Anti‐Inflammatory and Antiosteoclastogenic Activities of Parthenolide on Human Periodontal Ligament Cells In Vitro

Abstract

Periodontitis is an inflammatory disease that causes osteolysis and tooth loss. It is known that the nuclear factor kappa B (NF-κB) signalling pathway plays a key role in the progression of inflammation and osteoclastogenesis in periodontitis. Parthenolide (PTL), a sesquiterpene lactone extracted from the shoots of Tanacetum parthenium, has been shown to possess anti-inflammatory properties in various diseases. In the study reported herein, we investigated the effects of PTL on the inflammatory and osteoclastogenic response of human periodontal ligament-derived cells (hPDLCs) and revealed the signalling pathways in this process. Our results showed that PTL decreased NF-κB activation, I-κB degradation, and ERK activation in hPDLCs. PTL significantly reduced the expression of inflammatory (IL-1β, IL-6, and TNF-α) and osteoclastogenic (RANKL, OPG, and M-CSF) genes in LPS-stimulated hPDLCs. In addition, PTL attenuated hPDLC-induced osteoclastogenic differentiation of macrophages (RAW264.7 cells), as well as reducing gene expression of osteoclast-related markers in RAW264.7 cells in an hPDLC-macrophage coculture model. Taken together, these results demonstrate the anti-inflammatory and antiosteoclastogenic activities of PTL in hPDLCs in vitro. These data offer fundamental evidence supporting the potential use of PTL in periodontitis treatment.

Effects of Plants on Osteogenic Differentiation and Mineralization of Periodontal Ligament Cells: A Systematic Review

“…These components may exhibit antioxidant and antiinflammatory effects (Chib et al ., ; Baharfar et al ., ). Several plants have also demonstrated antimicrobial, wound healing, and differentiation potential, as well as enhanced gene expression for osteogenic activities (Inaba et al ., ; Zhao et al ., ; Jeong et al ., ; Zhang et al ., ).…”

Anti-inflammatory and Anti-tumor Activities of Parthenolide: An Update

“…References Cell Proliferation/ Apoptosis associated Molecules References NFκB [14], [30], [31], [35], [43], [48], [90] NFκB [17], [18], [21], [52], [54], [64], [78][79], [90] IKK-β [30][31][32], [48] [ERK/MEK/MAPK/ELK1] [14], [37], [48], [51] iNOS [39] β1-arrestin, Csk, FAK, FGFR2, PKC [51] STAT1/STAT3 [36], [51], [83][84][85][86][87][88] STAT1/STAT3 [36], [51], [55][56], [83][84][85][86][87][88] Cyclooxygenase (COX) [27][28][29], [37] JNK [42], [43], …”

“…Histamin [26] Survivin [57], [58] GSH [16], [14], [43] GSH [68] Nrf2-ARE [20], [43], [71] Caspases [50], [49] Thioredoxin reductase1& 2 [70] Bax, Beclin, ATG5, ATG3 [49] P53 [51] C/EBPα, FRA-1, HOXA-4, c-MYB, SNAIL, SP1, SRF, STAT3, XBP1…”

“…In in vitro experiments scientists have shown the nuclear factor kappa B (NFκB) inhibiting abilities of PTL [13]. Zhang et al showed that PTL inhibits the activation of NFκB and ERK signaling pathways, as well as the expression of inflammatory and osteo-clastogenic genes in lipo-polysaccharide (LPS)-stimulated hPDLCs in vitro [14]. It also inhibits proliferation and eliminates various cancer cells predominantly by inducing apoptosis [15].…”

Inhibitory Effect of Low‐Intensity Pulsed Ultrasound on the Expression of Lipopolysaccharide‐Induced Inflammatory Factors in U937 Cells

“…Inflammation, characterized as redness, swelling, heat, and pain, is a defense response to stimulus as toxins and pathogens. Lipopolysaccharide (LPS), which is recognized as an inflammatory initiation factor, stimulates macrophages to produce inflammatory cytokines, such as tumor necrosis factor α (TNF‐α), interleukin 1β (IL‐1β), IL‐6, and IL‐8 . Macrophages are involved in immune and inflammatory responses and play important roles in periodontitis .…”