The Preventive Effects of Xanthohumol on Vascular Calcification Induced by Vitamin D3 Plus Nicotine

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dc.contributor.author Liou, Shu-Fen
dc.contributor.author Nguyen, Thi Tuyet Ngan
dc.contributor.author Hsu, Jong-Hau
dc.contributor.author Sulistyowati, Erna
dc.contributor.author Huang, Shang-En
dc.contributor.author Wu, Bin-Nan
dc.contributor.author Lin, Ming-Chung
dc.contributor.author Yeh, Jwu-Lai
dc.date.accessioned 2021-10-14T01:41:53Z
dc.date.available 2021-10-14T01:41:53Z
dc.date.issued 2020-10-06
dc.identifier.uri https://www.mdpi.com/2076-3921/9/10/956
dc.identifier.uri http://repository.unisma.ac.id/handle/123456789/2031
dc.description [ARCHIVES] Copyright Article from: MDPI journals en_US
dc.description.abstract Vascular calcification (VC) is highly prevalent in patients with atherosclerosis, chronic kidney disease, diabetes mellitus, and hypertension. In blood vessels, VC is associated with major adverse cardiovascular events. Xanthohumol (XN), a main prenylated chalcone found in hops, has antioxidant effects to inhibit VC. This study aimed to investigate whether XN attenuates VC through in vivo study. A rat VC model was established by four weeks oral administration of vitamin D3 plus nicotine in Sprague Dawley (SD) rats. In brief, 30 male SD rats were randomly divided into three groups: control, 25 mg/kg nicotine in 5 mL corn oil and 3 × 105 IU/kg vitamin D3 administration (VDN), and combination of VDN with 20 mg/L in 0.1% ethanol of XN (treatment group). Physiological variables such as body and heart weight and drinking consumption were weekly observed, and treatment with XN caused no differences among the groups. In comparison with the control group, calcium content and alkaline phosphatase (ALP) activity were increased in calcified arteries, and XN treatment reduced these levels. Dihydroethidium (DHE) and 2′,7′-dichloroflurescin diacetate (DCFH-DA) staining to identify Superoxide and reactive oxygen species generation from aorta tissue showed increased production in VDN group compared with the control and treatment groups. Hematoxylin eosin (HE) and Alizarin Red S staining were determined to show medial vascular thickness and calcification of vessel wall. Administration of VDN resulted in VC, and XN treatment showed improvement in vascular structure. Moreover, overexpression of osteogenic transcription factors bone morphogenetic protein 2 (BMP-2) and runt-related transcription factor 2 (Runx2) were significantly suppressed by XN treatment in VC. Moreover, downregulation of vascular phenotypic markers alpha-smooth muscle actin (α-SMA) and smooth muscle 22 alpha (SM22α) were increased by XN treatment in VC. Furthermore, XN treatment in VC upregulated nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expressions. Otherwise, Kelch-like ECH-associated protein 1 (Keap1) was alleviated by XN treatment in VC. In conclusion, our findings suggested that XN enhances antioxidant capacity to improve VC by regulating the Nrf2/Keap1/HO-1 pathway. Therefore, XN may have potential effects to decrease cardiovascular risk by reducing VC. en_US
dc.language.iso en en_US
dc.publisher MDPI journals en_US
dc.relation.ispartofseries MDPI journals;Vol.9, Issue 10, Page 1-16
dc.subject xanthohumol en_US
dc.subject vascular calcification en_US
dc.subject vitamin D3 en_US
dc.subject nicotine en_US
dc.subject osteogenic transition en_US
dc.subject oxidative stress en_US
dc.title The Preventive Effects of Xanthohumol on Vascular Calcification Induced by Vitamin D3 Plus Nicotine en_US
dc.type Article en_US


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