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16.1 of DhHP-6 has not daf-16 dependency again. Then we examined xpa-1 which is partof nucleotide excision repair [7], msh-2 involved in mismatch repair [8] and hus-1 one ofthe cell cycle checkpoint gene in C. elegans [9] to focus on DNA repair signaling pathway.The results show that the expression of three genes were all decreased after given DhHP-6in wild-type indicating that the DhHP-6 can reduce the mistake in DNA replication. Underthe heat stress the heat shock-dependent up-regulation of hus-1 and the down-regulation oftwo genes involved gene repair as well as the results for hsp-16.1 above suggest a possibleregulation to resistance to the heat stress in C. elegans: heat shock makes an increase ofintracellular oxidative stress and causes an increase of DNA replication mistakes leading toincrease the expression of cell checkpoint gene subsequently and regulate the protection ofthe protein as the main resistant pathway for stress, when the DNA repair as the secondary.On the one hand the presence of DhHP-6 can decrease the oxidation levels, on the otherhand DhHP-6 can speed up the rate of the up-regulation for HSP and thus protect thebiological functions in C. elegans. Finally we detected cep-1 the homologous of p53 in C.elegans to investigate the influence of heat stress and DhHP-6 to apoptosis. The resultsshow that the expression of cep-1 is significantly decreased in the presence of DhHP-6 inwild type but independent heat shock indicating that DhHP-6 can reduce the apoptosis invivo and short-term heat shock has little effect on apoptosis. The change trend of cep-1 wassimilar in daf-16 mutant and wild-type worm suggesting the effect has no daf-16dependency.In conclusion DhHP-6 can protect C.elegans from the heat stress in a sir-2.1 anddaf-16 independent way and the possible mechanism is that the presence of DhHP-6 candecrease the high oxidation level caused by heat shock and accelerate the main response tostress by shortening the time for hsp's up-regulation.AcknowledgmentsWe would like to thank the Product Quality Supervision Inspection of Jilin for providing the real timePCR used in this research. We would like to thank the Caenorhabditis Genetics Center for providingstrains used in this research.References1. Wu,D., Cupser, J.R., Yashin, A.L., Johnson, T.E. J. of Gerontology 63(7), 660-668 (2008).2. Guan, S., Li, P., Luo, J., Li, Y., Huang, L., Wang, G., Zhu, L., Fan, H., Li, W., Wang, L. Free RadicRes. 44(7), 813-820 (2010).3. Lin, K., Hsinh,Libina, N., Kenyon, C. Nat. Genet. 28(2), 139-145 (2001).4. Berdichevsky, A., Guarente, L. Cell Cycle. 5(22), 2588-2591 (2006).5. Taub, J., Lau, J.F., Ma, C., Hahn, J.H., Hoque, R., Rothblatt, J., Chalfie, M. Nature. 399(6732), 162-166 (1999).6. Candido, E.P., Jones, D., Dixon, D.K., Graham, R.W., Russnak, R.H., Kay, R.J. Genome. 31(2):690-697 (1989).7. Park, H.K., Yook, J.S., Koo, H.S., Choi, I.S.,Ahn, B. Mol. Cells 14(1), 50-55 (2002).8. Tijsterman, M., Pothof, J., Plasterk, R.H. Genetics 161(2), 651-660 (2002).9. Hofmann, E.R., Milstein, S., Boulton, S.J., Ye, M., Hofmann, J.J., Stergiou, L., Gartner, A., Vidal,M., Hengartner, M.O. Curr. Biol. 12(22), 1908-1918 (2002).10. Schumacher, B., Hofmann, K., Boulton, S., Gartner, A. Curr. Biol. 11(21), 1722-1727 (2001).349