CASP3 ELISA kit
- Known as:
- CASP3 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CASP3-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CASP3 ELISA kit
Related genes to: CASP3 ELISA kit
- Gene:
- CASP3 NIH gene
- Name:
- caspase 3
- Previous symbol:
- -
- Synonyms:
- CPP32, CPP32B, Yama, apopain
- Chromosome:
- 4q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-22
- Date modifiied:
- 2016-10-05
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- Although artificial intelligence is rapidly advancing, its application in translational dermatological research remains limited. In this study, we established an artificial intelligence-based image analysis workflow for the quantification of proliferation and apoptosis within the human epidermis using 3,3'-diaminobenzidine-based immunohistochemical staining. Human skin cultured in a 3-dimensional in vivo model was processed using paraffin embedding and immunohistochemical staining for Ki-67 and cleaved Caspase-3. We implemented an artificial intelligence-based 2-model workflow: a custom-trained convolutional neural network-based model for cell detection and a semantic-segmentation model that specifically segregates the epidermis. By combining both models, we restricted cell annotation and classification to the epidermis-our structure of interest-enabling epidermis-constrained quantification on whole-slide images. Validation against manual counts showed high agreement for both markers (Ki-67 mean accuracy = 95.43%; cleaved Caspase-3 = 97.0%) across staining batches and time points. To test the experimental applicability of our workflow, we treated human skin cultured on the chorioallantoic membrane with hydroxytyrosol. The artificial intelligence-based workflow minimized subjective bias and provided a coherent readout, showing reduced proliferation without inducing apoptotic responses in hydroxytyrosol-treated samples. Overall, the workflow achieved strong performance with modest training effort and annotation, offering a scalable approach that supports translational dermatological research and holds potential for dermatopathological applications. - Source: PubMed
Publication date: 2026/07/16
Mei ValeriaMaurer SandraKainz PhilippEttner-Sitter AndreasBauer TheaAung ThihaHaerteis SilkeRötzer Vera - Skin aging involves interconnected inflammatory, oxidative, hormonal, extracellular matrix (ECM), and cellular senescence-related mechanisms, supporting the need for multitarget approaches. This study aimed to evaluate the effects of a multicomponent natural product-based injectable formulation developed in Korean medicine practice, Dong-An Pharmacopuncture (DAP), on skin aging-related pathways. A network pharmacology approach was used to identify the active compounds, predicted molecular targets, and signaling pathways associated with DAP. Sixty-two active compounds from 11 constituent materials were screened, and 70 final targets were identified using STITCH-based prediction, intersection with GeneCards-derived skin aging-related targets, and quality filtering. Herb-compound-target network analysis yielded 225 compound-target interactions across 292 edges. Protein-protein interaction analysis identified a highly connected network with 1,334 edges, and hub analysis converged on 10 core targets: , , , , , , , , , and . Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses identified four major mechanistic axes: inflammatory and oxidative stress regulation, hormonal skin homeostasis, tissue repair and ECM remodeling, and cellular senescence-related regulation. Because DAP is administered by injection, a Good Laboratory Practice-compliant single-dose subcutaneous toxicity study was additionally conducted in Sprague-Dawley rats, which showed no mortality, abnormal clinical signs, or histopathological findings attributable to DAP at 1.0 mL/head. The findings in this study provide a systems-level framework for the predicted multitarget mechanisms of DAP in skin aging-related pathways and support the need for further experimental validation of its predicted mechanisms and repeated-dose safety. - Source: PubMed
Publication date: 2026/08/20
