data presented here claim that Cip1 p21 and JNK signaling pathway might represent attractive targets to GSE induced apoptosis in human leukemia cells. In a recent review, GSE has demonstrated an ability to inhibit cell growth and cause GW9508 dissolve solubility G1 stage cell cycle arrest and apoptosis in human colorectal cancer cells, regulate cell cycle regulators with a strong effect for Cip1/p21 up-regulation. Consistent with this outcome, GSE mediated apoptosis in Jurkat cells may be associated with Cip/p21 up-regulation and cell cycle arrest. Additional mechanistic studies, nevertheless, are required in future to elucidate how Cip1/p21 plays a role in GSE induced apoptosis in human leukemia cells. In today’s study, we provide evidence that GSE causes up-regulation of Cip1/p21 through the activation of JNK in human leukemia cells. A connection between the upregulation of Cip1/p21 and activation of JNK is provided by the truth that SP600125, a selective inhibitor of JNK, effectively inhibits Cip1/p21 up-regulation caused by GSE. Similar are given by a report where galectin Skin infection 8 induces cell cycle arrest and apoptosis through up regulation of Cip1/ p21 by activation of JNK. Inhibition of JNK activation by a selective inhibitor of JNK, SP600125, completely prevents the up-regulation of Cip1/p21 mediated by galectin 8, indicating that JNK generally seems to play the major role in the process underlying the upregulation of Cip1/p21. Another evidence supports a model in which transcription of Cip1/p21 gene is activated by early progress response 1 independently of p53 in response to curcumin therapy in U 87MG human glioma cells. Egr 1 expression is induced by curcumin through activation of JNK, suggesting that JNK/Egr 1 signal cascade is required for p53 unbiased transcriptional activation of Cip1/p21. Jointly, our findings suggest a structure of activities in GSE induced lethality PFT alpha in which JNK activation represents the early insult, which cause Cip1/p21 up-regulation and caspase activation and apoptosis. In summary, the current study has presented evidence that GSE triggers human leukemia cell death with all the activation of caspases 3, 8, and 9 in addition to PARP cleavage, and that GSEinduced apoptosis is proceeded from the activation of JNK and thus up regulation of Cip1/p21. The of this study might have implications for the incorporation of agents such as GSE to the chemopreventive In this study, we focused to recognize whether eupatilin, an extract from Artemisia argyi folium, stops H2O2 induced damage of cultured feline esophageal epithelial cells. Cell viability was measured by the traditional MTT reduction assay. Western blot analysis was conducted to investigate the appearance of 5 lipoxygenase by treatment in the absence and presence of inhibitors. Cell viability was decreased to 4000-6000, when cells were subjected to 600 uM H2O2 for 24-hours.