Interventions

  • name effect species mean median maximum
    Carboxyfullerene SOD mimetic treatment Administration of a small-molecule synthetic enzyme superoxide dismutase mimetic to wild-type (i.e. non-transgenicm non-senescence accelerated) mice starting at middle age significantly extends lifespan and reduces age-associated oxidative stress and mitochondrial radical production. Treatment also improves performance on Morris water maze learning and memory task and therefore rescues age-related cognitive impairment [17079053].
    NAM treatment Treatment with NAM reduces mean and maximum replicative lifespan by 28 and 37%. NAM treatment blocks the lifespan extending effect of rapamycn [20947565]. Yeast -28 -37
    Ascrobate treatment Hypersensitivity to oxygene and significantly decreased replicative lifespan of SOD1 deletion can be ameliorated by exogenous ascorbate. If acorbate's negative effects of auto-oxidation are prevented by exchange of medium, ascorbate prolongs mean and maximum replicative lifespan in the atmosphere of air and pure oxygene [15621721]. Yeast
    D-glucosamine treatment Addition of 0.5 mg/ml D-glucosamine to the growth media suppresses the short replicative lifespan and temperature sensitive growth of mpt5 mutant, but fails to extend the lifespan of wild-type cells [11805047]. Yeast
    Hesperidin treatment Hesperidin derived from the Citrus genus extends replicative lifespan at doses of 5 and 10 microMolar. Hesperdin inihibts ROS and UTH1 gene expression, but increases Sir2 and SOD gene expression. UTH1 and SKN7 are involved in lifespan extension mediated by hesperidin [22484922]. Yeast
    Gonadermasides D treatment Application of gonadermasides D significantly increases the replicative lifespan in the K6001 strain by regulating UTH1 [21512225]. Yeast
    Ganodermasides C treatment Application of gonadermasides C significantly increases the replicative lifespan in the K6001 strain by regulating UTH1 [21512225]. Yeast
    Ganodermasides A treatment Application of Ganodermasides A extends the replicative lifespan in K6001 strain by regulating UTH1 expression [20093034]. Yeast
    Ganodermasides B treatment Application of Ganodermasides B extends the replicative lifespan in K6001 strain by regulating UTH1 expression [20093034]. Yeast
    Beauveriolide I treatment Treatment with beauveriolide I (20 microgram/mL) extends chronological lifespan in BY4741 by around 50% [22790951]. Yeast +50
    Resveratrol supplementation Resveratrol significantly extends the lifespan [12939617]. Yeast
    Rapamycin treatment Treatment with rapamcyin increases mean and maximum replicative lifespan by 19 and 16% Rapamycin fails to extend the lifespan of sir2 mutants or NAM treated wild-type cells [20947565]. Rapamcyin treatment increases mean chronological lifespan by by approximately by 80% in BY4742 [22790951]. Rapamycin extends chronological lifespan proportional with increasing concentrations from 100 pg/mL to 1 ng/mL [16418483] Yeast +19 to +50 +16
    concA treatment The specific V-ATPase inhibitor concanatmycin A (concA) blocks VMA1 or VPH2 overexpression mutations ability to produce normal, tubular mitochondria. Treatment of young cells causes vacuolar acidity and loss of mitochondrial depolarization. Loss of ΔΨ is followed by mitochondrial fragmentation and aggregation that resembles mitochondrial phenotypes present in aged cells [23172144]. Yeast
    Rapamycin treatment Treatment with rapamcyin increases mean, median, 75th %ile and maximum lifespan by 19-29, 17-29, 24-32 an 19%, respectively on OP50. On HT115 rapamycyin extends mean, median and 75th %ile of lifespan by 8-36, 4-46 and 12-44%, respectively. Rapamycin robustly increases lifespan in two daf-16 mutants (mgDf47 and mu86) with or without FUdR and with growth on either the standard strain OP50 or the feeding RNAi strain HT115 [22560223]. Worm +8 to +29 +4 to +46 +19
    Icariin treatment Icariin and its derivate icariside II extend lifespan. Animals treated with icariin have high levels of icariside II [22216122]. Worm
