it is possible that the PI3 kinase/Akt process is involved with FGF 2 induced GDNF launch through still another transcription factor with the exception of Egr 1. While crosstalk between the AZD5363 kinase pathway and the PI3 kinase/Akt pathway is situated in signaling, in our research, the activation of PI3 kinase/Akt pathway influences FGF 2 induced GDNF launch independently of p44/ p42 MAP kinase or SAPK/JNK from cells. We furthermore demonstrated that PD98059 didn’t affect FGF 2 caused SAPK/ JNK phosphorylation, and SP600125 did not lower FGF 2induced p44/p42 MAP kinase phosphorylation. Therefore, it is most likely that the p44/p42 MAP kinase pathway, the SAPK/ JNK pathway and the PI3 kinase/Akt pathway control FGF 2induced GDNF launch in C6 glioma cells independently of one another. The potential mechanism of FGF 2 triggered DGNF launch shown here is described in Fig. 9. Further investigations are essential to clarify the exactmechanismbehind FGF2 mediated signaling in astrocytes. Concerning the PI3 kinase/Akt pathway in neurons, phosphorylation of Akt, especially at Ser473 deposit, increases after reperfusion in swing. Different growth factors, including FGF Mitochondrion 2, have already been proven to upregulate Akt phosphorylation after ischemia. Since improvement of Akt phosphorylation is related to inhibition of caspases 9 and 3, it’s suggested that growth facets stop apoptosis through phosphorylation of Akt. The PI3 kinase/Akt route stops neural cell death. Astrocytes are a key factor in the mind in response to injury. Activated astrocytes encourage antioxidant chemical expression, membrane transporters and trophic facets that help neural and glial survival and tissue repair. It has been noted that apoptosis of rat cultured cortical astrocytes after experience of anaerobic insult is suppressed by PI3 kinase inhibitor. For that reason, it makes us speculate that the activation of PI3 kinase/Akt pathway characteristics defensive in both neurons and astrocytes. In the present study, we showed that FGF 2 enhanced release of GDNF, which will be regarded as a potent neuroprotective representative, at least partly through the PI3 kinase/Akt route. Based on our findings, it is probable that the Hesperidin solubility PI3 kinase/Akt pathway has a important role in astrocytes and a effect on the CNS. In summary, our results strongly suggest that the PI3kinase/Akt process plays a part in part involved in FGF 2 aroused GDNF launch independently of p44/p42 MAP kinase or SAPK/JNK in C6 glioma cells. GDNF enzyme linked immunosorbent assay kit was purchased from Promega Co.. FGF 2, PD98059, SP600125, SB203580 and LY294002 were obtained from Calbiochem Novabiochem Co.. Wortmannin was obtained from Sigma Chemical Co..