Ecklonia cava Extract Exerts Anti-Inflammatory Effect in Human Gingival Fibroblasts and Chronic Periodontitis Animal Model by Suppression of Pro-Inflammatory Cytokines and Chemokines.
Jae-In JungSeonyoung KimSeung-Min BaekSoo-Im ChoiHwan Hee LeeJee-Young ImmPublished in: Foods (Basel, Switzerland) (2021)
Periodontitis is one of the most common chronic inflammatory diseases. The anti-inflammatory effect of the extract from brown algae Ecklonia cava was analyzed in lipopolysaccharide (LPS)-stimulated human gingival fibroblasts (HGF-1), the most abundant cells in gingival tissue. The gene expressions of cyclooxygenase-2 and interleukin-6 were decreased by 78 and 50%, respectively, at 100 μg/mL Ecklonia cava extract (ECE) treatment. The gene expressions of matrix metalloproteases (MMP-2 and MMP-8) and chemokines (macrophage inflammatory protein 1-alpha and stromal cell-derived factor 1) were also significantly down-regulated by ECE treatment (p < 0.05). The increased reactive oxygen species (ROS) production in HGF-1 cells by LPS stimulation was decreased by 30% at 100 μg/mL ECE treatment. The mitogen-activated protein kinase pathway and the nuclear factor-kappa B (NF-κB) signal activated by ROS were suppressed by ECE in a dose-dependent manner. ECE treatment (400 mg/kg, 8 weeks) significantly improved alveolar bone resorption in the ligature-induced chronic periodontitis rat model. ECE supplementation also lowered elevated mRNA expression of the receptor activator of nuclear factor-kappa B (RANKL)/osteoprotegerin (OPG) in the gingival tissue (p < 0.05). Therefore, ECE mitigated gingival tissue destruction and bone resorption associated with chronic periodontitis condition.
Keyphrases
- nuclear factor
- anti inflammatory
- toll like receptor
- reactive oxygen species
- oxidative stress
- inflammatory response
- induced apoptosis
- bone loss
- cell death
- dna damage
- signaling pathway
- lps induced
- nitric oxide
- genome wide
- body composition
- drug induced
- adipose tissue
- bone marrow
- combination therapy
- replacement therapy
- endoplasmic reticulum stress
- small molecule
- cell cycle arrest
- binding protein
- protein protein
- cell migration