Jak stat and apoptotic rate inhibited in the riluzole pretreatment group. Our results of riluzole preventing apoptosis were similar with the conclusion that riluzole can attenuate morphine induced apoptosis in the lumbar spinal cord of rats. Alternatively or additionally to preventing death, riluzole may thereby stimulate a recovery process in noise damaged hair cells. It was also found that riluzole was able to increase the cell survival of T cells from HIV 1 infected patients and inhibit spontaneous apoptosis. However, the data about the effects of riluzole on cell cycle were few. The precise molecular mechanism by which riluzole protects astrocytes against Mn neurotoxicity is not clear. In many studies, the protective effects of riluzole have been explained by an anti neuronal signaling toxic mechanism. It may involve an inhibition of Glu release, an inactivation of voltage dependent sodium channels, an inhibition of calcium influx, or an activation of a G protein dependent process.
Therefore, it had presumed that riluzole acted neuroprotective PKC Pathway effects on astrocyte to reverse Mn cytotoxicity by inhibiting Glu release, promoting Glu uptake and GluTs activity, inhibiting calcium influx, or antagonizing oxidative stress. Basing the present study, it may demonstrate that riluzole exert the protective effects to reverse Mn induced cytotoxicity, cell cycle arrest, and apoptosis on astrocytes. In conclusion, Mn exposure cause inhibition of cell viability, elevation of LDH leakage, injury of astrocyte morphology, G0/G1 phase arrest, and apoptosis in the cultured astrocytes. These data suggested the hypothesis that Mn induced toxicity on astrocytes. The results presented herein demonstrate that riluzole can inhibit Mn toxicity on astrocytes. There have been few studies about the use of riluzole to prevent Mn toxicity on the cultured astrocytes. Therefore, the present study may provide a new way to prevent manganism. In both second and third line settings, PFS and OS were not significantly different between the two groups. One more retrospective study evaluated the effectiveness of erlotinib and gefitinib in patients with relapsed NSCLC in second and third cisplatin line settings, and compared this with that of docetaxel. No statistically significant difference in OS between these three drugs in either setting was present.
However, based on the BR.21 trial, erlotinib should be administered as second line treatment in patients considered unfit for chemotherapy, or in a subgroup of patients with positive predictive clinical and/or molecular factors especially in never smokers, and as third line therapy. The positive results of the INTEREST trial conducted in patients who were fit for further chemotherapy after the failure of one or two previous chemotherapy regimens support the consideration of EGFR inhibitors as a reasonable alternative to second line chemotherapy and especially in third line treatment after pemetrexed or docetaxel failure. Regarding the comparative differences between erlotinib and gefitinib in terms of efficacy, Kim et al. recently retrospectively studied 467 patients who had received either of these EGFR inhibitors after progression on prior therapies. There was no statistically significant difference with regards to OS and PFS.