GLP 1 receptor agonists have potentially essential applications in the treatment of diabetes. Within our current study, we also found that exendin 4 inhibited t BHP induced B mobile apoptosis by 77. 60-acre. The t BHPinduced increase was reduced by pretreatment of cells with exendin 4 in JNK phosphorylation by 50. Four or five Gemcitabine clinical trial and paid down the t BHP induced increase in d JUN by 84. 95-page. These results were similar to those observed following pre-treatment with the JNK chemical, SP600125, suggesting that exendin 4 attenuates t BHP induced apoptotic demise by modulating JNK c JUN signaling in T cells. High quantities of ERS bring about the apoptosis of pancreatic B cells. Islet B cells are protected by the GLP 1 receptor agonist, exendin 4, by reducing the degree of ERS. Exendin 4 protects B cells against free fatty acids via the induction of the ER chaperone BiP and the anti-apoptotic protein JunB, which mediate B cell survival under lipotoxic conditions. We show that a specific degree of oxidative injury produces apparent pyrazine ERS and that the domain of the ER transmembrane protein, IRE1, undergoes selfdimerization and phosphorylation induced activation. IRE1 activation may possibly market apoptosis, and exendin 4 can inhibit the activation of IRE1 to reduce the ERS answer, thereby protecting pancreatic B cells. Recently, the protective mechanisms of GLP 1 have now been elucidated. Cornu et al. showed that regulation of B cell numbers and characteristics by GLP 1 is dependent upon the cAMP/protein kinase A mediated induction of IGF 1R expression and the increased action of an IGF 2/IGF 1R autocrine loop. Klinger et al. demonstrated the cAMP/protein kinase A/CREB andMAPK/ERK1/2 paths can additively get a grip on T cell proliferation, whereas Aikin et al. shown that PI3K/AKT suppresses the JNK pathway in islets and that this crosstalk represents a vital anti-apoptotic consequence of PI3K/AKT activation. Widenmaier BMS-708163 Avagacestat et al. . Discovered that GLP 1 suppresses p38 MAPK and JNK via Akt mediated changes in the phosphorylation state of the apoptosis signal regulating kinase 1 in human islets and INS 1 cells, which in the inhibition of its activity. MIN6 cells were preincubated with exendin 4 or with SP600125 for 18 h and then exposed to t BHP for 1 h. Representative european blot images unveiled the expression degrees of phospho JNK and phospho c JUN, total JNK protein and total c JUN. The histogram displays the quantification of the protein data. Levels of phosphorylated protein were normalized to the levels of total protein and expressed as the relative fold change when compared with the control samples. Values match the mean SD. The present study has shown that exendin 4 has a protective effect against t BHP mediated B mobile apoptosis through the inhibition of ER stress. We’ve shown that IRE1 JNK h Jun caspase 3 pathways are involved.