Ask about this productRelated genes to: HTA125 TLR4
- 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: HTA125 TLR4
Related articles to: HTA125 TLR4
- This study aimed to evaluate the efficacy of cinnabarinic acid (CA) in regulating the barrier function and inflammatory responses of primary intestinal epithelial cells (IECs) derived from chicken embryos subjected to hyperthermia, so as to provide a theoretical basis for alleviating heat stress in broilers. The IECs were randomly divided into 4 groups, a thermoneutral group (37 °C), a hyperthermia group (43 °C), a hyperthermia + CA group and a hyperthermia + CA + aryl hydrocarbon receptor (AhR) inhibitor group. A hyperthermia cell model was established by exposing IECs to 43 °C for 6 h, and the experimental treatments consisted of 1 µmol/L CA and 1 µmol/L AhR inhibitor. According to the results, the supplementation of 1 µmol/L CA into the basal culture medium markedly improved the relative cell viability of hyperthermia-treated IECs, decreased the levels of lactate dehydrogenase (LDH), tumor necrosis factor alpha (TNF-α), and interleukin (IL)-1β in cell culture supernatants, downregulated the mRNA expression of heat shock protein (HSP)70, HSP90, claudin2, toll-like receptor (TLR)4, TLR5 and TLR21, increased AhR protein expression and the mRNA expression of occludin, increased the secretion of IL-22 of IECs treated with hyperthermia. Notably, the protective and regulatory effects of CA were markedly abolished by the AhR inhibitor under hyperthermic conditions. In conclusion, CA activated AhR in IECs, promoted IL-22 secretion, inhibited inflammatory responses, increased tight junction proteins genes expression, enhanced epithelial barrier integrity. - Source: PubMed
Publication date: 2026/06/08
Li QiufenOuyang JingxinDeng ChenxiChen XiaolianLiu YichunZhou HuaLi Guanhong - Osteoarthritis (OA) represents a significant unmet clinical need, where current management strategies primarily alleviate symptoms but fail to halt disease progression and are often associated with adverse effects. Curcumin, a natural polyphenol, has emerged as a promising therapeutic candidate. To systematically evaluate its efficacy and mechanisms, we conducted a systematic review and meta-analysis of studies from databases including PubMed, Web of Science, CNKI, and Wanfang up to October 2025. Nineteen preclinical studies meeting the inclusion criteria were analyzed. The results demonstrated that curcumin significantly improved OARSI scores (MD = - 3.36), knee diameter (SMD = - 4.40), paw withdrawal threshold (MD = 4.36), and reduced apoptotic chondrocytes (SMD = - 9.50). Mechanistically, it enhanced antioxidant defense via SOD activity (SMD = 5.17) and suppressed the TLR4/NF-κB pathway, reducing key upstream signaling mediators (TLR4: SMD = - 1.41; NF-κB: SMD = - 3.72) and downstream pro-inflammatory cytokines (TNF-α: SMD = - 3.37; IL-6: SMD = - 10.19). Furthermore, it preserved cartilage metabolism by increasing type II collagen (SMD = 2.00) and decreasing MMP-13 (SMD = - 3.51) and COMP (SMD = - 2.95). These findings indicate that curcumin exerts multi-target protective effects in OA by mitigating oxidative stress, suppressing the TLR4/NF-κB inflammatory pathway, and reducing cartilage degradation, providing a theoretical foundation for its clinical translation. Future research employing standardized methodologies will be crucial to fully elucidate the mechanistic basis of curcumin's action and optimize its therapeutic potential for clinical applications. - Source: PubMed
Publication date: 2026/06/08
Liu HaoYe ZixiangWu ChenjiaCai ChennuoFang HuilingWang Qinglai - Phenotypic switching in vascular smooth muscle cells (VSMCs) is key to the formation and progression of intracranial aneurysms (IAs). High-mobility group box 1 (HMGB1), a damage-associated molecule, significantly influences the progression of various diseases. Ferroptosis is an iron-dependent cell death process that is controlled by extensive membrane damage induced by lipid peroxidation. However, few studies have investigated the associations between VSMCs, HMGB1, ferroptosis, and IAs. To analyze the associations between VSMCs, HMGB1, ferroptosis, and IAs, we collected human tissue and blood samples, established an oxidative damage model in VSMCs induced using hydrogen peroxide, and analyzed the effects of interventions related to ferroptosis and HMGB1 on VSMC phenotypic changes in vitro. We measured ferroptosis levels, proliferation, migration capacity, and inflammatory molecule expression in VSMCs. In addition, we analyzed the nuclear-cytoplasmic translocation of HMGB1 and the nuclear factor κ light chain-enhancer of activated B cells (NF-κB) protein subunit p65. Then, we investigated the effects of HMGB1 inhibition on IA formation and progression in an elastase-induced rat model. Clinical experiments using human samples confirmed significant correlations between VSMC phenotypic switching, HMGB1, ferroptosis, and IAs. HMGB1 was activated and underwent translocation from the nucleus to the cytoplasm under oxidative stress conditions. By binding to TLR4, HMGB1 activated the NF-κB p65 pathway, promoted NF-κB p65 nuclear translocation, and induced inflammatory responses and ferroptosis, thereby mediating VSMC phenotypic switching. In animal studies, HMGB1 inhibition markedly reduced IA formation and progression. HMGB1 regulates VSMC phenotypic switching and contributes to the development of IAs by mediating ferroptosis. - Source: PubMed
Publication date: 2026/06/08
Zhu HuaxinZeng YanyangXiao ZhipengTan JiacongXin WenqiangZheng ZhifanZhao YeyuLi Meihua - Hypoxia-stimulated adipose-derived mesenchymal stem cells (ADSCs)-derived exosomes (Hypo-Exo) have a positive impact on diabetic wound healing. Neutrophil extracellular traps (NETs) can delay wound healing under diabetic hyperglycemia. This study aimed to investigate the mechanisms by which Hypo-Exo influence NETs formation. - Source: PubMed
Publication date: 2026/06/08
Qian LiMeng XianxiFang BairongPi Li - Docetaxel (DTX) resistance limits therapeutic efficacy in gastric cancer (GC). Through RNA sequencing of DTX-resistant GC cells, we identified insulin-like growth factor-like family member 2 (IGFL2) as a key upregulated gene. We demonstrate that IGFL2 overexpression enhances GC cell proliferation, migration, and invasion while suppressing apoptosis, thereby reducing DTX sensitivity. Mechanistically, IGFL2 directly binds the Toll-like receptor 4 (TLR4) promoter, activating the TLR4/MyD88/p65 pathway and upregulating drug efflux pumps MDR1 and BCRP. Knockdown of IGFL2 resensitizes resistant cells to DTX both and in mouse xenograft models. These findings establish IGFL2 as a regulator of DTX resistance via TLR4 signaling, suggesting its relevance as a therapeutic target for overcoming chemoresistance in GC. - Source: PubMed
Publication date: 2026/05/29
Huang WeiTao ZhiruiXu XiaolinCao HuangmingCheng LiLi Jin