HorseAlbumin, IgA, IgGa, IgGb, IgG(T), IgM, TNF-alpha
- Known as:
- HorseAlbumin, Immunoglobulin A, IgGa, IgGb, Immunoglobulin G(T), Immunoglobulin M, TNF-a
- Catalog number:
- CT007
- Product Quantity:
- 1 x 96
- Category:
- -
- Supplier:
- Celltrend
- Gene target:
- HorseAlbumin IgA IgGa IgGb IgG() IgM TNF-alpha
Related products to: HorseAlbumin, IgA, IgGa, IgGb, IgG(T), IgM, TNF-alpha
Related articles to: HorseAlbumin, IgA, IgGa, IgGb, IgG(T), IgM, TNF-alpha
- Many lines of evidence suggest that circular RNAs (circRNAs) are closely associated with the occurrence and progression of colon cancer. The objective of this study was to investigate the regulatory effects and mechanisms of circ_0075829 on ferroptosis and immune escape in colon cancer. We utilized colon cancer cell lines and a xenograft mouse model to analyze the function of circ_0075829 in vitro and in vivo. The gene expression level was assessed by qRT-PCR and western blotting. Cell proliferation was evaluated using the CCK-8 assay. The targeting relationships between circ_0075829, miR-330-5p, and TCF4 were analyzed through a dual-luciferase reporter experiment and RNA pull-down experiment. Cytokine levels were measured using the ELISA assay. Fe2+, MDA, and SOD levels were tested using appropriate kits, and the ROS level was detected by immunofluorescence. Knockdown of circ_0075829 resulted in increased levels of Fe2+, ROS, and MDA and decreased levels of GPX4 and xCT proteins in cells. Furthermore, silencing of circ_0075829 increased the cell proliferation rates of CD8+T cells co-cultured with colon cells. Moreover, it also enhanced IFN-γ, IL-2, and TNF-α concentration in the supernatants of the co-culturing system and reduced PD-L1 protein expression levels. Subsequently, silencing of circ_0075829 induced ferroptosis and inhibited immune escape in vivo. Meaningfully, we certified that circ_0075829 functions as a sponge for miR-330-5p, leading to the upregulation of TCF4 expression. TCF4 was identified as a downstream target of miR-330-5p. Additionally, co-transfection with anti-miR-330-5p or TCF4 overexpression plasmid reversed the effects observed following the knockout of circ_0075829. Collectively, our research indicates that the circ_0075829 plays a significant role in regulating ferroptosis and immune escape in colon cancer by sponging miR-330-5p to modulate TCF4 expression. - Source: PubMed
Fan HuajunDing YuXiao ZheLi ShengboZheng Yongbin - Spinal cord injury (SCI) is one of the devastating neurological disorders that leads to a loss of motor and sensory functions. Long non-coding RNA small nucleolar RNA host gene 6 (lncRNA SNHG6) plays a crucial role in inflammatory regulation across various diseases. This study investigates the role of SNHG6 in SCI development and its underlying regulatory mechanisms. Two experimental models were established: an in vitro model using LPS-challenged (100 ng/mL) mouse microglia BV2 cells and an in vivo model employing controlled spinal cord impact in mice. SNHG6, miR-182-5p, and NEUROD4 expression levels were quantified through RT-qPCR and Western blot. Functional and histological assessments were performed using the Basso mouse scale (BMS) and Nissl staining, respectively. Putative binding sites between SNHG6 and miR-182-5p, as well as between miR-182-5p and NEUROD4, were predicted using the ENCORI/starBase platform. These molecular interactions were validated through dual-luciferase reporter assays and RNA pull-down experiments, with further confirmation by qRT-PCR and Western blot analyses. Both LPS-stimulated BV2 cells and spinal cord tissues from SCI mice exhibited elevated SNHG6 expression. Downregulation of SNHG6 enhanced LPS-induced polarization of BV2 cells from M1-type to M2-type, significantly modulated the expression of pro-inflammatory factors (TNF-α, IL-1β, and IL-6) and anti-inflammatory factors (TGF-β, IL-10, and IL-13), and reduced injury severity in SCI mice. Our mechanistic studies revealed that SNHG6 functions as a molecular sponge for miR-182-5p to regulate NEUROD4 expression. This study demonstrates that SNHG6 knockdown promotes microglial M2-type polarization and alleviates inflammatory responses through modulation of the miR-182-5p/NEUROD4 axis, suggesting SNHG6 as a potential therapeutic target for SCI treatment. - Source: PubMed
Publication date: 2025/01/20
