Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) (CT)
- Known as:
- Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) (CT)
- Catalog number:
- pc-598
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) ()
Related genes to: Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) (CT)
- 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: Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) (CT)
Related articles to: Polyclonal Toll Interactin Protein (TOLLIP/TOLIP) (CT)
- To investigate the anxiolytic effects of Baihe Dihuang decoction (, BDD) and its underlying molecular mechanisms, focusing on cannabinoid type 2 receptor (CB2R)-mediated regulation of microglial polarization and the toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB) signaling pathway. - Source: PubMed
Qiaoyun LuoYuanshan HanYang LiuLin TangTianyu WangYuhong WangHongqing Zhao - Metabolic dysfunction-associated fatty liver disease (MAFLD) has become the most common chronic liver disease worldwide, currently affecting approximately 32% of the global adult population.Initially presenting as simple hepatic steatosis, MAFLD often progresses to severe cardiovascular complications, imposing significant healthcare and economic burdens. Current clinical management relies primarily on lifestyle interventions, with few targeted pharmacotherapies available, highlighting the urgent need for deeper mechanistic understanding and innovative treatments. A growing body of research highlights the critical role of intestinal homeostasis in the development and progression of MAFLD. Modern studies refer to the bidirectional communication between the gut and liver via the biliary tract, portal vein, and systemic circulation as the "gut-liver axis." This structural connection makes the liver more susceptible to damage from gut-derived microbes, metabolites, endotoxins, and inflammatory mediators, positioning the liver as a key target organ exposed to the intestinal microenvironment. For instance: LPS (endotoxin) a component of Gram-negative bacteria, activates the TLR4 signaling pathway, triggering NF-κB and promoting the release of pro-inflammatory cytokines such as TNF-α and IL-6. This amplifies inflammation and compromises the intestinal barrier, allowing bacteria and their products to enter the liver via the portal vein and induce liver injury. Short-chain fatty acids (SCFAs, e.g., butyrate), produced by the fermentation of dietary fiber, inhibit histone deacetylase (HDAC) and activate G-protein-coupled receptors (e.g., GPR43, GPR109A). These mechanisms promote the differentiation of regulatory T cells (Treg) and the production of IgA antibodies, thereby suppressing inflammation and strengthening the mucosal barrier.Secondary bile acids (e.g., 3-oxoLCA), generated through microbial modification of bile acids, can regulate the Treg/Th17 balance via nuclear receptors such as the vitamin D receptor (VDR). Numerous studies have observed microbial dysbiosis in MAFLD, characterized by an increase in Bacteroidetes and a decrease in Firmicutes.Emerging therapies targeting gut microbiota-including microbial metabolite modulators (HDCA, 4-HPAA) and multi-target traditional Chinese medicines (silymarin, Cornus officinalis glycosides)-demonstrate promising therapeutic potential when combined with interventions like probiotics and fecal microbiota transplantation. - Source: PubMed
Publication date: 2026/08/10
Xue LihongWang HaojieShan BowenLi ChangwenChen HongyanYu ChangqingXia ChangyouZhang He - Diabetic foot ulcers (DFUs) represent a severe complication of diabetes, with persistent nonhealing closely associated with bacterial colonization and excessive inflammation. S100A8 participates in immune regulation, but its mechanism in DFU healing remains unclear. This study aimed to investigate whether S100A8 regulates the DFU healing process via the TLR4/NF-κB pathway. - Source: PubMed
Wang QiSun TongXu YanFeiZhang LiLi JiaoGuo Lei - Icariside II (ICS II), a PDE5 inhibitor, is a flavonoid glycoside and primary metabolite of icariin, derived from the herb Herba epimedii, and exhibits promising neuroprotective potential in various pre-clinical studies. The current review provides evidence that ICS II shows neuroprotective potential against various neurological disorders, mainly including Alzheimer's disease, Parkinson's disease and Cerebral ischemia through modulating neuroinflammation, oxidative stress, neural apoptosis, neurogenesis, mitochondrial and cognitive dysfunction. It regulates multiple signalling pathways including PI3K/Akt, Keap1/Nrf2, TLR4/MyD88/NF-κB, cGMP/PKG/CREB, TGFB1/Smad, Wnt/β-catenin signaling and BDNF/TrkB/CREB. The pre-clinical evidence suggests that ICS II attenuates oxidative stress through increasing antioxidant enzymes SOD, GSH, catalase, and HO-1, with decreasing MDA and lipid peroxidation. Neuroinflammation is suppressed by inhibition of pro-inflammatory cytokines and down-regulation of IL-1β, IL-6, TNF-α, COX-2, iNOS levels and up-regulation of tight-junction proteins like occludin, claudin-5, ZO-1. Apoptosis is regulated via altering PARP, Bcl-2, Bax/Bcl-2 ratio and reducing caspase-3 activation. Mitochondrial dysfunction is ameliorated by restoring Complex I activity and increasing mitofusin-1/2 expression and reducing mitochondrial fission factors. Collectively, these molecular mechanisms show promise for ICS II as a potential candidate in different in vivo and in vitro studies of neurological disorders. - Source: PubMed
Solanki AshutoshSharma KhushiJain JagratiSingh Niraj KumarKrishnamurthy Praveen T - Reproductive disorders from viral infections cause major economic losses in livestock. This review provides a comprehensive mapping of natural compounds (monomers, extracts, and traditional Chinese medicine formulas) against 12 key viruses causing reproductive disorders in pigs, cattle, and sheep. A total of 297 independent studies were included. The compounds targeted multiple nodes within four conserved host signaling networks: NF-κB (TLR4, p65, IRF3, IκBα, ERK1/2), MAPK (p38 MAPK, JNK), apoptosis-related factors (Caspase-3, Bcl-2, Bax), and autophagy-related factors (AKT, p62). By modulating these networks, this multi-target, on-demand regulatory strategy endows natural compounds with broad-spectrum regulatory effects on host responses and the ability to reduce drug resistance. These findings consequently provide a theoretical basis for developing a single natural product combination that is effective against multiple reproductive disorder viruses. - Source: PubMed
Publication date: 2026/08/24
Su QilingWu JiangShi QinyaoChen HaienHu ChongkaiHuang YidanKang Kai