Mouse IL-6 ELISA kit
- Known as:
- Mouse Interleukin-6 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- BEK1109
- Product Quantity:
- 96 T
- Category:
- Elisa Kits
- Supplier:
- Biospect
- Gene target:
- Mouse IL-6 ELISA kit
Related genes to: Mouse IL-6 ELISA kit
- Gene:
- CEBPB NIH gene
- Name:
- CCAAT enhancer binding protein beta
- Previous symbol:
- TCF5
- Synonyms:
- LAP, CRP2, NFIL6, IL6DBP, C/EBP-beta
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-02-27
- Date modifiied:
- 2018-02-23
- Gene:
- CEBPD NIH gene
- Name:
- CCAAT enhancer binding protein delta
- Previous symbol:
- -
- Synonyms:
- CRP3, CELF, C/EBP-delta, NF-IL6-beta
- Chromosome:
- 8q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-24
- Date modifiied:
- 2018-02-23
- Gene:
- ENTPD6 NIH gene
- Name:
- ectonucleoside triphosphate diphosphohydrolase 6
- Previous symbol:
- CD39L2, IL6ST2
- Synonyms:
- NTPDase-6, dJ738P15.3
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-20
- Date modifiied:
- 2019-02-28
- Gene:
- IL6 NIH gene
- Name:
- interleukin 6
- Previous symbol:
- IFNB2
- Synonyms:
- IL-6, BSF2, HGF, HSF
- Chromosome:
- 7p15.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-07-12
- Gene:
- IL6RP1 NIH gene
- Name:
- interleukin 6 receptor pseudogene 1
- Previous symbol:
- IL6RL1
- Synonyms:
- -
- Chromosome:
- 9q22.2
- Locus Type:
- pseudogene
- Date approved:
- 1991-08-18
- Date modifiied:
- 2014-11-19
Related products to: Mouse IL-6 ELISA kit
Related articles to: Mouse IL-6 ELISA kit
- Peripheral neurotoxicity represents a debilitating complication of cancer chemotherapy. Although cyclophosphamide (CP) is an alkylating agent with lower clinical propensity for classic peripheral neuropathy than platinum compounds or taxanes, its reactive metabolites provoke significant neurotoxic injury in experimental settings. This study investigated whether remogliflozin (Remo), a sodium-glucose cotransporter-2 inhibitor (SGLT2) with pleiotropic antioxidant and anti-inflammatory properties, attenuates CP-associated peripheral neurotoxicity in an experimental rat model. Twenty-four male Wistar rats were divided into four groups: control, CP alone (100 mg/kg intraperitoneally once weekly), CP plus Remo 25 mg/kg/day orally, and CP plus Remo 50 mg/kg/day orally, all for one month. Behavioral assessments revealed that CP treatment was associated with altered motor coordination and nociceptive responses, which showed dose-related numerical improvements with Remo treatment. Biochemically, Remo treatment was associated with a favorable shift in redox markers, evidenced by higher Nrf2, glutathione, and superoxide dismutase levels, alongside reduced malondialdehyde. Remo treatment was associated with lower concentrations of inflammatory markers, including NF-κB, MCP-1, TNF-α, IL-6, and IL-1β. Furthermore, Remo treatment was associated with increased BDNF and CREB concentrations, PI3K, and total/phosphorylated Akt (with an improved p-Akt/total Akt ratio), along with lower concentrations of caspase-3 and BAX, and higher BCL-2. Histopathological and immunohistochemical analyses demonstrated that Remo was associated with preserved nerve structural integrity, attenuated myelin loss, and elevated Nrf2 and p-Akt immunoreactivity. These findings suggest that Remo is associated with attenuation of CP-induced peripheral neurotoxicity in rats, presenting a phenotypically consistent biomarker profile that warrants further causal and mechanistic evaluation. - Source: PubMed
Publication date: 2026/09/28
Almarghalani Daniyah AQadri MarwaAlarifi AbdulazizFayed Hany MA Shokry Aya - Metabolic dysfunction-associated steatotic liver disease (MASLD) affects approximately 25% of the global population and is a major health concern. Liver sinusoidal endothelial cells (LSECs) undergo morphological and functional alterations during MASLD progression, resulting in endotheliopathy characterized by pro-inflammatory phenotypes. We hypothesize that lipotoxicity synergistically exacerbates LSEC dysfunction in MASLD via IL-6 trans-signaling. - Source: PubMed
Publication date: 2026/09/28
Ueda YasuhikoKawaguchi NaoInomata YosukeArima JunIshida MitsuakiIto YukoLee Sang-WoongTaniguchi Kohei - Placental Cd accumulation was associated with altered Zn, Fe, and Cu homeostasis and increased lipid peroxidation, indicating redox imbalance. Cd exposure upregulated metallothionein II expression and altered the gene expression of the redox-sensitive markers Nrf2, FOXO3, and HO-1, consistent with modulation of stress-responsive gene expression. Gene expression of stress-responsive and vascular markers was evaluated by semi-quantitative RT-PCR. Concomitantly, VEGF and eNOS expression were increased, suggesting redox-sensitive changes in angiogenic and vasoactive gene expression under Cd exposure, while IL-6 elevation indicated a pro-inflammatory environment. Notably, the soy-based diet differentially modulated these responses, being associated with higher GPx activity, and lower IL-6 expression. Histological and immunohistochemical analyses confirmed structural alterations and dysregulation of the apoptosis-proliferation balance in placental tissue. Collectively, these findings indicate that Cd-induced placental dysfunction involves redox-associated changes in the expression of NO-dependent angiogenic and inflammatory mediators, and that dietary soy partially shifts this response toward improved redox balance and vascular response. - Source: PubMed
