A study executed by our laboratory also confirmed that Bcl 2, another protein, may mediate survival signals of osteoblasts. reported that Lapatinib clinical trial, a 2 inhibitor, decreased cellular Bcl XL levels, then activated caspases 3 and 9, and induced apoptosis of prostate cancer cells. Thus, the SNP caused nitrosative pressure can stimulate apoptosis through downregulation of Bcl XL mRNA and protein expression. The oxidative stress induced inhibition of Bcl XL expression requires the transcription factors, NF B and AP 1. In parallel, SNP reduced Bcl XL mRNA and protein syntheses. c Jun is just a essential member of transcription factor AP 1. AP 1 binding components and nf B are found in the promoter region of the bcl xL gene. Throughout the means of cell protection, service of Runx2, another transcription factor, may be involved in managing antiapoptotic bcl 2 gene expression. Ergo, the SNP activated nitrosative pressure may induce apoptotic Lymph node insults to rat osteoblasts via curbing antiapoptotic gene expression, including bcl xL or bxcl 2. In cardiac muscle cells and neuronal cells, nitrosative tension attenuates c Jun/AP 1 activation and therefore induces cell apoptosis. In addition, downregulation of NF B activation is demonstrated to mediate NO induced apoptosis of macrophages and T lymphocytes. This study furthershowed that nitrosative stress might reduce the translocation of c Jun and NF B from the cytoplasm to nuclei and therefore lowered Bcl XL mRNA expression and cell survival. MAPKs take part in nitrosative stress caused modifications in NF Bs and AP 1s translocation, Bcl XL phrase, and osteoblast harm. Exposure of rat osteoblasts to SNP decreased the degrees of p38 MAPK, JNK1/2, and phosphorylated ERK1/2 in time dependent ways. ERK1/2, JNK1/2, and p38 MAPK are important members of MAPK family proteins. Following service, phosphorylated GW0742 MAPKs may modulate certain gene expressions and regulate cell mitosis, growth, and apoptosis. In individual osteosarcomaMG 6-3 cells, JNK/SAPK participates in NO induced cell apoptosis. This research showed that application of JNK1 and ERK1 siRNAs in to rat osteoblasts lowered the translation of those two MAPKs. At the same time, therapy with JNK1 and ERK1 siRNAs potentially increased nitrosative stressinduced apoptosis of rat osteoblasts.