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Medical Science Monitor Basic Research


eISSN: 1643-3750

Rosiglitazone Reduces Apoptosis and Inflammation in Lipopolysaccharide-Induced Human Umbilical Vein Endothelial Cells

Xiao-xia Ji, Xiao-jing Ji, Qian-qian Li, Xiao-xian Lu, Liang Luo

Department of Critical Care Medicine, Wuxi No.2 Hospital affiliated to Nanjing Medical University, Wuxi, Jiangsu, China (mainland)

Med Sci Monit 2018; 24:6200-6207

DOI: 10.12659/MSM.910036

Available online:

Published: 2018-09-06


BACKGROUND: Although the peroxisome proliferator-activated receptor-g (PPARg) agonist rosiglitazone has significant anti-inflammatory properties, no scientific studies have provided new insights in its pharmacological properties with respect to acute respiratory distress syndrome (ARDS). The present investigation aimed to evaluate whether rosiglitazone can reduce apoptosis and inflammation in a lipopolysaccharide (LPS)-induced acute respiratory distress syndrome in vitro model.
MATERIAL AND METHODS: Human umbilical vein endothelial cells (HUVECs) were treated with 1 µg/ml LPS in the absence or presence of 10 µM rosiglitazone for 24 h. Cell viability was measured by MTT assay. Flow cytometry was used to examine the cell apoptosis and ROS production in HUVECs response to LPS and rosiglitazone. The levels of pro-inflammatory cytokine factors, including TNF-α, IL-6, CXCL12, and CXCR4, were measured by ELISA, real-time PCR, and Western blot assay, respectively. The expression of PPARg, Bcl-2, and Bax and the activity of JAK2 and STAT3 were also investigated by Western blot assay.
RESULTS: We found that rosiglitazone significantly inhibited LPS-induced cell apoptosis, ROS production, and inflammation in HUVECs. Furthermore, we found a significant reduction of JAK2/STAT3 activation and the Bax/Bcl-2 ratio in LPS-induced HUVECs response to rosiglitazone treatment.
CONCLUSIONS: Treatment with rosiglitazone can reduce apoptosis and inflammation in HUVECs induced by LPS.

Keywords: Apoptosis, Inflammation, Janus Kinase 2, Respiratory Distress Syndrome, Adult, STAT3 Transcription Factor