Essential oil from Fructus Alpinia zerumbet (fruit of Alpinia zerumbet (Pers.) Burtt.et Smith) protected against aortic endothelial cell injury and inflammation in vitro and in vivo

• Published in: Journal of ethnopharmacology 2019-06, Vol.237, p.149-158
• Main Authors: Ji, Yun-peng, Shi, Ting-yu, Zhang, Yan-yan, Lin, Dan, Linghu, Ke-gang, Xu, Yi-ni, Tao, Ling, Lu, Qing, Shen, Xiang-chun
• Format: Article
• Language: English
• Subjects: Endothelial injury; Fructus Alpinia zerumbet; Inflammation; LPS; NF-κB; TLR4
• ISSN: 0378-8741; 1872-7573
• DOI: 10.1016/j.jep.2019.03.011

Fructus Alpinia zerumbet (FAZ), a dry and ripe fruit of Alpinia zerumbet (Pers.) Burtt. et Smith, is widely used as a spice to treat cardiovascular diseases in clinic as a miao folk medicine in Guizhou Province of China. Essential oil extracted from FAZ (EOFAZ) is the key bioactive ingredients. This study aimed to examine the effects and mechanisms of EOFAZ on lipopolysaccharide (LPS)-induced endothelial cell injury, inflammation and apoptosis in vitro and in vivo. For the in vitro study, LPS-treated human aortic endothelial cells were used to perform PCR, western blot analysis and immunofluorescence. For the in vivo study, male mouse were divided into four groups, vehicle control group and LPS group received 0.5% Tween-80 in saline; and two EOFAZ groups receive different dose of EOFAZ (90 mg kg −1·day−1, 180 mg kg −1·day−1) respectively. Each group was fed for 7 days by intragastrical administration at daily base. Then, except vehicle control group received saline, mice in other three groups were administered with LPS (1 mg kg −1, dissolved in saline) by intraperitoneal injection. 24 h later, Aorta tissue was collected and frozen immediately in liquid N2, stored at −80 °C for western blot analysis. We found that EOFAZ completely prevented LPS-induced HAEC activation and inflammation in vitro and in vivo, as assessed by expression of endothelial adhesion molecules, ICAM-1 and VCAM-1. Similarly, EOFAZ significantly blunted LPS-induced endothelial injury, as tested by MTT assay, LDH release and caspase-3 activation. We further demonstrated that TLR4-dependent NF-κB signaling may be involved in the process. EOFAZ protected against LPS-induced endothelial cell injury and inflammation likely via inhibition of TLR4-dependent NF-κB signaling. [Display omitted]