ArticleImmunity, inflammation and disease2025
EGCG Regulates the Effect of HDAC6 on Oxidative Stress of Human Periodontal Ligament Fibroblasts Induced by Lipopolysaccharide.
Article in Immunity, inflammation and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Epigallocatechin gallate in dentistry: Therapeutic applications, biomaterial integration, and translational challenges.Journal of dental sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundEpigallocatechin gallate (EGCG) has anti-inflammatory and antioxidative stress effects in periodontitis. However, the specific mechanisms involved remain unclear. Our study explored whether the mechanism by which EGCG on alleviates inflammation and oxidative stress in human periodontal ligament fibroblasts (hPDLCs) involves HDAC6.
methodsWe treated hPDLCs with lipopolysaccharide (LPS) and EGCG, and detected the resultant effects on cell proliferation by the CCK-8 method. Cells were divided into three groups: control, LPS, and EGCG + LPS. The expression of tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) was detected by enzyme-linked immunosorbent assay (ELISA), and the expression of reactive oxygen species (ROS) was detected using 2',7'-dichlorofluorescein diacetate. The expression of histone deacetylase 6 (HDAC6), p62, heat shock protein 70 (Hsp70), Kelch-like ECH-associating protein (Keap1), nuclear factor E2-related factor 2 (Nrf2), and heme oxygenase-1(HO-1) mRNA was detected by real-time quantitative polymerase chain reaction (RT-qPCR). The protein expression of HDAC6, Nrf2, and nod-like receptor protein 3 (NLRP3) was detected by western blotting.
resultsAt concentrations of less than 100 μmol/L, EGCG can promote cell proliferation and significantly inhibit the levels of TNF-α and IL-1β. Moreover, EGCG can activate the Nrf2 pathway and inhibit ROS production. Furthermore, EGCG inhibited the expression of HDAC6 and promoted the expression of p62 and Hsp70, indicating that the anti-inflammatory and antioxidant effects of EGCG are closely related to HDAC6.
conclusionsEGCG can regulate LPS-induced oxidative stress levels of hPDLCs through the Keap1/Nrf2/HO-1 pathway and reduce the expression of HDAC6-related factors. Therefore, HDAC6 may be a potential target for EGCG in the treatment of periodontal inflammation and oxidative stress.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.