The effects of AST were mediated through the downregulation of Bcl-2 associated X, apoptosis regulator (Bax), and cleaved caspase-3 and through the upregulation of B-cell lymphoma 2 (Bcl-2).
The protein levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X (Bax), X-linked inhibitor of apoptosis (XIAP), total poly (ADP-ribose) polymerase (PARP), caspase-3 and caspase-8 were examined using western blotting.
Ocimum basilicum L. significantly decreased testicular levels of nuclear factor-kappa B and B-cell lymphoma-2 (Bcl2)-associated protein X, along with caspase-3 immunohistochemical staining.
After 30 min of ischemia and 120 min of reperfusion, cardiac function, infarct size, cardiac marker enzymes, antioxidative parameters, inflammatory factors, histopathological changes, cardiomyocyte apoptosis, and B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein and caspase‑3 expression were determined using a multi‑channel physiological recording system, nitrotetrazolium blue chloride, biochemical kits, radioimmunoassay kits, hematoxylin and eosin, terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling assay, immunohistochemistry and reverse transcription‑quantitative PCR, respectively.
Furthermore, morin was able to down regulate the levels of inflammatory and apoptotic markers such as nuclear factor kappa B (NF-κB), neuronal nitric oxide synthase (nNOS), tumor necrosis factor-α (TNF-α), p53, cysteine aspartate specific protease-3 (caspase-3) and B-cell lymphoma-2 (Bcl-2).
As a result, we observed higher level of XIST and Smurf1, but lower level of miR-27a in SCI rats and lipopolysaccharide (LPS)-induced primary microglial cells. in vitro, LPS induced SCI microglia cells as described by decreased cell viability and B cell lymphoma 2 (Bcl-2) expression, and increased cell apoptosis rate, Bax and cleaved caspase 3 levels, and tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) secretions. in vivo, a T10 laminectomy caused SCI rats as evidenced by decreased Basso-Beattie-Bresnahan Locomotor Rating Scale (BBB) score and induced expression of Bax, cleaved caspase 3, TNF-α and IL-6.
Furthermore, based on Western blot experiment, cell apoptosis induced by <b>a14</b> also involved the expression of B-cell lymphoma-2 (Bcl-2) family and Caspase 3 protein.
Meanwhile, oxidative stress induced a significant improvement in the mRNA expression of occludin (OCLN) and caspase-3, and remarkably inhibited the expression of L-type amino acid transporter 1 (LAT1) or B cell lymphoma-2 (Bcl-2), respectively.
After transfection of overexpressed miR-590-3p or si-RIPK1, declined RIPK1, NF-κB, Toll-like receptor 4, caspase-3, FasL, p53, and c-myc levels, increased B-cell lymphoma-2 level, promoted cell proliferation, promoted cell cycle distribution and inhibited apoptosis of myocardial cells were found.
The expression of B‑cell lymphoma (Bcl)‑2, Bcl‑2‑associated X (Bax), and caspase‑3 were detected by western blot analysis and reverse transcription‑quantitative polymerase chain reaction.
RT-qPCR and western blot analyses were also performed to determine the effects of miR-210-3p on the expression levels of SIN3A, B-cell lymphoma 2 (Bcl-2) and Caspase-3.
Moreover, we found enhanced expression of Bcl2-associated X, apoptosis regulator (Bax), and cleaved caspase-3, and reduced expression of B-cell lymphoma 2 (Bcl-2) in the LPS-treated group, which were markedly reversed in the LPS + caffeine co-treated group.
B-cell lymphoma (Bcl)-2 mRNA and protein expression levels were decreased however caspase-3, caspase-9 and dynamin-related protein 1 (Drp-1) mRNA and protein expression levels were increased.
Because PC-corr network inference integrated with a protein-protein interaction network prediction also showed that MURC is involved in the apoptotic pathway, we confirmed the upregulation of STAT3 (signal transducer and activator of transcription 3) and BCL2 (B-cell lymphoma 2) and the inactivation of caspase 3 in I/R-injured hearts of MURC knockout mice compared with those of wild-type mice.
In this study, we identified CD122<sup>high</sup> stem cell antigen-1 (Sca-1) <sup>high</sup> B cell lymphoma 2 (Bcl-2) <sup>high</sup> CD4<sup>+</sup> stem cell-like memory T cells (TSCMs) as a distinct memory T cell subset, which preferentially reside in the BM, where they respond vigorously to blood-borne antigens.
Immunoblotting demonstrated that levistolide A enhanced doxorubicin‑induced cell death by decreasing the expression levels of B‑cell lymphoma 2 and increasing caspase 3 expression.
Depletion of ROS by diphenyleneiodonium decreased HG‑induced cell death, and suppressed increases in caspase 3 activity and B‑cell lymphoma 2‑associated X protein levels.
Furthermore, CBE also prevented UVB-induced apoptosis and significantly downregulated B cell lymphoma 2 (Bcl-2)-associated X, cytochrome-c, and caspase-3 expression, while upregulating Bcl-2 expression.
We also found that EEL enhanced the apoptosis of Bel-7402 and Huh-7 cells by regulating the expressions of Bcl-2 associated X (Bax), B cell lymphoma 2 (Bcl-2) and Cytochrome-C and the activity of caspase-3 and therefore promoted cell cycle arrest.
At the gene level, CADM1 expression level upregulated caspase-3 activity and expression of Bax and p27 protein and downregulated levels of B cell lymphoma-2, cyclinD1, cyclinE1 and cyclin dependent kinase 2 proteins.
Furthermore, LncRNA RAB5IF depletion suppressed cell proliferation and colony formation, increased sub G1 population, cleavage of poly ADP-ribose polymerase (PARP) and cysteine aspartyl-specific protease (caspase 3) and attenuated the expression of procaspase 3, pro-PARP and B-cell lymphoma 2 (Bcl-2) in HepG2 and Hep3B cells.
Activation of apoptosis was analyzed by western blot analysis of B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated x protein (Bax), cytochrome c (Cyt c), caspase‑3 and caspase‑9 levels.
The anti-apoptotic proteins B-cell lymphoma 2 (Bcl-2) and Bcl-xL were significantly upregulated, whereas the pro-apoptotic proteins BCL2-associated X (Bax), H<sub>2</sub>O<sub>2</sub>-induced cleaved caspase-3, and the DNA damage marker, phosphorylated histone (γH2A.X) foci, were significantly downregulated upon histochrome treatment of hCPCs in vitro.
Furthermore, the expression of anti-apoptotic protein B-cell lymphoma 2 decreased and the expression of the pro-apoptotic proteins active caspase-3 and apoptosis regulator BAX increased in the Hep G2 cells following JTC-801 treatment.