ELISA Rat , TNF-alpha
- Known as:
- Enzyme-linked immunosorbent assay test Rat , TNF-a
- Catalog number:
- RBMS622R
- Product Quantity:
- 96 wells (1 kit)
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- ELISA Rat TNF-alpha
Related products to: ELISA Rat , TNF-alpha
Related articles to: ELISA Rat , TNF-alpha
- Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by motor neuron degeneration, oxidative stress, and neuroinflammation. This study evaluated the neuroprotective potential of caffeic acid phenethyl ester (CAPE) against MTME + 5-induced neurotoxicity in an ALS-like pathology model. CAPE (50 and 100 mg/kg., p.o.) demonstrated significant therapeutic efficacy by improving motor and cognitive deficits, restoring oxidative balance, and mitigating neuroinflammatory and apoptotic pathways. Behavioral assessments, including the open field, grip strength, forced swim, and Morris water maze, highlighted CAPE's ability to restore neuromuscular coordination and cognitive function in a dose-dependent manner. Cellular and Molecular analyses revealed that MTME5 exposure significantly disrupted Klotho/SIRT-1/Nrf2/HO-1 antioxidant signaling, increased pro-inflammatory cytokines (TNF-α, IL-1β), and elevated apoptotic markers (Bax, caspase-3) while depleting anti-inflammatory cytokines (IL-10) and neuroprotective proteins. Furthermore, CAPE treatment restored these parameters, reduced oxidative stress, and enhanced antioxidant defenses (SOD, CAT, r-GSH). Furthermore, CAPE normalized neurotransmitter imbalances, including acetylcholine, dopamine, GABA, serotonin, and glutamate, alleviating excitotoxicity. Histopathological and gross morphological analyses confirmed CAPE50 and CAPE100 ability to preserve neuronal and myelin integrity across key brain regions, including the cerebral cortex, hippocampus, striatum, midbrain, and cerebellum. CAPE also reduced methylmercury accumulation in the brain and cerebrospinal fluid, indicating detoxifying effects. Co-administration of vitamin B1 (VTB1(200)) further amplified CAPE's therapeutic efficacy. Complete blood count (CBC) analysis demonstrated MTME5-induced hematological abnormalities, including reduced RBCs, hemoglobin, WBCs, and platelets, alongside elevated eosinophils and basophils. CAPE treatment normalized these parameters, indicating systemic recovery. These findings establish CAPE as a promising neuroprotective agent for ALS, capable of targeting neurocomplications. - Source: PubMed
Publication date: 2026/04/27
Rana RaviMehan SidharthMukherjee RitamKhan M D NasiruddinDas Gupta GhanshyamNarula Acharan S - Osteoarthritis (OA) is a degenerative joint disease with high global prevalence, and YKL-40 is an important factor related to the pathological process of OA. Increased levels of YKL-40 exert a protective influence against TNF-α-induced apoptosis in chondrocytes, thereby enhancing chondrocyte survival and activation, while counteracting TNF-α-driven expression of specific inflammatory mediators such as S100A8/A9.This study aims to evaluate the role and molecular mechanism of YKL-40 on chondrocytes in OA and provide a potential therapeutic avenue requiring further validation. A meta-analysis compared serum YKL-40 and TNF-α levels between OA patients and healthy controls. In vitro experiments examined the effects of YKL-40 on TNF-α-induced OA chondrocytes, assessing proliferation, differentiation, apoptosis, and inflammatory pathways. Meta-analysis revealed significantly elevated serum levels of YKL-40 and TNF-α in osteoarthritis (OA) patients compared to healthy controls. In vitro, TNF-α (10 ng/mL) induced extracellular matrix (ECM) degradation in chondrocytes, significantly reducing glycosaminoglycan (GAG) and type II collagen content. This degradation was effectively rescued by YKL-40 (100 ng/mL). RNA sequencing identified differentially expressed genes in TNF-α-treated chondrocytes, enriched in pathways like IL-17 and NF-κB signaling. YKL-40 treatment reversed the expression of key genes altered by TNF-α. Crucially, these differentially expressed genes (including S100A8/A9, ISG15, CDSN, BAAT, PTPN4, NPTX1, SMARCA1) were validated in independent OA cartilage and synovium GEO datasets. Protein-protein interaction (PPI) networks highlighted central genes within treatment groups. Western blotting confirmed YKL-40 counteracted TNF-α-induced NF-κB pathway activation (reduced p65 and IκBα phosphorylation) and modulated key targets (S100A8/A9, ASB7, ZFPM2), consistent with qRT-PCR data. YKL-40 is a promising biomarker and therapeutic target for OA. Its interplay with TNF-α provides a molecular basis for novel therapies targeting chondrocyte dysfunction, guiding future translational research. - Source: PubMed
Publication date: 2026/04/27
Li ZhuozhengSun XueXie YongfangHong ZexinDou ZeminYan ShichaoZhang YulongQin HeLiu DanFeng TingtingWang Guohui - Gastrointestinal inflammation could contribute to the early development of Parkinson's disease (PD). This study investigated gut inflammation, intestinal barrier function, and integrity in patients with isolated REM sleep behavior disorder (iRBD), a prodromal stage of PD. Sigmoid colon biopsies from patients with iRBD (n = 20), PD (n = 34), and controls (n = 20) were analyzed by qPCR to measure the expression levels of proinflammatory cytokines and enteric glial markers, along with fecal calprotectin. Gut permeability was evaluated in biopsies mounted in Ussing chambers, and the integrity of the intestinal epithelial barrier was assessed by analyzing the expression of tight junction protein by Western blot. We found that the mRNA expression levels of interleukin-1β and interleukin-8 were increased in both patients with iRBD and PD relative to controls; the expression of TNF-α was also higher in PD but not in iRBD patients. We did not observe any differences in colonic permeability, tight junction proteins expression, and calprotectin levels groups. Our study is the first to characterize the inflammatory profile in the gut in iRBD. Our findings provide evidence that enteric inflammation is present at a moderate level in prodromal PD, not higher than in individuals with established PD, and without concurrent changes in intestinal permeability. - Source: PubMed
Publication date: 2026/04/27
Sellier Montaigne LoïcLassozé Simonde Guilhem de Lataillade AdrienOullier ThibauldVibet Marie-AnneBach-Ngohou KalyaneRolli-Derkinderen MalvyneDurand TonyLe Dily SéverineJirka-Alebic IvaCoron EmmanuelMichaux QuentinNeunlist MichelMadaro GiuseppeCervino AlessandraDerkinderen PascalLeclair-Visonneau Laurène - To investigate the mechanism by which aerobic exercise improves transverse aortic constriction (TAC)-induced heart failure in mice. - Source: PubMed
Zhang GuodongWei SiangWang HongXie YanliHe HuiLi Rong - To investigate the therapeutic effect of Lotus Seed Drink (QISD) on renal injury in mice with diabetic kidney disease (DKD) and its mechanism. - Source: PubMed
Xie JiarunLuo YanyuXia JinjinWang Ming