ABT-199 Bcl-2 inhibitor
- Known as:
- ABT-199 Bcl-2 suppressor
- Catalog number:
- a-1231
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ActivBio Active Biochem
- Gene target:
- ABT-199 Bcl-2 inhibitor
Related genes to: ABT-199 Bcl-2 inhibitor
- Gene:
- BCL2 NIH gene
- Name:
- BCL2 apoptosis regulator
- Previous symbol:
- -
- Synonyms:
- Bcl-2, PPP1R50
- Chromosome:
- 18q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: ABT-199 Bcl-2 inhibitor
Related articles to: ABT-199 Bcl-2 inhibitor
- High-fat diet and alcohol are often co-exposed in real life, contributing to cognitive deficits and posing a significant yet modifiable public health challenge. We extensively evaluated the efficacy of polysaccharides extracted from Polygonatum kingianum (PP) in mitigating cognitive deficits in high-fat-diet-induced obese mice exposed to alcohol in females and males. PP alleviated cognitive deficits assessed via open-field and Y-maze tests, with a more pronounced efficacy in females, accompanied by restored hippocampal histopathology and improved synaptic integrity markers. PP also ameliorated metabolic dysregulation (i.e., hyperglycemia, dyslipidemia, oxidative stress), improved colon morphology and tight junction proteins (ZO-1, Claudin-1). Sex-specific alterations were significantly prominent in remodeling gut microbiome and fecal metabolome induced by PP. For instance, Parabacteroides goldsteinii, Bacteroides caecimuris, and the families Staphylococcaceae and Prevotellaceae were elevated in females while Lactobacillus spp. and Clostridium spp. exclusively elevated in males. Mendelian randomization using large-scale human GWAS data demonstrated causal relationships between certain gut bacteria and cognitive function. Metabolomics identified largely non-overlapping sets of PP-regulated metabolites and pathways in females and males. Correlation analysis linked microbiota to microbiota-derived metabolites and network pharmacology identified core targets (e.g., BCL2, CASP3, TNF, STAT3, PTGS2, PPARG) involved in PP's cognition protection benefits. Molecular docking validated the binding ability of core targets to 8 pharmacokinetically favorable metabolites regulated by PP in each sex, reinforcing the sex-specific mechanism. Collectively, our findings provide novel insights into the benefits of PP in alleviating diet-induced cognitive deficits and underscore the necessity of considering sex as a critical biological variable in developing microbiome-targeted nutritional therapies. - Source: PubMed
Publication date: 2026/06/29
Lv JiayaoQu YizheYan QixinCheng KenWu QingyangZhang JiayiDuan XintingHan ShanshanTian HongleiShi Lin - The poor prognosis and limited treatment options for cholangiocarcinoma (CCA) continue to drive the search for novel therapeutics with clear mechanisms of action. 10-hydroxy-2-decenoic acid (10-HDA) is a unique bioactive fatty acid isolated from royal jelly, yet its therapeutic potential in CCA is unknown. In this study, we evaluated the anti-CCA properties of 10-HDA across cell-based, computational, transcriptomic, and animal models. Cell viability and clonogenic assays showed that 10-HDA strongly suppressed HUCCT1 and RBE cell growth by triggering extensive apoptosis. We also observed a marked decline in cell migration and invasion; rather than a purely targeted anti-metastatic effect, transcriptomic data suggested this motility loss is tightly linked to the drug's primary cytotoxicity and a parallel disruption of actin cytoskeleton dynamics. Computational predictions initially pointed toward apoptosis networks as primary targets, which was corroborated by our RNA-seq data highlighting a strong enrichment in both general apoptotic and specific TNF signaling pathways. Protein-level validation confirmed a dual-activation mechanism: 10-HDA upregulates the intrinsic p53/Bax axis while simultaneously engaging the extrinsic TNF/Caspase-8 cascade, both converging on Caspase-3 cleavage. These mechanisms translated effectively in vivo, where 10-HDA administration severely restricted xenograft tumor growth in nude mice without noticeable systemic toxicity. These findings identify 10-HDA as a potent, defined natural agent that halts CCA progression by activating comprehensive apoptotic programs. - Source: PubMed
Publication date: 2026/08/21
