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Inhibitory Effects of Standardized Boesenbergia pandurata Extract and Its Active Compound Panduratin A on Lipopolysaccharide-Induced Periodontal Inflammation and Alveolar Bone Loss in Rats

Authors
Kim, HaebomKim, ChangheeKook, Kyo EunYantiChoi, SeungmokKang, WonkuHwang, Jae-Kwan
Issue Date
Oct-2018
Publisher
MARY ANN LIEBERT, INC
Keywords
alveolar bone; Boesenbergia pandurata Roxb.; gingival tissue; panduratin A; periodontitis
Citation
JOURNAL OF MEDICINAL FOOD, v.21, no.10, pp 961 - 970
Pages
10
Journal Title
JOURNAL OF MEDICINAL FOOD
Volume
21
Number
10
Start Page
961
End Page
970
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/737
DOI
10.1089/jmf.2017.4155
ISSN
1096-620X
1557-7600
Abstract
Periodontitis, an inflammatory disease of the gingival tissue, triggered by microbial-derived elements, such as lipopolysaccharide (LPS), collapses the periodontal tissues and resorbs the alveolar bone. This study evaluated the inhibitory effects of standardized Boesenbergia pandurata extract (BPE) and panduratin A (PAN) on periodontitis-induced inflammation and alveolar bone loss. Sprague-Dawley rats with LPS-induced periodontitis were orally administered BPE (50 and 200mg/kg/day) and PAN (20mg/kg/day) for 8 days. Histological analysis revealed that BPE- and PAN-administered groups showed decreased cell infiltration and alveolar bone resorption. Furthermore, the BPE and PAN significantly alleviated the mRNA and protein expression levels of nuclear factor kappa B (NF-B), interleukin-1, matrix metalloproteinase (MMP)-2, and MMP-8. BPE and PAN also inhibited the expression of nuclear factor of activated T cells, cytoplasmic 1, c-Fos, and ostoclastogenesis-related enzymes, including cathepsin K and tartrate-resistant acid phosphatase (ALP). BPE and PAN not only upregulated the osteoblastogenesis-associated markers, such as collagen type I (COL1A1) and ALP, but also increased the ratio of osteoprotegerin to receptor activator of NF-B ligand. Collectively, BPE and PAN efficiently prevent destruction of periodontal tissues and stimulating the loss of alveolar bone tissues, strongly indicative of their potential as natural antiperiodontitis agents.
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