Ask about this productRelated genes to: CASP3 Blocking Peptide
- 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
Related products to: CASP3 Blocking Peptide
Related articles to: CASP3 Blocking Peptide
- As the most frequently occurring cancer worldwide, lung cancer is notoriously diagnosed at advanced stages, resulting in high mortality rates. The primary factor underlying this persistent global health burden remains tobacco consumption. Nicotine, a key component of cigarette smoke, is one of the major contributing factors to the development of lung cancer, but the molecular mechanisms remain incompletely elucidated. α7-nAChR, β2-AR, and HGF/c-Met are known to contribute to lung cancer development, respectively. However, the specific signaling cascade through which they interact in nicotine-induced malignancy is unclear. In this study, using CCK-8 assays across a range of concentrations (0-5 μM), we determined that 1 μM nicotine treatment for 48 h optimally enhances A549 cell proliferation, establishing this condition for subsequent experiments. This study uncovers nicotine's role in driving malignant behaviors including proliferation, migration, and invasion in nonsmall cell lung cancer A549 cells. Notably, nicotine potently stimulated migration and invasion, accompanied by upregulation of Cyclin D1 and MMP-2, and downregulation of BAX, BAD, and Caspase-3. Mechanistically, nicotine induced synergistic engagement of α7-nAChR and β2-AR, leading to activation of the HGF/c-Met/PI3K/AKT axis and enhancing the secretion of both HGF and MMP-2. Importantly, we reveal a previously unrecognized bidirectional regulatory loop between α7-nAChR and β2-AR that functionally converges on the HGF/c-Met axis, which acts as a critical signaling hub to drive the downstream PI3K/AKT pathway and facilitate tumor progression. Our findings provide the first evidence of a coordinated α7-nAChR/β2-AR interface regulating HGF/c-Met signaling that orchestrates both intracellular signaling and extracellular secretory programs in nicotine-promoted lung cancer progression. This offers innovative insights for identifying potential antitumor therapeutic targets and presents novel perspectives for the prevention and clinical management of lung cancer, particularly in smokers with nonsmall cell lung cancer. - Source: PubMed
Publication date: 2026/05/20
Li ZihanXie BoxuanLiu XileiHe ZihanZhang ZhongweiZhou JianmingZhou TongWang Huai - Neonatal white matter injury (WMI), a leading cause of cerebral palsy, results from microglial-driven neuroinflammation that affects oligodendrocyte precursor cell (OPC) survival and differentiation. Our prior in vivo research indicated that inosine may protect against maternal inflammation-induced WMI by modulating microglial polarization and inhibiting TLR4/MyD88/NF-κB signaling, but its direct effects on microglia are unknown. This in vitro study used a microglia-conditioned medium (MCM)-OPC approach to explore this question. Primary microglia were stimulated with lipopolysaccharide (LPS) and treated with inosine, followed by the measurement of inflammatory cytokines (TNF-α, IL-1β, IL-6) and TLR4 pathway proteins via ELISA and Western blot. MCM derived from differentially treated microglia was then applied to OPC cultures, where OPC viability, death, proliferation, and differentiation were assessed using CCK-8 assay, propidium iodide (PI) staining, immunofluorescence, and Western blot. Inosine co-treatment significantly decreased LPS-induced secretion of TNF-α, IL-1β, and IL-6 from microglia (P < 0.05) and downregulated TLR4, MyD88, and p-NF-κB p65 expression (P < 0.001, P < 0.01). MCM from inosine-treated microglia mitigated OPC damage caused by activated microglia, as demonstrated by enhanced OPC viability (P < 0.01), reduced apoptosis (evidenced by decreased PI positivity and Cleaved Caspase-3 expression, P < 0.01, P < 0.05), increased proliferation (indicated by elevated Ki67 positivity and NG2 expression, P<0.001, P < 0.01), and improved differentiation (reflected by increased expression of CNPase, Olig2, and MBP, P < 0.001, P < 0.01). These findings suggest that inosine can directly inhibit the overactivation and inflammatory response of microglia in vitro, an effect associated with TLR4/MyD88/NF-κB downregulation. Furthermore, it can indirectly ameliorate the injurious microenvironment for OPC, thereby providing cellular-level mechanistic clues for explaining its neuroprotective role in vivo. - Source: PubMed
