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首页> 外文期刊>Arteriosclerosis, thrombosis, and vascular biology >Premature senescence of vascular cells is induced by HIV protease inhibitors: implication of prelamin A and reversion by statin.
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Premature senescence of vascular cells is induced by HIV protease inhibitors: implication of prelamin A and reversion by statin.

机译：HIV蛋白酶抑制剂可诱导血管细胞过早衰老：含prelamin A和他汀类药物可逆转。

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OBJECTIVE: To determine whether and how protease inhibitors (PIs) could affect vascular aging. METHODS AND RESULTS: HIV therapy with PIs is associated with an increased risk of premature cardiovascular disease. The effect of ritonavir and a combination of lopinavir and ritonavir (for 30 days) on senescence, oxidative stress, and inflammation was evaluated in human coronary artery endothelial cells (HCAECs). These HCAECs were either cotreated or not cotreated with pravastatin or farnesyl transferase inhibitor (FTI)-277 or with 2 antioxidants (manganese [III] tetrakis [4-benzoic acid] porphyrin [MnTBAP] and N-acetyl cysteine). Senescence markers were evaluated in peripheral blood mononuclear cells (PBMCs) from HIV-infected patients under PI treatment. PIs induced senescence markers, prelamin A accumulation, oxidative stress, and inflammation in HCAECs. Senescence markers and prelamin A were also observed in PBMCs from HIV-infected patients under ritonavir-boosted PIs. Pravastatin, FTI-277, and antioxidants improved PI adverse effects in HCAECs. Senescence markers were lower in PBMCs from PI-treated patients cotreated with statins. CONCLUSIONS: PIs triggered premature senescence in endothelial cells by a mechanism involving prelamin A accumulation. Accordingly, circulating cells from HIV-infected patients receiving PI therapy expressed senescence markers and prelamin A. Statin was associated with improved senescence in endothelial cells and patient PBMCs. Thus, PIs might promote vascular senescence in HIV-infected patients; and statins might exert beneficial effects in these patients.
机译：目的：确定蛋白酶抑制剂（PI）是否以及如何影响血管衰老。方法和结果：用PI进行HIV治疗会增加心血管疾病的风险。在人冠状动脉内皮细胞（HCAEC）中评估了利托那韦以及洛匹那韦和利托那韦的组合（持续30天）对衰老，氧化应激和炎症的影响。这些HCAEC与普伐他汀或法呢基转移酶抑制剂（FTI）-277或不与2种抗氧化剂（锰[III]四[4-苯甲酸]卟啉[MnTBAP]和N-乙酰基半胱氨酸）共同治疗或不共同治疗。在PI治疗下，对来自HIV感染患者的外周血单个核细胞（PBMC）评估了衰老标记。 PI在HCAEC中诱导衰老标记，prelamin A积累，氧化应激和炎症。在利托那韦增强PI的情况下，在HIV感染患者的PBMC中也观察到了衰老标记和prelaminA。普伐他汀，FTI-277和抗氧化剂可改善HCAEC中PI的不良反应。在用他汀类药物治疗的PI治疗患者的PBMC中，其衰老标记物较低。结论：PIs通过涉及prelamin A积累的机制触发了内皮细胞的过早衰老。因此，接受PI治疗的HIV感染患者的循环细胞表达衰老标志物和prelaminA。他汀与内皮细胞和患者PBMC的衰老改善有关。因此，PI可能会促进HIV感染患者的血管衰老。他汀类药物可能对这些患者产生有益作用。

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