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Periodontitis is a common disease involving inflammation and tissue destruction in the periodontal region. Although uncontrolled long-term inflammation in the gingiva may lead to loss of the periodontal ligament, treatments or preventive solutions for periodontitis are scarce. The aim of this study is to find anti-inflammatory material from a natural source that can be used to treat or protect against periodontitis. Daphne species (Thymelaeaceae) are important and popular components of traditional Chinese medicine and are used as anti-inflammatory agents. Daphne jejudoensis is an endemic plant that grows on Jeju Island and was identified as a new species in 2013. In this study, for the first time, we investigated the anti-inflammatory effect of D. jejudoensis leaf extract (DJLE) on human periodontal ligament cells. The gene expression levels of pro-inflammatory cytokines (interleukin-1β and 6 and tumor necrosis factor-α) and inflammation-inducible enzymes (inducible nitric oxide synthase and cyclooxygenase-2) were reduced after DJLE treatment with/without lipopolysaccharide stimulation. The findings of this study indicate that D. jejudoensis possesses anti-inflammatory activities, suggesting that DJLE may be a potential preventive and therapeutic agent for periodontitis.

"Forces of Nature: New Perspectives on Korean Environments" is an edited volume that explores the role of nature in Korean history. The book covers a wide range of topics, including ecology, energy systems, and climate events, and examines how these forces shaped the relationship between humans and their environment. The chapters in the book span different time periods, political contexts, and geographical locations, shedding light on the co-production of nature and people in Korean history. While some contributors take a climate-determinist perspective, the editors aim to put human actors in their physical and material surroundings. The book is organized thematically rather than chronologically or geographically, and includes chapters on imperial interventions, responses to environmental crises, processes of dispossession, and reclaiming life through environmental movements and sciences. The editors also propose a new framework for future research, focusing on everyday ecologies and the intersection of science, technology, and the environment in Korea. [Extracted from the article]

The roles and molecular mechanisms of Delta-like 1 (DLK1) in periodontitis remain largely unknown. Here, we investigated the expression of DLK1 and NF-κB p65 in Porphyromonas gingivalis (Pg.)-induced periodontitis in vivo. Periodontal inflammation and alveolar bone resorption were analyzed using western blotting, micro-computed tomography, TRAP staining, immunohistochemistry, and immunofluorescence. Raw246.7 cells were stimulated with 1 μg/ml Porphyromonas gingivalis lipopolysaccharide (Pg.LPS) to assess DLK1 expression in vitro. DLK1 overexpression was achieved, and transfection efficiency was confirmed using western blotting and immunofluorescence. The NF-κB and MAPK pathways were activated by treating cells with 1 μg/ml Pg.LPS to explore related mechanisms. Compared with normal tissues, both DLK1 and NF-κB p65 expression increased in periodontitis gingival tissues. DLK1-positive expression was observed in inflammatory infiltrating cells and osteoclasts in the marginal lacunae of the alveolar bone. DLK1 expression in CD68-positive macrophages was detected by immunofluorescence. However, DLK1 expression in Raw246.7 cells decreased after Pg.LPS stimulation and during osteoclast differentiation. DLK1 levels negatively correlated with TNF-α, IL-1β, and NFATC1. Increased DLK1 in Raw246.7 cells further inhibited COX2 and iNOS expressions. Mechanistically, DLK1 overexpression down-regulated NF-κB p65 and JNK levels. In summary, these findings suggest that DLK1 overexpression inhibits periodontal inflammation through the NF-κB p65 and JNK pathways. Interventions targeting increased DLK1 levels may have therapeutic implications for periodontitis., Competing Interests: Declarations. Conflict of interest: The authors declare no conflicts of interest., (© 2024. The Author(s), under exclusive licence to The Society of The Nippon Dental University.)