Publication date: 2026/05/20
Han YongChen JinWang PeilianSun JinpingNiu JianguoMa Quanrui - Myocardial infarction (MI) induces brain injury. Myrtenol has antioxidant and anti-inflammatory effects. This study investigated the neuroprotective effect of myrtenol following myocardial infarction induced by isoproterenol (ISO) in male rats. This experimental study involved 36 male Wistar rats. They were divided into six groups. Rats received ISO (85 mg/kg) for two days. Subsequently, they were treated with vehicle or myrtenol (5, 25, or 50 mg/kg) once daily, one hour after the last ISO injection, for seven days. Behavioral tests (spontaneous alternation and passive avoidance) were conducted post-treatment. Hemodynamic parameters and serum troponin were assessed. Tissue samples (heart/brain tissue) underwent histopathological examination via H&E and Nissl staining methods. The activities of glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD), along with malondialdehyde (MDA) content and total antioxidant capacity (TAC) were measured in heart and brain tissue. Western blot analysis was used for the assessment of inflammatory (TNF and NF-κB), cell death (Bax, Bcl2, and Cleaved caspase-3), and nuclear factor erythroid-related factor-2 (Nrf2) markers in brain tissue. ISO significantly reduced latency time and spontaneous alternation compared to control (p < 0.001). Myrtenol improved these parameters at 25 mg/kg (p < 0.01) and 50 mg/kg (p < 0.001). Myrtenol also reduced MDA content, Bax, Cleaved caspase-3, TNF, and NF-κB protein expression and also increased Bcl2, and Nrf2 proteins, TAC level, SOD, GPx, and catalase enzyme activity in heart/brain tissues when compared to ISO group (p < 0.05). Myrtenol improved memory function and hemodynamic parameters. It decreases brain oxidative stress, inflammation and cell death markers, highlighting its potential as a therapeutic agent. - Source: PubMed
Publication date: 2026/05/20
Petrudi Nima RahimiHassanshahi JalalZeinali HosseinRezvan SajjadShafiei Seyed Ali - This study investigated the effects of genistein-3'-sodium sulfonate (GSS) on chronic cerebral hypoperfusion (CCH) and the involvement of Takeda G-protein-coupled receptor 5 (TGR5) (also known as GPBAR1 (G protein-coupled bile acid receptor 1)) in its mechanism of action. In a mouse model of CCH, induced by bilateral common carotid artery stenosis (BCCAS), GSS treatment was combined with stereotaxic injection of TGR5 siRNA or expression vectors. Anxiety and depressive behaviors were evaluated using the elevated plus maze, light-dark box, tail suspension, and forced swim tests. Histological changes and blood-brain barrier (BBB) integrity were assessed by hematoxylin and eosin and Evans blue staining. Furthermore, an in vitro low-glucose hypoxia (LGH) microglia activation model was used. Protein and mRNA levels of TGR5, tight junction proteins, microglial markers, inflammatory molecules and caspase-3 were measured by western blotting and qRT-PCR. GSS treatment or TGR5 overexpression reversed the LGH-induced decrease in BV2 cell viability, whereas TGR5 knockdown had the opposite effect. In CCH mice, GSS or TGR5 overexpression improved behavior, alleviated histopathology, reduced injury scores and preserved BBB integrity. Along with these changes, TGR5, ZO-1, claudin-5, and CD206 increased, while the expression of IBA-1, iNOS, CD40, CD68, NF-κB p65, IL-1β, and caspase-3 decreased at protein and mRNA levels. In addition, TGR5 silencing promoted the effects of BCCAS and LGH. Overexpressing TGR5 promoted the effects of GSS, while TGR5 silencing partly abrogated these effects. These findings indicate that GSS can inhibit microglial mobilization and neuroinflammation by activating TGR5, offering a potential targeted therapy for cerebral ischemia and mitigating behavioral changes in CCH through TGR5 regulation. - Source: PubMed
Publication date: 2026/05/20
Fan MengyaoLi Xiao - Oxidative stress-induced liver injury can progress to severe hepatic conditions. Polysaccharides are promising therapeutic agents, but the protective effects of polysaccharide (ADP) against this injury remain unclear. - Source: PubMed
Publication date: 2026/05/20
He Xue-QinLi Yi-ZhangXu Li-BaWu Chun-FengWei Du-DongLiu Hao-YuQiu Fen