thatS 22.2 35 untreated animals to 62, indicating that the treatment of OSU 03,012 k can further RAD001 reduce the IIS pathway activity t in a background sensitized daf second Overall, our results are consistent with a model that celecoxib and OSU 03102 a component of the IIS pathway, probably PDK 1, the life of C. influence ridiculed Ngern elegans. Celecoxib and OSU 03,012 treatments reduce disease years with an intriguing question in biology is connected, as is the normal aging process is coupled with age-related diseases. Is a drug that agrees on leased getting the onset of age-related diseases Reduced IIS pathway activity T been shown to improve the appearance and severity of age-related progressive neuronal degeneration associated with aberrant protein aggregations and tumor growth in models C. elegans disease. For instance, form YFP fusions expressed 35 glutamine repeats in cells of the K Rperwand muscles aggregates and loss of mobility T due to the age of the animals. Since the formation of aggregates and durable polyQ proteotoxicity mutants are in the way IIS galv Siege and accelerated by short-lived mutants of the IIS pathway. To test whether treatment OSU 03 012 can also improve proteotoxicity YEARS Ring aggregation by inhibiting the process of a screw in IIS model we have initially Highest the formation of aggregates, depending on the age of the animals analyzed polyQ drugs treated. We found that polyQ aggregation in animals exposed to 03,012 OSU compared to control animals is zinc Siege. Proteotoxicity the associated aggregation was also significantly improved in treated animals OSU 03,012.
Mutations in gld 1, a tumor suppressor gene required for oocyte development in C. elegans, germ cell tumors cause death. The growth of these tumors lived significantly reduced in the period mutants of the way IIS. To determine whether the progression of tumor growth in a germ gld mutants by celecoxib and OSU 03012 galv Gert be k Nnte, we followed the growth of germ cell tumors drugtreated mutants. As expected, the growth of germ cell tumors in a gld mutants is inhibited by celecoxib and OSU 03012 treatment, probably by inhibition of PDK-1 activity T. The inhibitory effect of these drugs on the proliferation VX-222 of germ cells appears to occur only when a mutated gld as both clutch size S and duration of the breeding stock of N2 not by treatment with celecoxib ge Be changed. Interestingly, these two compounds have been as a cancer drug Chemopr Proposed intervention. Our results showed that celecoxib, a compound commonly used as an anti-inflammatory drug in humans, life extending and progression of age-related proteotoxicity and tumor growth in C. elegans. Discussion In this study, we report that celecoxib stero, not one To the anti-inflammatory both the average and maximum life span in C. elegans extends. Zus Tzlich the k Physical health, such as the decay rate with the age of the motor activity Associated t is implied significantly improved in the celecoxib-treated animals. The effect of celecoxib on aging is not the result of a Ver Change in the N Hrwerts of bacteria from the celecoxib had no effect on the growth of bacteria. These findings quickly to a critical question: What is the mechanism by which celecoxib extends lifespan Celecoxib is an original