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.
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.
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.
Analysis of apoptosis‑associated proteins revealed that Rsf‑1 positively regulated B‑cell lymphoma 2 (Bcl‑2), cellular inhibitor of apoptosis 1 (cIAP1) and cIAP2, and downregulated Bcl‑2‑associated X protein expression.
In addition, PTS treatment significantly increased the expression of anti-apoptotic B-cell lymphoma 2 (BCL2), with a concomitant reduction in the apoptotic Bcl-2-associated X protein (BAX) and Caspase-3 genes in the embryo.
The results demonstrated that the expression levels of AURKA, B‑cell lymphoma 2 (Bcl‑2), cyclin‑dependent kinase 1, cyclin B1, proliferating cell nuclear antigen and heterogeneous nuclear ribonucleoprotein K, as well as the phosphorylation of p53 and mouse double minute 2 homolog, were significantly decreased in Huh‑7 cells treated with 5 µmol/l cinobufagin for 24 h. Conversely, the expression levels of Bcl‑2‑associated X protein, p21, p53 upregulated modulator of apoptosis and phorbol‑12‑myristate‑13‑acetate‑induced protein 1, were significantly increased by cinobufagin treatment.
Moreover, the expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in brain tissues were detected via immunohistochemistry, and the relative protein expressions of PI3K p85, PI3K p110, and p-Akt were detected via Western blotting.
Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) was used to detect the expression of B-cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated X protein (Bax) and aspartate proteolytic enzyme-3 (Caspase-3) mRNA.
Terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling assays were used to detect apoptotic cells, and western blotting was performed to determine the expression of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), and cleaved caspase-3, as well as oxidative stress and inflammation-related proteins, such as nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Toll-like receptor 4 (TLR4), and nuclear factor-κB (NF-κB).
By the western blotting analysis, FXS-3 increased the expression of B-cell lymphoma-2 (Bcl-2) associated X protein (Bax)/Bcl-2 ratio, inhibited matrix metalloproteinase (MMP)-2 and MMP-9, and regulated the extracellular signal-regulated kinase (ERK)/p38, c-Jun N-terminal kinase (JNK), protein kinase B (AKT)/mechanistic target of rapamycin (mTOR), as well as mitogen-activated protein kinase (MEK)/ERK signaling pathways.
Moreover, IL-21 promoted the uncontrolled proliferation of AA-FLS through induction of B cell lymphoma-2 (Bcl-2) and diminished expression of Bcl-2 associated X protein (BAX) via PI3K/Akt signaling.
Treatment with 3DC2ME also significantly reduced expression of active caspase-8 and -3, Bcl-2-associated X protein (Bax), and B cell lymphoma 2 (Bcl-2), indicating the inhibition of apoptosis pathways in the kidneys.
BACKGROUND B-cell lymphoma 2 (BCL-2) ovarian killer (BOK) is a Bcl-2 family member with sequence homology to pro-apoptotic BAX and BAK, but its physiological and pathological roles remain largely unclear.
MCAO mice showed overexpression of interleukin-6 (IL-6), IL-17, and IL-23, and increased positive protein expression of PTGS2, as well as expression of PTGS2, nuclear factor-κB (NF-κB), tumor suppressor region 1 (TSP-1) and Bcl-2-associated X protein (Bax), but underexpression of vascular endothelial growth factor (VEGF), S-phase kinase associated protein 2 (Skp2), and B-cell lymphoma 2 (Bcl-2).
Shikonin increased mitochondrial membrane depolarization and altered the levels of apoptosis-related proteins, with a decrease in B cell lymphoma (Bcl)-2 and an increase in Bcl-2-associated X protein, and subsequently, increased expression of cleaved forms of caspase-9 and -3.
The effects of FerA at doses of 80 and 100 mg/kg on mitochondrial B‑cell lymphoma-2 (Bcl‑2)‑associated X protein‑related apoptosis were attributed to the activation of Akt/mTOR/4E‑BP1/Bcl‑2 anti‑apoptotic signaling, and eventually contributed to suppression of the cytochrome c/caspase‑3 activation pathway in the penumbral cortex 7 days following permanent cerebral ischemia.
The results revealed that GA inhibited the proliferation and induced the apoptosis of NSCLC A549 cells in dose‑ and time‑dependent manners, which was associated with upregulated B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax) and downregulated Bcl‑2.
The effects of cisplatin include activation of caspases, proteolysis of enzyme poly ADP ribose polymerase (PARP), control of apoptosis modulators B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and BH3-interacting domain death agonist (Bid), and cell cycle arrest in G2/M phase.