Yan GuohongZhang JiakaoLu ZiyanMo ShutianHe YongfeiQin WeiWei YongguangChen MeifengLiang JiamingHan ChuangyeYe Xinping - Quercetin, a flavonoid derived from astragalus and other medicinal plants, exhibits anti-cancer activity; however, its mechanisms in gastric cancer, especially regarding tumor immunity, remain incompletely understood. The aim of this study is to elucidate the mechanism of quercetin against gastric cancer. - Source: PubMed
Publication date: 2026/08/20
Liu YaliKang XiaojuanWang JiaxuanZhou XinyangTan WushuangKang TingtingShi WenguiZhang Dekui - Gastric ulceration is a common dose-limiting adverse effect associated with the use of non-steroidal anti-inflammatory drugs (NSAIDs). Asiatic acid (AA) is a naturally occurring pentacyclic triterpenoid that has been reported to possess antioxidant, anti-inflammatory, and healing properties. The present study investigated the potential protective effect of AA against indomethacin-induced gastric ulceration in rats. Male rats were divided into five groups: control, indomethacin (50 mg/kg), indomethacin + AA (25 mg/kg), indomethacin + AA (50 mg/kg), and indomethacin + omeprazole (30 mg/kg). Indomethacin administration produced marked gastric mucosal injury, whereas pretreatment with AA significantly reduced ulceration as confirmed by a reduction in the macroscopic ulcer index and by histopathological examination. AA also reduced lipid peroxidation and prevented the depletion of endogenous antioxidant enzymes, indicating a protective antioxidant effect. In addition, AA suppressed the immuno-expression of cyclooxygenase-2, tumor necrosis factor-α, interleukin-6, and nuclear factor-κB, suggesting a significant anti-inflammatory action. AA was also associated with a reduction in the indomethacin-induced increase in the immuno-expression of interferon-γ (IFN-γ), JAK-1, and phosphorylated STAT3. At the molecular level, AA decreased the mRNA expression of the pro-apoptotic gene Bax and increased the expression of the anti-apoptotic gene Bcl-2. These findings indicate that AA ameliorates indomethacin-induced gastric ulceration in rats. This gastroprotective effect is associated with antioxidant, anti-inflammatory, and anti-apoptotic activities, as well as downregulation of the IFN-γ/JAK-1/STAT3 signaling pathway. - Source: PubMed
Publication date: 2026/08/14
Binmahfouz Lenah SBagher Amina MBinmahfouz Najlaa SEzzeddine Dana WDawood Monana FGaddaa Yara SAyoub Nahla AEid Basma G - Parkinson's disease (PD) is a complex neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons. This study aimed to elucidate the dynamic interplay between these pathological pathways in a rotenone-induced rat model of PD. Adult male Wistar rats were chronically treated with rotenone. Behavioral assessments included Rotarod, Open Field, Rotating Pole, and Cylinder tests. On days 7, 14, and 21, gene expression levels of key markers including α-synuclein, NLRP3 inflammasome components (NLRP3, ASC), inflammatory cytokines (IL-1β, TNF-α, IL-6), upstream signaling molecules (TLR4, NF-κB), antioxidant defense factors (Nrf2, HO-1), apoptotic regulators (Bax, Bcl-2, Caspase-3), and tyrosine hydroxylase (TH) were quantified via qPCR. Crucially, protein abundance for all major markers was validated using ELISA, alongside biochemical assessment of oxidative stress markers (MDA and SOD). Rotenone treatment caused a progressive decline in motor performance across all behavioral assays (p < 0.001), including reduced rotarod latency, decreased open field distance, increased pole test latency, and heightened cylinder asymmetry. The PD group exhibited significant time-dependent increases in α-synuclein, TLR4, NF-κB, NLRP3, ASC, IL-1β, IL-6, TNF-α, Bax, Caspase-3, and MDA levels. Conversely, expression levels of Nrf2, HO-1, Bcl-2, and SOD activity showed marked decreases (p < 0.01). Finally, TH expression decreased progressively, reaching roughly 50% of control levels at day 21. Correlation analysis confirmed strong links between α-synuclein accumulation, inflammation, oxidative damage, and neuronal loss. These findings suggest a synergistic pathogenic cascade where α-synuclein accumulation contributes to neuroinflammation and oxidative stress, suppressing antioxidant defenses and activating apoptotic pathways, ultimately leading to dopaminergic neuron death and severe motor dysfunction. - Source: PubMed
Publication date: 2026/08/18
Pour Homa ValiAlfateh MohamadShanjani Sanaz MirzayanTajeri MaryamAbbasi-Maleki Saeid