The protein expression levels of apoptosis-related genes, including B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax), were detected via Western blotting.
The present study investigated the association between the G(-248)A single nucleotide polymorphism (SNP) in the promoter region of B-cell lymphoma 2 (Bcl-2) associated X protein (Bax), which is a pro-apoptosis gene and the clinicopathological parameters and prognosis of patients with esophagus cancer.
Aβ<sub>25-35</sub> -induced changes in Ca<sup>2+</sup> and B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X (Bax) protein and gene levels in cells were also reversed by genistein.
Expression levels of phosphorylated (p)-MEK1/2, p-ERK1/2, p-NF-kappaB (p-p65), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), Caspase3, and B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) were measured by Western blot assay or/and quantitative real-time polymerase chain reaction (qRT-PCR), respectively.
In addition, immunoreactivities of NMDAR1, NMDAR2A/B, B-cell lymphoma 2 (Bcl-2) and Bcl-2- associated X protein (Bax) are closely related with neuroexcitotoxicity.
The expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-6, B-cell lymphoma (Bcl)-2 associated X protein (Bax), and caspase-3 in the PFC-PL of OB rats were significantly increased as compared with the sham rats, but the Bcl-2 and IL-10 expressions were decreased, whereas BI-1 overexpression significantly suppressed the changes of these proteins in the PFC-PL of OB rats.
Then, apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assay, and the gene expression levels of apoptosis-related proteins [cytochrome c (Cyt c), B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax)] were detected by reverse transcription-polymerase chain reaction (RT-PCR).
Compound 9i was further evaluated for protective effect against myocardial I/R injury on the basis numerous parameters, for example, hemodynamic parameters (left ventricular developed pressure [LVDP], ±dp/dtmax, coronary flow [CF], and heart rate [HR]), myocardial enzymes (creatine kinase and lactate dehydrogenase), thiobarbituric acid reactive substance (TBARS), oxidative stress (super oxide dismutase [SOD], catalase [CAT], glutathione [GSH], and glutathione peroxidise [GPx]), histopathology, western blots analysis for B-cell lymphoma 2 (Bcl-2), Bcl-2-associated x protein (Bax), lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), and NF-κB in cardiac tissues.
Western blot analysis was performed in order to determine the differential expression levels of Janus kinase (JAK), signal transducer and activator of transcription 3 (STAT3) and apoptosis associated proteins B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax) and Bcl-2 associated agonist of cell death (Bad).
The levels of apoptosis were examined by flow cytometry utilizing Annexin V-fluorescein isothiocyanate/propidium iodide double staining, and the protein expression levels of cleaved caspase-3, phosphorylated phosphoinositide 3'-kinase (p-PI3K), p-protein kinase B (p-AKT), hypoxia inducible factor (HIF-α), pyruvate kinase M2 (PKM2), B-cell lymphoma (Bcl-2)-associated X protein (Bax), Bcl-2 and cytochrome c were detected by western blot analysis.
These results suggest that inhibition of apoptosis through bax gene mutations is unlikely to be a common event in B-cell lymphoma, at least in the major types of nodal and extranodal B-cell lymphomas.
Our results showed that 200-800 μM PA treatment reduces cell viability, induces cell apoptosis, enhances the expression of apoptosis-related genes (Caspase 3 and B-cell lymphoma-2 (BCL-2) associated X protein (BAX)), and activates the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)).
To investigate the influences of remifentanil on myocardial ischemia-reperfusion injury in rats and the expressions of b-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and other apoptosis-related proteins.
Allicin significantly suppressed CCA cell proliferation by activating the caspase cascade, inducing apoptosis, and reducing the expression of proteins downstream of STAT3, such as B-cell lymphoma 2 (Bcl-2), while upregulating Bcl-2-associated X (Bax) protein.
The expression levels of apoptosis-related proteins, such as B-cell lymphoma 2 (Bcl-2), Bcl-2 Associated X Protein (Bax), cysteine-aspartic acid protease-3 and protease-9 (caspase-3 and caspase-9), cytochrome c (cyt-C), brain-derived neurotrophic factor (BDNF), and cAMP-response element binding (CREB) protein, were evaluated by western blot.
The increased intracellular level of ROS appeared to induce the activation of p53 and elevate the B‑cell lymphoma 2 (Bcl‑2)‑associated X protein/Bcl‑2 ratio, which modulates ΔΨm and triggers the release of cytochrome c, and may increase the activities of apoptotic protease activating factor 1, caspase‑3, ‑8 and ‑9 to further trigger the destruction of structural and specific proteins and thereby cell apoptosis.
Levels of B‑cell lymphoma-2 (Bcl‑2), apoptosis regulator Bax (BAX), caspase-9, caspase‑3 and cleaved caspase‑3 expression were analyzed using western blot analysis.
Finally, western blotting was employed to detect the protein expression of cyclin D1, p21, B cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax).
B‑cell lymphoma (Bcl)‑2‑associated X protein/Bcl‑2 ratio, reactive oxygen species generation and caspase‑3 activation were also increased following ZFP580 inactivation.
In the apatinib combined with DDP group, the levels of cleaved caspase-3, cleaved caspase-9 and B-cell lymphoma-2 (Bcl-2)-associated X (BAX) proteins were significantly upregulated, while the level of Bcl-2 proteins was downregulated.
The present study demonstrated that miR‑98 expression was increased in OA chondrocytes in response to IL‑1β stimulation, and the expression levels of apoptosis-associated proteins, including Fas cell surface death receptor, caspase‑3, caspase‑8 and B‑cell lymphoma‑2 (Bcl‑2)-associated X protein, were also increased in IL‑1β‑stimulated chondrocytes.
In this study, to our knowledge, we provide for the first time mechanistic evidence that VB1-induced apoptosis in the human breast cancer line, MDA-MB-231, is associated with the generation of reactive oxygen species (ROS), the activation of caspases and the modulation of the expression of myeloid leukemia cell differentiation protein 1 (Mcl‑1), B cell lymphoma‑2 (Bcl-2) and Bcl-2-associated X (Bax) proteins.
Western blotting assays were used to measure the influence of HCS on apoptosis-related proteins, including B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), and Cleaved-Caspase-3.