TNF-alpha antibody Polyclonal Antibodies Primary antibodies
- Known as:
- TNF-a (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100003
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- TNF-alpha antibody Polyclonal Antibodies Primary antibodies
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Related articles to: TNF-alpha antibody Polyclonal Antibodies Primary antibodies
- This study aimed to investigate the effects of Mediterranean and Western diet models on telomere length, oxidative stress, inflammatory markers, and total hippocampal cell count in rats. - Source: PubMed
Publication date: 2026/04/19
Tilekli Mehmet MustafaAcar Tek Nilüfer - To compare the therapeutic effects of intravenous (IV) and intratracheal (IT) delivery of adipose-derived stem cells (ADSCs) in a mouse model of bleomycin (BLM)-induced idiopathic pulmonary fibrosis (IPF). - Source: PubMed
Publication date: 2026/02/28
Ng Yan-YanChiang Chen-YuNi Yung-LunShen Huan-TingLee Chien-YingLee Tai-PingSieber MartinTseng Ching-ChiTsao Thomas Chang-YaoKuan Yu-Hsiang - This study investigated the role of TGF-β-activated kinase 1 (TAK1) in synovial inflammation and hyperplasia in JIA synovial fibroblasts (JIASFs). - Source: PubMed
Publication date: 2026/04/17
Shanta Meena ALough Donavon CHenderson Lauren ANigrovic Peter AAhmed Salahuddin - Acute pancreatitis is a complex inflammatory disease with high morbidity and mortality, closely associated with intestinal barrier dysfunction, gut microbiota dysbiosis and abnormal lipid metabolism. Akkermansia muciniphila has been shown to exert beneficial effects on the host via bioactive components such as Amuc proteins. Here, we investigate the effect of Amuc_1098 on acute pancreatitis in mice induced by caerulein combined with lipopolysaccharide or L-arginine. We show that oral administration of Amuc_1098 reduces pancreatic tissue injury and the levels of serum amylase and lipase. Mechanistically, it suppressed NF-κB signaling partially dependent on TLR2, thereby reducing the levels of pro-inflammatory factors (TNF-α, IL-1β, IL-6) and the proportion of macrophages in the spleen, pancreas and intestine, and reversed downregulation of colonic tight junction proteins via TLR2 to protect intestinal barrier function. Amuc_1098 improves disrupted glycerophospholipid metabolism seen in both acute pancreatitis patients and mice. Together, these results suggest that Amuc_1098 alleviates acute pancreatitis severity by exerting anti-inflammatory effects, reducing macrophage infiltration, enhancing colonic tight junction proteins, and regulating intestinal flora and glycerophospholipid metabolism. - Source: PubMed
Publication date: 2026/04/18
Wang LijuanZhang RuilinZhao LiangtaoXiao LiuxiangZhang XiaoyanLiu LingyiWang JiajuChen KuiyuanLi JinyangZhang MaosenLi JieLin Wei - Preterm birth (PTB) is a principal contributor to neonatal morbidity, wherein inflammation and dysregulated cell death pathways are implicated as key drivers in its pathogenesis. However, the role of the RIPK1/RIPK3-MLKL signaling axis, a critical regulator of necroptosis and inflammatory responses, remains poorly characterized in the context of PTB. Here, we sought to elucidate the role of RIPK1-mediated activation of the RIPK3-MLKL pathway in placental inflammation and its involvement in PTB pathogenesis. In vitro experiments were conducted using TNF-α-stimulated HTR8/SVneo trophoblasts, while an LPS-induced murine model was employed to mimic inflammation-associated PTB. RIPK1 expression was modulated via shRNA-mediated knockdown or pharmacological inhibition with GSK2982772 and Nec-1. Molecular analyses included qPCR, Western blotting, ELISA, and the assessment of necroptosis via PI staining. We found that TNF-α and LPS significantly upregulated RIPK1 expression and activated the RIPK3-MLKL pathway in both the cellular and animal models. RIPK1 knockdown or pharmacological inhibition attenuated TNF-α-induced proinflammatory cytokine release (IL-1β, IL-6, TNF-α), uric acid accumulation, RIPK3-MLKL pathway activation, and necroptosis in trophoblasts at both 24 and 48 h. Notably, in vivo treatment with Nec-1 ameliorated LPS-induced placental damage. Collectively, our findings demonstrate that RIPK1 drives inflammation and necroptosis in PTB through RIPK3-MLKL activation, suggesting that targeting RIPK1 may represent a promising therapeutic strategy for inflammation-associated preterm labor. - Source: PubMed
Publication date: 2026/04/18
Bing XuexiangWang YongqingZheng JiacuiGao GuodongJiang JinxiaoLiu LanlanZhang Xue