Mechanism of action of Coptidis Rhizome in treating periodontitis based on network pharmacology and in vitro validation.

OBJECTIVE: Explore the therapeutic mechanism of Coptidis Rhizome (CR) in periodontitis using network pharmacology, and validate it through molecular docking and in vitro experiments. METHODS: Screened potential active components and target genes of CR from TCMSP and Swiss databases. Identified periodontitis-related target genes using GeneCards. Found common target genes using Venny. Conducted GO and KEGG pathway analysis. Performed molecular docking and in vitro experiments using Berberine, the main active component of CR, on lymphocytes from healthy and periodontitis patients. Assessed effects on inflammatory factors using CCK-8, flow cytometry, and ELISA. RESULTS: Fourteen active components and 291 targets of CR were identified. 30 intersecting target genes with periodontitis were found. GO and KEGG analysis revealed oxidative stress response and IL-17 signaling pathway as key mechanisms. Molecular docking showed strong binding of Berberine with ALOX5, AKT1, NOS2, and TNF. In vitro experiments have demonstrated the ability of berberine to inhibit the expression of Th17 + and other immune related cells in LPS stimulated lymphocytes, and reduce the secretion of IL-6, IL-8, and IL-17. CONCLUSION: CR treats periodontitis through a multi-component, multi-target, and multi-pathway approach. Berberine, its key component, acts through the IL-17 signaling pathway to exert anti-inflammatory effects.

The associations of two novel inflammation indexes, systemic immune-inflammation index (SII) and system inflammation response index (SIRI), with periodontitis: evidence from NHANES 2009-2014.

OBJECTIVES: The research's goal is to look for any potential relationships between the systemic immune-inflammation index (SII) and the system inflammation response index (SIRI), along with inflammation indicators and the likelihood of periodontitis. METHODS: Ten thousand two hundred eighty-two individuals in sum were determined to be eligible for this cross-sectional study from the National Health and Nutrition Examination Survey (NHANES) between 2009 and 2014. Multiple logistic regression, generalized additive model, smooth curve fitting, subgroup analysis, and interaction tests were done for analyzing the association between periodontitis and SII, SIRI, and other inflammatory indicators. RESULTS: The analysis, adjusted for population weighting, revealed that individuals with moderate/severe periodontitis had SII levels of 545.46 (95% CI (529.10, 561.82), P = 0.0044) and SIRI levels of 1.33 (95% CI (1.29, 1.37), P < 0.0001). In a fully adjusted multivariate logistic regression model, SII was not sensibly associated with moderate/severe periodontitis among the continuous and quartile Q1-Q4 groups (OR = 0.97, 95% CI (0.91, 1.02)). The continuous variable of SIRI (OR = 1.11, 95% CI (1.06, 1.17)) and the quartile Q4 group (OR = 1.58, 95% CI (1.28, 1.94)) had a deemed significant positive association with moderate to severe periodontitis. In addition, other inflammatory indicators, especially NLR, PPN, PLR, MLR, PC, NC, and MC were observed to be notably involved moderate/severe periodontist in this research. CONCLUSION: We explored the association between periodontitis and two novel comprehensive markers of inflammation (SII and SIRI). CLINICAL RELEVANCE: These inflammatory markers are expected to serve as tools to assist clinicians in diagnosing periodontitis.

Causal association between asthma and periodontitis: A two-sample Mendelian randomization analysis.

BACKGROUND: A unified view of whether asthma and periodontitis interact and the direction of action is not found in previous studies. Therefore, in this article, we will elucidate bidirectional causality by two-sample Mendelian randomization (MR). METHODS: We obtained summary-level data for asthma and periodontitis from the massive GWAS databases of several publicly available. Meanwhile, it will ensure no confounders like smoking using the Phenoscanner website to have a search over each SNP. The F statistic value of each SNP is calculated as more significant than 10. This MR analysis mainly used five MR methods: MR-Egger, weighted median, inverse variance weighted (IVW), simple mode, and weighted mode. As a result, we performed heterogeneity and horizontal pleiotropy tests. RESULTS: We have found supporting evidence to verify the hypothesis that asthma may be a protective factor for periodontitis (IVW OR = 0.34; 95% CI = [0.132,0.87]; p = 0.025). The consistent impact direction is shown when additional asthma GWAS dataset are used (MR-Egger OR = 0.118; 95%CI = [0.016,0.883]; p = 0.04). There is no evidence of a causal effect of periodontitis at the risk of asthma in the reverse analysis (p > 0.05). CONCLUSIONS: Our analysis found that people with asthma may have a lower risk of periodontitis than those without. This MR analysis could have significant implications for the clinical process and future research.