Hwang Ji HyeJung Chul - Neuropathic pain (NP) is driven by neuroimmune interactions where in activated microglia release pro-inflammatory mediators that sustain central sensitization. Platelet-rich plasma (PRP) is a promising therapy, but its efficacy depends on its biochemical composition. This study aimed to evaluate how modifying the molecular profile of PRP influences its capacity to modulate neuroinflammation in a human-derived co-culture model. We compared standard PRP (sPRP) and balanced protein-concentrate plasma (BPCP), enriched in extraplatelet molecules, using an iPSC direct co-culture of sensory neurons (hSNs) and microglia (hMG). Neuroinflammation was induced for 24 h with serum-free (SF) or 10% sPRP or BPCP supplementation. Neuroinflammation, microglial activation, apoptosis, and neuronal plasticity were analyzed via RT-qPCR and Luminex. Both formulations attenuated pro-inflammatory mediators. However, BPCP demonstrated superior suppressive efficacy, reducing the levels of major cytokines (IL-1β, TNF-α, IL-6, IL-8) by half as compared to sPRP. BPCP significantly decreased IL-6, IL-8, and MCP-1 protein levels; kept microglial activation markers (CD86, CTSS) downregulated; and downregulated the apoptotic cascade (BAX, CASP9, CASP3). Conversely, sPRP displayed a distinct pro-resolving and neuroprotective trend, upregulating IL-10 and TGF-β1 and rescuing the expression of (KCC2), which regulates neuronal excitability. sPRP and BPCP modulated neuroinflammation via complementary mechanisms. BPCP acted as an immunomodulatory shield suppressing macro-inflammation, while sPRP drove inflammation resolution and neuroplastic rescue. - Source: PubMed
Publication date: 2026/08/08
Mercader-Ruiz JonMarijuan-Pinel DanielDelgado DiegoLasuen Aguirre DeieneSansinanea XabierGuadilla JorgeSánchez Mikel - Chronic exposure to endocrine-disrupting chemicals has been increasingly recognized as a potential contributor to cancer progression. Monobutyl phthalate (MBP), a major metabolite of dibutyl phthalate, is widely detected in human biological samples, yet its long-term impact on anaplastic thyroid cancer (ATC) has not been systematically investigated. CAL-62 cells were continuously exposed to an environmentally relevant concentration of MBP (10 nM) over 3 months to establish a chronic exposure model that mimics long-term environmental exposure. Transcriptomic profiling was integrated with network toxicology to identify key molecular pathways and hub genes, followed by molecular docking and Western blot validation. Chronic MBP exposure significantly enhanced cell viability, proliferation, colony formation, and tumorsphere formation, indicating promotion of malignant phenotypes. Transcriptomic profiling revealed extensive molecular remodeling characterized by activation of inflammation-associated pathways, including cytokine-cytokine receptor interaction, IL-17, TNF, and JAK-STAT signaling, accompanied by suppression of p53- and mTOR-related pathways. Integrated analysis identified 57 overlapping KEGG pathways, with IL6 and CSF2 emerging as central hub genes. Molecular docking demonstrated favorable binding affinities between MBP and representative target proteins, including IL6, TP53, CASP3, BCL2, and PPARG. Western blot analysis further confirmed increased IL6 and BCL2 expression together with decreased TP53, CASP3, and PPARG expression following chronic MBP exposure. Chronic environmentally relevant MBP exposure promotes ATC malignant progression through coordinated inflammation-associated molecular network remodeling accompanied by suppression of apoptosis-related signaling. Integrating network toxicology with transcriptomic profiling provides an effective systems-level strategy for identifying biologically relevant molecular networks underlying chronic environmental toxicant exposure. - Source: PubMed
Publication date: 2026/08/04
Deng YuTan SongweiWei JinlanGuo XingyueHu LongqingQu XincaiZhou Jing - Intervertebral disc degeneration (IDD) is a multifactorial spinal degenerative condition influenced by inherited susceptibility and environmental exposures. Genetic evidence from Chinese Han populations remains limited. This study aimed to evaluate GWAS-informed and previously reported candidate single-nucleotide polymorphisms (SNPs) associated with IDD and to explore potential gene-gene and gene-environment interaction patterns. - Source: PubMed
Publication date: 2026/08/18
Lei RidanZhang MengyuanLuo ManjunRuan XiaoruiWei JianhuiLi ZiyeQin Jiabi