The effects of pectins on life span and stress resistance in Drosophila melanogaster

被引:0
|
作者
Mikhail Shaposhnikov
Dmitrii Latkin
Ekaterina Plyusnina
Lyubov Shilova
Anton Danilov
Sergey Popov
Alexander Zhavoronkov
Yuri Ovodov
Alexey Moskalev
机构
[1] Komi Science Center of Russian Academy of Sciences,Laboratory of Molecular Radiobiology and Gerontology, Institute of Biology
[2] Syktyvkar State University,Institute of Physiology, Komi Science Centre
[3] The Urals Branch of the Russian Academy of Sciences,undefined
[4] Center for Pediatric Hematology,undefined
[5] Oncology and Immunology,undefined
[6] Moscow Institute of Physics and Technology,undefined
来源
Biogerontology | 2014年 / 15卷
关键词
Pectins; Lifespan; NF-κB; Anti-inflammatory activity;
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中图分类号
学科分类号
摘要
The composition of diet is one of the major determining factors for lifespan. The dietary pectins are known to have anti-inflammatory properties and may influence aging and longevity. Here we demonstrate the lifespan-extending effect of the low methyl esterified (LM) commercial pectins CU701 and AU701 in wild-type strain of Drosophila melanogaster. The high methyl esterified (HM) pectin CU201 did not affect lifespan. LM pectin did not increase lifespan of males with a mutation in the Toll adaptor Myd88 gene and in both males and females with a mutation in the NF-κB ortholog Relish. LM pectin CU701 increased imagoes survival in stress conditions (oxidation, hyperthermia and starvation). However, the fertility of LM and HM pectins treated flies decreased. The treatment of the imagoes with LH and HM pectins induced the activation of whole-body expression of genes involved in DNA repair (D-GADD45, mei-9, spn-B), apoptosis (wrinkled/hid) and heat shock response (hsp70Aa). In contrast, the expression of proinflammatory PARP-1 gene decreased. In the intestines LH and HM pectins induced the mRNA expression of the NF-κB-dependent antimicrobial genes Defensin, Drosomycin and Metchnikowin. These results indicate that the observed lifespan-extending effect of the LM pectins may be mediated by intracellular pathways that involve NF-κB signalling and activation of stress resistance genes.
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页码:113 / 127
页数:14
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