEHP和/或Caspase-1抑制剂Ac-YVAD-CHO治疗HEMEC，评估其乳酸脱氢酶（LDH）释放水平。暴露于MEHP后，通过逆转录定量聚合酶链反应（RT-qPCR）和western blot检测NLRP3的表达。检测MEHP和/或siNLRP3诱导的HEMEC中LDH释放和凋亡水平。MEHP能显著诱导HEMEC的细胞活力并抑制其凋亡，且呈浓度依赖性。此外，MEHP暴露后HEMEC中Bcl-2/Bax比率明显降低，Caspase-3表达增加。Western-blot和免疫荧光结果证实MEHP显著增强了HEMECs中Caspase-1的表达。此外，经MEHP处理的HEMEC中LDH释放水平得到加强，与Ac-YVAD-CHO共处理后LDH释放水平得到改善。在mRNA和蛋白质水平上，暴露于MEHP的HEMEC中NLRP3的表达显著增加。NLRP3基因敲除显著改善MEHP暴露诱导的HEMEC LDH释放增加和细胞凋亡。我们的研究结果表明，暴露于MEHP可通过NLRP3炎症体促进HEMEC的凋亡和热下垂。

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