Rat IL1b ELISA
- Known as:
- Rat IL1b Enzyme-linked immunosorbent assay test
- Catalog number:
- kt-18885
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Rat IL1b ELISA
Related genes to: Rat IL1b ELISA
- Gene:
- IL1B NIH gene
- Name:
- interleukin 1 beta
- Previous symbol:
- -
- Synonyms:
- IL1F2, IL-1B, IL1-BETA
- Chromosome:
- 2q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-31
- Date modifiied:
- 2016-10-05
Related products to: Rat IL1b ELISA
Related articles to: Rat IL1b ELISA
- Adenomyosis, a common gynecologic condition of the uterus, affects women with diverse symptoms including pain. Traditionally evaluated pathologically, advanced imaging modality has led to more diagnoses including asymptomatic women. This noninvasive diagnosis has raised questions about disease progression and symptom development. This study aimed to investigate the cellular and molecular patterns associated with adenomyosis and adenomyosis-related pain, focusing on inflammatory processes. We employed an integrative, retrospective bioinformatic design combining publicly available bulk RNA-sequencing data from adenomyotic and control endometrium and myometrium with single-cell RNA-sequencing data from adenomyosis patients stratified by the presence of pain. - Source: PubMed
Publication date: 2026/07/08
Kwon KanghyunKwon Ji YoungSheen KisungYu SanghyeonKim Ye-AhYoo Eun HeeLee KiwonKim Man S - Aortic dissection (AD) is a life-threatening vascular condition characterized by acute inflammation and structural deterioration of the aortic wall. This study aimed to delineate the immune landscape, particularly T cell-mediated responses, and identify conserved inflammatory mechanisms driving AD pathogenesis across human and murine models. - Source: PubMed
Publication date: 2026/07/11
Zhang ShenZhang YongguiSun YaodongZhu MinfangWu Naishi - Indoleamine 2,3-dioxygenase 1 (IDO1) facilitates tumoral immune evasion via the kynurenine (Kyn) pathway, while ABCB1-mediated efflux drives multidrug resistance. Previously, miconazoles were reported as potent IDO1 inhibitors and some azole antifungals inhibit efflux pumps. Herein, we report a miconazole analogue, 1g, which inhibits both mechanisms. An in-house library of miconazole analogues, incorporating oxime ether derivatives with imidazole and pyrazole rings, was screened against Kyn production in IDO1-expressing SK-OV-3 and HeLa cells, yielding the hit pyrazole derivative 1g (IC = ∼5.8µM). In vitro LDH assay showed minimal cytotoxicity for 1g and it was well tolerated by in vivo zebrafish model at 2 × IC concentrations. Molecular modelling and biochemical assays indicated apo-form preference for 1g, which suppressed Kyn production without affecting IDO1 protein levels or inducing apoptosis. In indirect co-cultured models, 1g reversed Kyn-mediated immunosuppression, significantly restoring pro-IL1B and TNF levels in LPS-induced THP-1 macrophages. Furthermore, 1g restored Jurkat T cell proliferation, aggregate formation, and PDCD1 expression independent of direct 1g exposure, confirming a Kyn-dependent mechanism. Finally, 1g inhibited ABCB1 function in a dose-dependent manner and enhanced the sensitivity of ABCB1-expressing cells to paclitaxel, demonstrating its efficacy as a multidrug resistance (MDR) reversal agent. Our findings characterised 1g as a promising low-micromolar dual inhibitor of apo-IDO1 and ABCB1 with minimal cytotoxicity. It simultaneously disrupts the immunosuppressive Kyn axis and modulates ABCB1-mediated efflux, which provides a robust pharmacological basis for further development of next-generation combinatorial therapies. - Source: PubMed
Publication date: 2026/07/11
Chen Pin-ChenChang Yung-ChiehHo Yun-YunTseng Kai-YuLin Kai-HsuanSari SuatÖzdemir ZeynepReynisson JóhannesLeung EuphemiaCheung Chun Hei Antonio - Migraine is associated with an increased risk of ischemic stroke, but the molecular mechanisms linking these two disorders remain unclear. - Source: PubMed
Publication date: 2026/07/11
Rong WenzhengXu JingLi BoZhang XiaofengLi YapengSong BoXu Yuming - Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy, and their side effects, such as cardiotoxicity, have become critical complications. Herein, we explored the potential mechanism of ICIs-related cardiotoxicity. Healthy male C57BL/6 J mice were intraperitoneally injected with a PD-1/PD-L1 inhibitor (BMS-1) at a total dose of 60 mg/kg. BMS-1 treatment led to cardiac injury, with elevated cardiac enzyme levels, numbers of apoptotic cells, cardiomyocyte cross-sectional areas, and α-SMA expression. BMS-1-induced H9c2 cardiomyocyte injury was immune cell dependent. Compared with the control treatment, BMS-1 treatment did not significantly alter the T-cell composition in the peripheral blood or spleen. However, fluorescence imaging revealed increased numbers of CD3 T cells, F4/80 macrophages, and Ly6G neutrophils in the hearts of BMS-1-treated mice. In addition, BMS-1 treatment also increased PD-L1 expression and activated inflammatory pathways, including AKT, p38 MAPK, mTOR, and STAT3. Interestingly, the expression of the inflammatory genes Il1b, Il17a, and Ifng; the T-cell activation genes Nkg7 and Cst7; the exhaustion genes Klrg1 and Tigit; and the transcription factors Tbx21 and Rora were markedly elevated in the thymus, but their expression was unchanged in the peripheral blood and spleen. Furthermore, electron microscopy revealed mitochondrial swelling and lipid droplets in the hearts of BMS-1-treated mice. Compared with those in control hearts, the levels of the lipid metabolism proteins p-ACC, p-ACLY, FASN, and Lipin 1 were consistently upregulated in the hearts of BMS-1-treated mice. Taken together, these findings suggested that the PD-1/PD-L1 inhibitor BMS-1 induced inflammation in the heart. Alterations in cardiac lipid metabolism might be correlated with ICIs-related cardiotoxicity. - Source: PubMed
Publication date: 2026/07/09
Ye CongJiang Zhi-TingYan ChenLi Xin-RanZhu Yu-HuaZeng Ling-YuLuo Lan