Ask about this productRelated genes to: TLR4 antibody
- Gene:
- TLR4 NIH gene
- Name:
- toll like receptor 4
- Previous symbol:
- -
- Synonyms:
- hToll, CD284, TLR-4, ARMD10
- Chromosome:
- 9q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-01-21
Related products to: TLR4 antibody
Related articles to: TLR4 antibody
- L. (CR), a globally pervasive weed with dual agricultural and medicinal significance, undergoes vinegar-processed (VCR) to enhance its hepatoprotective properties. This study investigated the phytochemical and functional changes induced by vinegar processing and elucidated the role of α-cyperone, a key bioactive sesquiterpene, in modulating gut-liver axis homeostasis. UPLC-Q-Exactive Orbitrap MS and HPLC analyses revealed a significant increase in α-cyperone content post-vinegar processing. In thioacetamide-induced acute and chronic liver injury models, VCR significantly outperformed CR in reducing serum ALT and AST, hepatic TNF-α and IL-6, and oxidative stress, while restoring gut barrier integrity via up-regulation of ZO-1 and occludin. Molecular docking supported α-cyperone's high-affinity binding to the TLR4/NF-κB pathway, corroborated by western blot and immunofluorescence. Gut microbiota analysis demonstrated VCR's capacity to reverse dysbiosis, notably enriching Bacteroidetes and improving microbial diversity. These findings highlight edible vinegar processing as a sustainable strategy to transform agricultural waste into a functional food-grade intervention for liver health, mediated by α-cyperone-driven modulation of the gut-liver axis. - Source: PubMed
Publication date: 2026/05/04
Jia-He GaoLi-Ting LinYue-Han LiuFu-Chao WangJun-Tong LiuTian-Hui Gao - Oxidative stress and inflammation are interconnected drivers of cellular damage in pathologies ranging from neurodegenerative disorders to sensorineural hearing loss. We aimed to develop a chitosan-Prussian blue nanozyme (CS-PB) to target these processes in sensorineural hearing loss. CS-PB (35 μg/mL) pretreatment of HO-injured HEI-OC1 cochlear cells for 4 h markedly decreased the levels of reactive oxygen species (ROS) inside cells (from 3.8 to 2.4 relative fluorescence intensity) by approximately 37% ( < 0.001)-and concomitantly significantly decreased expression of the oxidative damage markers 4-HNE and 3-NT (both < 0.001). The rate of apoptosis decreased from 27.5% in the HO-treated group to 14.1% following CS-PB treatment (P < 0.01). This reduction was accompanied by a significant downregulation of the pro-apoptotic proteins Bax (P < 0.05) and Cleaved-caspase-3 (P < 0.001), as well as an upregulation of the anti-apoptotic protein Bcl-XL (P < 0.01).Western blot analysis confirmed that CS-PB significantly downregulated TLR4 expression and inhibited downstream phosphorylation of p-P65/P65, while upregulating p-IκBα/IκBα protein (all < 0.01) associated with reduction in the production of inflammatory cytokines like TNF-α, IL-1β, and IL-6. Treatment with the specific TLR4 antagonist TAK-242 (2 μM) mimicked the effect of CS-PB, with coadministration showing no additional ant-inflammatory effect (although HEI-OC1 viability was additionally increased), indicating that the anti-inflammatory properties of CS-PB were facilitated via the TLR4/NF-κB signaling pathway. , CS-PB pretreatment (2 mg/mL, 2 μL) was administered by carefully applying the solution to the round window membrane (RWM) using a microsyringe in a noise-induced hearing loss rat model, which significantly curtailed the noise-induced activation of the TLR4/NF-κB pathway in the cochlea. After 24 hours, the levels of p-P65/P65 and TLR4 decreased by 54% and 50%, respectively. ( < 0.001), and levels of the inflammatory cytokines IL-6, TNF-α and IL-1β were decreased by 53%, 48%, and 51% ( < 0.001). Furthermore, the degree of pathway inhibition showed a strong correlation with cytokine reduction (r = 0.87-0.89, all < 0.001). CS-PB showed no significant cytotoxicity or , suggesting that its combined ROS-scavenging and TLR4/NF-κB-modulating properties may represent a potential therapeutic strategy, pending further mechanistic and translational validation. - Source: PubMed
Publication date: 2026/04/21
Li YongWang NaRen PengchengZhai YueyiXie PengZhang ChunhuanQu Yan - [This corrects the article DOI: 10.3389/fphar.2026.1655883.]. - Source: PubMed
Publication date: 2026/04/21
Xu ZiyanWu HaoFan WeiyangMeng FenzhaoHu ShuangfeiZou MuhanChen YixuanSu WeiweiLi Peibo - Childhood obesity is tightly linked to dyslipidemia, chronic low-grade inflammation, and insulin resistance (IR). CD36 has been implicated in metabolic disease, yet its pediatric mechanisms remain unclear. This study aims to investigate the CD36/ANXA1/TLR4/NF-κB axis as a potential therapeutic target for lipid metabolism and IR in childhood obesity. - Source: PubMed
Publication date: 2026/05/04
Yao YiqingYang WeimingCheng FengMao Shunfeng - Sjögren's syndrome (SS) is a chronic systemic autoimmune disorder characterized by lymphocytic infiltration of exocrine glands and a lack of effective therapeutic options. Jiajian Yiguan Decoction (JYD) has demonstrated promising clinical efficacy in SS patients, yet its underlying mechanism remains unclear. - Source: PubMed
Publication date: 2026/05/05
Liu ErxiongGao Le-NyuWang Yong