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).
Meanwhile, ACART increased the expression of the B cell lymphoma 2 (Bcl-2) and suppressed the expression of Bcl-2-associated X (Bax) and cytochrome-C (Cyt-C).
Compound 7a notably inhibited the expression and activity of PIM kinases, as evidenced by reduced B‑cell lymphoma‑2 (Bcl‑2)‑associated death promoter phosphorylation at Ser112.
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.
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.
The levels of Shrm4, GABA<sub>B1</sub>, Bcl-2-associated protein x (Bax), B cell lymphoma 2 (Bcl-2), cleaved Caspase-3, microtubule-associated protein 2 (MAP-2) as well as suppressor of cytokine signaling 2 (SOCS2) were detected to further assess the role of Shrm4 and GABA pathway in NSCs.
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).
We found that ectopic expression of gga-miR-16-5p in DF-1 cells enhanced IBDV-induced apoptosis by directly targeting cellular anti-apoptotic protein B-cell lymphoma-2 (Bcl-2), facilitating IBDV replication in DF-1 cells.
Western blot assay was conducted to examine the protein levels of B-cell lymphoma-2 (Bcl-2), BCL2-Associated X (Bax), matrix metalloprotein 2 (MMP2), MMP9 and PDCD4.
The current study sought to investigate the effect of modified exosome-containing plasmids expressing B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X-protein (Bax) short hairpin RNA (shRNA) on apoptosis and neural functions after TBI.
In addition, modulation of ZEB1 and subsequent change in MRP4 expression correlated with a lower apoptotic response to docetaxel, characterized by lower B-cell lymphoma 2 (Bcl2), high BCL2-associated X protein (Bax), and high active caspase 3 expression.
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.
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.
Furthermore, CP group showed toxic histopathological changes of marked cardiac damage in addition to a significant decrease in total antioxidant capacity (TAC), superoxide dismutase (SOD), eNOS gene expression, and B cell lymphoma 2 (Bcl2) immunoexpression.
CABYR-a/b downregulation suppressed cell proliferation and induced G1-phase arrest via decreasing cyclin D1 and cyclin dependent kinase 4, while promoted apoptosis by reducing B-cell lymphoma 2 (Bcl-2) and increasing Bcl-2-associated death promoter.
Diabetes-related physical and biochemical parameters, pancreatic histopathological changes, immunohistochemical staining, quantitative real-time polymerase chain reaction, and western blot were used to measure the expression of apoptosis signal-regulating kinase 1 (ASK1), Jun N-terminal kinase (JNK), Bcl-2 associated X protein (BAX), and B-cell lymphoma-2 (Bcl-2).
The mRNA and protein expression of apoptosis-related genes including Caspase-3, Caspase-9, Caspase-8, Cytochrome-C (Cyt-C), p53, B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax) were significantly altered in broilers BF.
Furthermore, exposure to Pb induced neurodegenerative cognitive impairment in rats, depressed the long-term potentiation (LTP) in the rat brain slices, increased the neuronal intracellular free calcium concentration ([Ca<sup>2+</sup>]i), inhibited the phosphorylation of Ca<sup>2+</sup>/calmodulin-dependent protein kinase II (CaMKII) and cyclic adenosine 3',5'-monophosphate (cAMP) response element binding protein (CREB) as well as the expression of anti-apoptotic protein B-cell lymphoma 2 (Bcl2), and activated the phosphorylation of extracellular regulated protein kinases (Erk) protein both in vitro and in vivo.
The potential protective effects of resveratrol (RES) on the modulation of hepatic biomarkers of apoptosis and survival, p53-Bax axis, and B-cell lymphoma 2 (Bcl-2) in an animal model of paracetamol-induced acute liver injury have not been investigated before.
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.