Abstract
Periodontitis is a chronic periodontal inflammatory disease and its etiology remains not fully understood. Chlorogenic acid (CA) is an ingredient isolated from nature product and exerts anti-inflammatory property. The purpose of the present study was to estimate the effect of CA on LPS-induced Human gingival fibroblasts (HGFs) and explore its mechanism. The CysLT1R inhibitor montelukast, Nrf2 inhibitor ML385, NLRP3 inhibitor MCC950 were employed to investigate the mechanism. As a result, the bioinformatic analysis indicated that CysLT1R, Nrf2, NLRP3 in the affected site of periodontitis patients gingival tissues were notably altered compared with those in unaffected site of healthy donors gingival tissues. The treatment with CA inhibited the contents of IL-1β, IL-18 both in LPS-induced HGFs. CA ameliorated the expressions of CysLT1R, Nrf2, HO-1, NLRP3, ASC, pro-caspase-1, active caspase-1 in vitro. CA treatment promoted the nuclear translocation of Nrf2, suppressed oxidative stress and elevated mitochondrial membrane potential. The co-treatment with montelukast, ML385, MCC950 proved that CysLT1R, Nrf2, NLRP3 participated in the CA-mediated anti-inflammatory reaction. Molecular docking showed that CA might combine with CysLT1R. In conclusion, our data suggested that CA could attenuate inflammation in HGFs, which was possibly through CysLT1R/Nrf2/NLRP3 signaling.
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