Aims: Periodontitis is a chronic disease affecting adult oral health. Transient receptor potential vanilloid 1 (TRPV1) expression is shown to upregulate in many inflammatory diseases. Nevertheless, its biological potential along with the molecular mechanism in periodontitis is unclear. Our study aimed to explore the biological role and underlying signaling pathway of TRPV1 in periodontitis., Methods: In the current research, human periodontal ligament stem cells (hPDLSCs) were stimulated by lipopolysaccharide (LPS) to induce inflammatory conditions in vitro. In vivo, the periodontitis mouse model was built by ligating the gingival sulcus of male C57BL/6J mice. Thereafter, the proliferation, apoptosis, inflammation, and oxidative stress-related processes were assessed., Results: We found that LPS induced apoptosis and inflammation in hPDLCs, along with oxidative stress, while simultaneously inhibiting hPDLC proliferation (p < 0.05). Notably, TRPV1 expression was elevated in LPS-treated hPDLSCs and gingival samples from patients with periodontitis. Interestingly, the increase in TRPV1 expression induced by Capsaicin, a TRPV1 agonist, inhibited cell proliferation while promoting LPS-stimulated apoptosis, inflammation, and oxidative stress in hPDLSCs (p < 0.01). In contrast, inhibition of TRPV1 expression using Capsazepine, a TRPV1 inhibitor, produced opposite effects (p < 0.01). In vivo experiments revealed that inhibition of TRPV1 attenuated ligation-induced periodontitis in mice, as evidenced by enhanced oxidative stress, inflammatory response, and elevated apoptosis (p < 0.01). Additionally, rescue assays indicated that TRPV1 promoted periodontitis-associated tissue inflammation and oxidative damage via activating the STAT3 signaling pathway (p < 0.01)., Conclusion: Our study demonstrates that TRPV1 expression is high in periodontitis and facilitates periodontitis-associated tissue inflammation and oxidative damage by regulating STAT3 signaling pathway, which implies that TRPV1 may represent a new therapeutic target for periodontitis., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Periodontitis, characterized by the progressive destruction of dental support tissues due to altered immune responses, poses a significant concern for public health. This condition involves intricate interactions between the immune response and oral microbiome, where innate and adaptive immune responses, with their diverse cell populations and inflammatory mediators, play crucial roles in this immunopathology. Indeed, cytokines, chemokines, growth factors, and immune cells perform key functions in tissue remodeling. Focusing on periodontal therapies, our attention turns to micro-immunotherapy (MI), employing low doses (LDs) and ultra-low doses (ULDs) of immunological signaling molecules like cytokines, growth factors, and hormones. Existing studies across various fields lay the groundwork for the application of MI in periodontitis, highlighting its anti-inflammatory and regenerative potential in soft tissue models based on in vitro research. In summary, this review underscores the versatility and potential of MI in managing periodontal health, urging further investigations to solidify its clinical integration. MI supports an innovative approach by modulating immune responses at low doses to address periodontitis. [ABSTRACT FROM AUTHOR]

Honokiol is a neolignan biphenol found in aerial parts of the Magnolia plant species. The Magnolia plant species traditionally belong to China and have been used for centuries to treat many pathological conditions. Honokiol mitigates the severity of several pathological conditions and has the potential to work as an anti-inflammatory, anti-angiogenic, anticancer, antioxidant, and neurotherapeutic agent. It has a long history of being employed in the healthcare practices of Southeast Asia, but in recent years, a greater scope of research has been conducted on it. Plenty of experimental evidence suggests it could be beneficial as a neuroprotective bioactive molecule. Honokiol has several pharmacological effects, leading to its exploration as a potential therapy for neurological diseases (NDs), including Alzheimer's disease (AD), Parkinson's disease (PD), cerebral ischemia, anxiety, depression, spinal cord injury, and so on. So, based on the previous experimentation reports, our goal is to discuss the neuroprotective properties of honokiol. Besides, honokiol derivatives have been highlighted recently as possible therapeutic options for NDs. So, this review focuses on honokiol's neurotherapeutic actions and toxicological profile to determine their safety and potential use in neurotherapeutics. [ABSTRACT FROM AUTHOR]