Publication date: 2026/09/28
Veronica BiaggioKarina AltamiranoLaura GaticaSilvana PiguillemVeronica FilippaVeronica Perez Chaca MaríaEugenia CiminariSilvina AlvarezSofía Gimenez MaríaGomez Nidia N - Pediatric perioperative respiratory adverse events (PRAE) pose significant risks during general anesthesia. Reliable predictive biomarkers reflecting early airway vulnerability remain scarce. This study aimed to evaluate the predictive value of miR-431-5p for PRAE and explore its underlying cellular mechanisms. A retrospective cohort of 202 children undergoing general anesthesia with tracheal intubation was analyzed. Preoperative serum miR-431-5p levels were quantified, and correlations with clinical outcomes and inflammatory markers were evaluated. Additionally, an in vitro lipopolysaccharide (LPS)-induced alveolar epithelial cell (AEC-II) model was established to investigate the molecule's protective function. Preoperative serum miR-431-5p was significantly downregulated in PRAE-positive patients, demonstrating high diagnostic efficacy (AUC = 0.891). Reduced miR-431-5p expression emerged as an independent risk factor for PRAE and correlated negatively with peak airway pressure, postanesthesia care unit stay, and postoperative serum SP-D and IL-6 levels. In vitro, LPS stimulation suppressed miR-431-5p expression in AEC-II cells. Conversely, miR-431-5p overexpression effectively restored cellular viability and attenuated the hypersecretion of IL-6 and TNF-α. Preoperative miR-431-5p deficiency independently associated with the occurrence of PRAE in pediatric patients. The molecule appears to modulate alveolar epithelial cell viability and suppress inflammatory responses in vitro, suggesting its potential as a noninvasive. These findings are derived from a single-center cohort and in vitro experiments; multicenter validation is warranted before clinical application. - Source: PubMed
Publication date: 2026/09/28
Liu JunLiu LiliZhang JianfengZhu RuiLei Yan - Berberine, a naturally occurring isoquinoline alkaloid found in several medicinal plants such as Berberis spp. and Coptis chinensis has long been used in traditional medicine. Recent evidence positions berberine as a pleiotropic modulator of multiple interconnected hallmarks of aging, making it a promising candidate for geroprotective interventions. This review critically examines the molecular mechanisms through which berberine influences energy metabolism, mitochondrial homeostasis, proteostasis, chronic inflammation, and cellular senescence. Berberine activates AMP-activated protein kinase (AMPK) via mild mitochondrial complex I inhibition, restoring cellular energy balance and suppressing mTOR-dependent anabolic pathways. Enhanced AMPK signaling stimulates autophagic flux and mitophagy, promoting clearance of damaged mitochondria and aggregated proteins. At the mitochondrial level, berberine improves respiratory efficiency, limits pathological excessive reactive oxygen species production while preserving physiological redox signaling, and upregulates endogenous antioxidant defenses through Nrf2. Furthermore, berberine exerts anti-inflammatory effects by inhibiting NF-κB nuclear translocation and reducing the transcription of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β). Notably, berberine acts as a senomorphic agent, attenuating the senescence-associated secretory phenotype (SASP) without inducing widespread apoptosis, partly through modulation of p16 and cyclin expression. By integrating these molecular insights, this review positions berberine as a multi-target geromodulator that addresses deregulated nutrient sensing, mitochondrial dysfunction, impaired proteostasis, chronic inflammation, and cellular senescence in a coordinated manner. The translational potential, pharmacokinetic challenges, and safety considerations of berberine in the context of healthy aging are also discussed. - Source: PubMed
Publication date: 2026/09/28
Alanazi Sultan MohammedAl-Kuraishy Hayder MAbdelaziz Ahmed MAlasmari Eidah MYousef Fatimah MMohamed Ahmed ASalama Mohamed MBatiha Gaber El-Saber