GLP 1 also inhibits B cell apoptosis and promotes B cell growth in cultured cells and animals in vitro. The continual administration of GLP 1 Cediranib structure also encourages B cell growth, insulin synthesis, and B cell neogenesis. An important locus for the regulation of GLP 1 scientific action is the N terminal of the peptide via dipeptidyl peptidase IV mediated cleavage in the position 2 alanine. The half-life of active GLP 1 in the circulation is about 2 min, which limits its clinical value. Exendin 4 is just a GLP 1 receptor agonist that is not cleaved by DPP 4. Therefore, it has an extended half life than GLP 1 and could bemore appropriate as a therapeutic agent. Currently, the action of GLP 1 around the ERS signaling pathway in pancreatic B cells hasn’t been fully discussed. Yusta et al. demonstrated that GLP 1 receptor signaling specifically modulates the ER stress response, ultimately causing the promotion of B cell adaptation and survival. Ferdaoussi et al. found that exendin 4 inhibits apoptosis elicited by IL 1, which highlights Skin infection the significance of GLP 1 mimetics as new effective inhibitors of cytokine induced JNK signaling. Tert butyl hydroperoxide is an organic lipid hydroperoxide analog, which can be widely used as a prooxidant to judge mechanisms involving oxidative stress in cells and tissues. In this research, we investigated whether t BHP can result in ERS. More over, we investigated whether exendin 4 can defend T cells from t BHP induced apoptosis. Moreover, we discovered the anti-apoptotic molecular mechanisms of exendin 4, including an assessment of the ERS and JNK signaling pathways, in t BHP treated T cells. Exendin 4, t BHP,Dulbeccosmodified Eagles choice, Hanks balanced salt solution, and fetal price Bosutinib bovine serum were obtained from Gibco. Key antibodies, including rabbit polyclonal antibodies to sheep P IRE1 and IRE 1, were ordered from Santa Cruz Biotechnology. Rabbit polyclonal antibodies to sheep NH2 terminal kinase, p JNK, c Jun, p c Jun, caspase 3 were ordered fromCell Signaling. The JNK inhibitor, SP600125, was purchased from Invitrogen. Hoechst 42/PI, caspase 3 activity assay kits, and the Annexin V FITC apoptosis equipment were purchased from Sigma Aldrich. The western blot chemiluminescent detection system was purchased from KPL. All reagents were of analytical or cell culture grade purity. The pancreatic MIN6 B cell line was a present from the Institute of Endocrinology of Ruijin Hospital, which is associated with Shanghai 2nd Medical University. MIN6 cells were maintained in DMEM supplemented with 1500-3000 FBS, 100 units/mL penicillin, and 100 ug/mL streptomycin and were kept at 37 C in humidified air with 5%CO2. The cells were passaged every 3 days and developed to 75%confluence. 2Cells were double stained with propidium iodide and Hoechst 42 to distinguish apoptotic cells from necrotic cells.