title: Effects of sappanchalcone on the cytoprotection and anti-inflammation via heme oxygenase-1 in human pulp and periodontal ligament cells.
abstract: Sappanchalcone has been demonstrated to possess several biological effects. However, the molecular mechanism underlying these effects is not fully understood. In this study, we examined the effects of sappanchalcone on hydrogen peroxide (H(2)O(2))-induced cytotoxicity using human dental pulp (HDP) cells, and lipopolysaccharide (LPS)-induced inflammation using human periodontal ligament (HPDL) cells. Sappanchalone concentration proportionately increased heme oxygenase (HO)-1 protein expression and enzyme activity in both HDP and HPDL cells. It also protected HDP cells from H(2)O(2)-induced cytotoxicity and reactive oxygen species production. The cytoprotective effect of sappanchalcone was nullified by HO-1 inhibitor, Tin protoporphyrin (SnPP). Sappanchalcone is seen to inhibit LPS-stimulated nitric oxide (NO), prostaglandin E(2) (PGE(2)), interlukine-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interlukine-6 (IL-6) and interlukine-12 (IL-12) release in addition to inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in HPDL cells. SnPP, a specific inhibitor of HO-1, partly blocked sappanchalcone mediated suppression of inflammatory mediator production, in LPS-stimulated HPDL cells. HDP and HPDL cells treated with sappanchalcone exhibited the transient activation of c-Jun NH2-terminal kinase (JNK) and NF-E2-related factor-2 (Nrf2). The expression of HO-1 protein by sappanchalcone was significantly reduced by pretreatment with JNK inhibitor. In conclusion, induction of HO-1 is an important cytoprotective mechanism by which sappanchalcone protects HDP cells from H(2)O(2) and in addition it also exhibits anti-inflammatory effects in LPS-stimulated HPDL cells. Thus, sappanchalcone could potentially be a therapeutic approach for periodontal, pulpal and periapical inflammatory lesion.
authors.affiliation: Zoonosis Research Center, Wonkwang University, Iksan 570-749, South Korea.
authors.forename: Gil-Saeng
authors.initials: GS
authors.lastname: Jeong
authors.forename: Dong-Sung
authors.initials: DS
authors.lastname: Lee
authors.forename: Bin
authors.initials: B
authors.lastname: Li
authors.forename: Hwa-Jun
authors.initials: HJ
authors.lastname: Lee
authors.forename: Eun-Cheol
authors.initials: EC
authors.lastname: Kim
authors.forename: Youn-Chul
authors.initials: YC
authors.lastname: Kim
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002460:Cell Line; D047188:Chalcones / Q000494:pharmacology*; D003782:Dental Pulp / Q000166:cytology / Q000187:drug effects / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects; D051547:Heme Oxygenase-1 / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000633:toxicity; D007249:Inflammation / Q000188:drug therapy* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity; D010513:Periodontal Ligament / Q000166:cytology / Q000187:drug effects / Q000473:pathology
chemical_list: D000893:Anti-Inflammatory Agents; D047188:Chalcones; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; C044363:sappanchalcone; D006861:Hydrogen Peroxide; D051547:Heme Oxygenase-1