The SIRT1 Agonist SRT1720 Effectively Decreased Il-1β Levels in Cerebral Microvascular Endothelial Cells Caused By CMV Infection and Ox-LDL Treatment

Author(s): Pian Ye, Mengen, Zhu, Shaoqiong, Zhou, Lihua Liu, Chibo Ai, Xin Fang

CMV infection may cause or worsen microvascular dysfunction induced by high cholesterol in mice, possibly through inflammation. Interleukin 1 Beta (IL-1β) can alter the permeability of brain endothelial cells. Sirtuin (SIRT1) inhibits the transcriptional activity of nuclear factor kappa B (NF-kB) as an upstream factor. Our objective is to verify the efficacy of correcting IL-1β levels by regulating the SIRT1/NF-κB pathway in brain microvascular endothelial cells (BMECs) induced by CMV infection and/ or ox-LDL treatment.


bEnd.3 cells were categorized into four groups: Mock, CMV (infection multiple of 10), ox-LDL (100 μg/ml), and both. The cell viability was evaluated using the CCK-8 assay. The expression levels of SIRT1, acetylation and phosphorylation of p65 NF-κB were examined through Immunofluorescence staining or Western Blot. Moreover, IL-1β levels were measured using the ELISA method.


In BMECs, CMV infection or ox-LDL treatment increases IL-1β levels. Additionally, CMV or/and ox-LDL causes a decrease in SIRT1 levels and an increase in acetylation and phosphorylation of p65 NF-κB. Importantly, the administration of any NF-κB inhibitor or a SIRT1 agonist reduces the IL-1β induced by CMV and/or ox-LDL.


Our findings offer novel insights into the impact of viral involvement in brain endothelial injury. It can be inferred that both the SIRT1 agonist SRT1720 and the NF-κB inhibitor helenalin effectively address the heightened IL-1β levels induced by CMV and/or ox-LDL in brain endothelial cells. Moreover, helenalin, as an NF-κB inhibitor, can reverse the reduced cell activity triggered by CMV and NF-κB, whereas SRT1720 fails to achieve this outcome.

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