    Icariside II treatment Icariside II and its derivate icarrin extend lifespan. Animals treated with icariin have high levels of icariside II. Icariside II also increases thermo and oxidative stress tolerance, slow locomotion decline in late adulthood and delay the onset of paralysis mediated by polyQ and ABeta(1-42) proteotoxicity. Lifespan extension by Icariside II is dependent on IIS, since daf-16(mu86) and daf-2(e1370) fails to sho exhibit lifespan extension upon icariside treatment. Incariside II treatment upregulates expression of DAF-16 targets in wild-type. HSF-1 has also a role in icariside II-dependent lifespan extension [22216122]. Worm
    Quercetin treatment Quercitin significantly extends the lifespan. Lifespan extension by quercitin has no effect on reproduction and body length. Quercitin induced lifespan extenison was neither dependent on a dietary restriction mimetic nor on sir-2.1 [19043800]. Worm
    NAD supplementation Supplementation with NAD extended lifespan and this extension was dependent on sir-2.1 and daf-16 and associated with upregulation of sod-3 [19370397]. Worm
    Apply polyphenol treatment Treatment with 100 microgram/mL apple polyphenol increases mean lifespan of wild-type N2 and FEM-1 by 12.0 and 5.3%, respectively [20717869]. Worm +5.3 to 12.0
    (-)-epicatechin treatment Treatment with (-)-epidcatechin do no extend lifespan [20717869]. Worm
    Procyanidin treatment Treatment with 65 microgram/mL Procyanidins from apple extends the lifespan of N2 and FEM-1 by 12.1 to 8.4%, respectively and does not modify grwoth, food intake of fecundity. Procyanidin treatment has no effect on mev-1 or sir-2.1 mutants [20717869]. Worm +8.4 to +12.1
    Eleutherococcus senticosus treatment Plant adaptogen Eleutherococcus senticosus (SHE-3; alias Acantopanax senticosus) increase stress resistance and mean lifespan in a dose-dependent manner. 250 microgram/ml SHE-3 signinifanclty increases lifespan between 10 and 20% 9 (P < 0.001), increase maximum lifepsan with 2-3 days and pospones the moment when the first individuals die. With higher concentrations, the effect is weakerm wheras at the highest concentrations (2500 microgram/mL) a lifespan shortenening effect of 15-25% (P < 0.001) occurs. Treatment with SHE-3 induces translocation of DAF-16 and activation of HSP-16 [18536978]. Worm +10 to +20
    Rhodiola rosea treatment Plant adaptogen Rhodiola rosea (SHE-5) increase stress resistance and mean lifespan in a dose-dependent manner. 10-25 microgram/ml SHE-5 signinifanclty increases lifespan between 10 and 20% 9 (P < 0.001), increase maximum lifepsan with 2-3 days and pospones the moment when the first individuals die. With higher concentrations, the effect is weaker whereas at the highest concentrations (250 microgram/mL) a lifespan shortenening effect of 15-25% (P < 0.001) occurs. Treatment with SHE-5 induces translocation of DAF-16 and activation of HSP-16 [18536978]. Worm +10 to +20
    DhHP-6 treatment Deuterohemin containing peptide deterohemin-AlaHisThrValGluLys (DhHP-6) significantly increases mean lifespan (P < 0.05), but not maximum lifespan. DhHP-6 also improves survival rate in acute heat-stress (35 degree Celsius) and rescues sensitivity to paraquat in acute oxidative stress. DhHP-6 treatment up-regulates SOD-3 and also regulates stress resistance genes such as hsp-16.1, hsp16.49 and sir-2.1 daf-16 and sir-2.1 genes are essential for the beneficial effect of DhHP-6 [20528576]. Worm
    DMSO treatment Treatment with 0.5 and 2% DMSO increases lifespan by 24.4 and 23.0%, respectively. 0.5% DMSO does not affect progeny number or lifespan under thermal stress. Treatment with 0.5% DMSO enhances the mRNA levels of hsp-16.2, hsp-70, lys-7, old-1, and sod-5 by 2.5, 2.9, 1.3, 2.3, and 4.5-fold, respectively, as well as the protein level of lys-7 by 1.5-fold. Lifespan extension confered by DMSO depends on sir-2.1 and daf-16 but not on eat-2 or hsf-1 [20828537]. Worm +23.0 to +24.4
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    • 25 of 79 interventions
    Interventions are an extension of GenAge and GenDR.