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.
We propose the anti-apoptotic BCL2-like and pro-apoptotic BH3-only members of the family arose through duplication and modification of genes for the pro-apoptotic multi-BH domain family members, such as BAX and BAK1.
In addition, LCC inhibited the JAK2/signal transducer and activator of transcription 3 pathway, upregulated p21, and downregulated Bcl-2, Mcl-1, and Survivin, while it disrupted mitochondrial membrane potential and subsequently caused cytochrome c release with activation of multi-caspase, eventually leading to apoptosis in HN22 and HSC4 cells.
Tumor samples were compared in their expression of p53, Bcl(2), Bcl(x), Bax, p21, p-glycoprotein (PGP), multi-drug resistance-associated protein (MRP), lung resistance protein (LRP), and glutathione S-transferase (GST) using immunohistochemistry.
Moreover, due to decrease of in vivo radiotracer uptake by parathyroid grafts, the expression of multi-drug resistance-involved factors, including P-glycoprotein (P-gp/mdr1), multi-drug resistance-associated protein (mrp) and bcl-2 have been investigated using RT-PCR.