Feng LuqianLi Gang - Sea buckthorn is a model of medicine and food homology, but the chemical composition and mechanism of anti-inflammatory effects are limited. In this study, the key components and mechanisms of the anti-inflammatory effects of sea buckthorn were identified based on UPLC-Q-TOF-MS, network pharmacology, molecular docking, molecular dynamics and RAW264.7 cells. The predicted key anti-inflammatory compounds in sea buckthorns were cianidanol, kaempferol, pelargonidin, and ent-epicatechin, and the key targets were EGFR, TNF, STAT3, and IL-10. The anti-inflammatory effects of sea buckthorn may be achieved via the synergistic regulation of multiple biological pathways. Furthermore, cianidanol significantly reduced the secretion of NO, IL-6, TNF-α, and IL-1β and the expression of phosphorylated JAK2 and STAT3 in LPS-stimulated RAW264.7 cells, as determined by ELISA and western blotting. Cianidanol from sea buckthorns exerts anti-inflammatory effects by reducing the expression of inflammatory mediators and pro-inflammatory cytokines, and inhibiting the JAK2/STAT3 signaling pathway. Thus, sea buckthorn can be developed into a promising functional food with anti-inflammatory properties. - Source: PubMed
Publication date: 2025/01/20
Liu ChuanYi XiangruiLi YafanXu HuijuanWang PengYang WenyuLi LingTu Ya - Fucoidan from Apostichopus japonicus (Aj-FUC) has shown anti-inflammatory activity, whereas its mechanism was not explicated. This study investigated the anti-inflammatory potential and mechanism of the fucoidan from green and purple A. japonicus (G-FUC and P-FUC) in lipopolysaccharide (LPS)-treated RAW264.7 cells. Results showed that Aj-FUCs at 25-400 µg/mL had no toxicity to cells after 24 h stimulation and promoted cell phagocytic activity. ELISA results indicated that Aj-FUC reduced the nitric oxide (NO), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-6 levels and increased IL-10 level. The Aj-FUC suppressed transcription of inflammatory-related genes (tnf-α, il-1β, il-6, nlrp3, inos, cox-2, tlr4, trif, and nf-κb) in LPS-treated RAW264.7 cells, among which G-FUC had stronger anti-inflammatory effects. Moreover, Aj-FUC upregulated the mRNA expression of autophagic genes (beclin1, lc3II, and lamp2). The immunoblotting and immunofluorescence analyses of Beclin-1 and LC3II supported that Aj-FUC enhanced autophagy activity. After autophagy inhibited by 3-methyladenine, the mRNA expressions of tnf-α, il-6, il-1β, and nlrp3 were significantly upregulated in LPS-induced cells treated with Aj-FUC, suggesting the suppressed inflammation by Aj-FUC mediated via autophagy. Summarily, the present study demonstrated that Aj-FUC showed anti-inflammatory effects by elevating autophagy activity in LPS-induced macrophages. - Source: PubMed
Publication date: 2025/01/20
Hou TingtingLiu XiaolinZhang ShuaiTang KuiLiu ShilinLiu JialiangFan XiaotengWang Zaizhao - Adenosine, a critical molecule regulating cellular function both inside and outside cells, is controlled by two human adenosine deaminases: ADA1 and ADA2. While ADA1 primarily resides in the cytoplasm, ADA2 can be transported to lysosomes within cells or secreted outside the cell. Patients with ADA2 deficiency (DADA2) often suffer from systemic vasculitis due to elevated levels of TNF-α in their blood. Monocytes from DADA2 patients exhibit excessive TNF-α secretion and differentiate into pro-inflammatory M1-type macrophages. Our findings demonstrate that ADA2 localizes to endolysosomes within macrophages, and its intracellular concentration decreases in cells secreting TNF-α. This suggests that ADA2 may function as a lysosomal adenosine deaminase, regulating TNF-α expression by the cells. Interestingly, pneumonia patients exhibit higher ADA2 concentrations in their bronchoalveolar lavage (BAL), correlating with elevated pro-inflammatory cytokine levels. Conversely, cord blood has low ADA2 levels, creating a more immunosuppressive environment. Additionally, secreted ADA2 can bind to apoptotic cells, activating immune cells by reducing extracellular adenosine levels. These findings imply that ADA2 release from monocytes during inflammation, triggered by growth factors, may be crucial for cell activation. Targeting intracellular and extracellular ADA2 activities could pave the way for novel therapies in inflammatory and autoimmune disorders. - Source: PubMed
Publication date: 2025/01/20
Dong LiangLu BingtaiLuo WenwenGu XiaoqiongWu ChengxiangTrotta LucaSeppanen MikkoZhang YuxiaZavialov Andrey V