Background: Nitric oxide, a diatomic free radical activated by phagocytic leukocytes, arginine a catalyzed product that is synthesized by nitric oxide synthases. It is one of the mechanisms which assists in the resolution of inflammation. A review of its effect on healing around dental implants is yet to be studied. Objective: To review the role of nitric oxide on healing around dental implants. Material and methods: A digital search was carried out using Google Scholar, Medline, and PubMed. The most related article was selected for the review. Conclusion: Osseointegration of dental implants is inclined by many factors which affect the bone-implant contact formation process, and it initiates by forming a hematoma, immunomodulation, and angiogenesis following osteogenesis. Nitric oxide shows a biphasic effect on osteoblast and osteoclast activity, which depends on the concentration of nitric oxide and it can be an important factor in achieving successful osseointegration. [ABSTRACT FROM AUTHOR]

Kaempferol (KPR), a flavonoid compound found in various plants and foods, has garnered attention for its anti-inflammatory, antioxidant, and anticancer properties. In preliminary studies, KPR can modulate several signaling pathways involved in inflammation, making it a candidate for treating cholecystitis. This study aimed to explore the effects and mechanisms of KPR on lipopolysaccharide (LPS)-induced human gallbladder epithelial cells (HGBECs). To assess the impact of KPR on HGBECs, the HGBECs were divided into control, KPR, LPS, LPS + KPR, and LPS + UDCA groups. Cell viability and cytotoxicity were evaluated by MTT assay and lactate dehydrogenase (LDH) assay, respectively, and concentrations of KPR (10-200 μM) were tested. LPS-induced inflammatory responses in HGBECs were to create an in vitro model of cholecystitis. The key inflammatory markers (IL-1β, IL-6, and TNF-α) levels were quantified using ELISA, The modulation of the MAPK/NF-κB signaling pathway was measured by western blot using specific antibodies against pathway components (p-IκBα, IκBα, p-p65, p65, p-JNK, JNK, p-ERK, ERK, p-p38, and p38). The cell viability and LDH levels in HGBECs were not significantly affected by 50 μM KPR, thus it was selected as the optimal KPR intervention concentration. KPR increased the viability of LPS-induced HGBECs. Additionally, KPR inhibited the inflammatory factors level (IL-1β, IL-6, and TNF-α) and protein expression (iNOS and COX-2) in LPS-induced HGBECs. Furthermore, KPR reversed LPS-induced elevation of p-IκBα/IκBα, p-p65/p65, p-JNK/JNK, p-ERK/ERK, and p-p38/p38 ratios. KPR attenuates the LPS-induced inflammatory response in HGBECs, possibly by inhibiting MAPK/NF-κB signaling., (© 2024 John Wiley & Sons Ltd.)

This study aimed to investigate the effect of fatty acid-ethanol amine (FA-EA) derivatives (L1-L10) on the mitigation of intracellular lipid accumulation and downregulation of pro-inflammatory cytokines in vitro. First, the series of FA-EA derivatives were synthesized and characterized. Then, their cytotoxic, intracellular lipid accumulation and inhibition of pro-inflammatory cytokines were evaluated. The oil red O staining experiment showed that the tested compounds L4, L6, L8, L9, and L10 could reduce intracellular lipid accumulation induced by palmitic acid (PA). Moreover, ω-3/ω-6 PUFA-EA derivatives showed inhibitory effect on the production of pro-inflammatory cytokines in lipopolysaccharide (LPS) -stimulated RAW 264.7 cells. ω-3/ω-6 PUFA-EA derivatives at a concentrations of 10 μM could significantly decrease mRNA levels of IL-6, IL-1β, and TNF-α, inhibit NO production, and alleviate the protein expression of IL-1β in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. These data suggest that ω-3 PUFA-EA derivatives can be beneficial for further pharmaceutical development to treat chronic low-grade inflammation diseases such as obesity., (© 2023 AOCS.)