Limits...
Catalpol Modulates Lifespan via DAF-16/FOXO and SKN-1/Nrf2 Activation in Caenorhabditis elegans.

Seo HW, Cheon SM, Lee MH, Kim HJ, Jeon H, Cha DS - Evid Based Complement Alternat Med (2015)

Bottom Line: We also found that elevated antioxidant enzyme activities and expressions of stress resistance proteins were attributed to catalpol-mediated increased stress tolerance of nematode.Moreover, locomotory ability of aged nematode was significantly improved by catalpol treatment, while lipofuscin levels were attenuated, suggesting that catalpol may affect age-associated changes of nematode.These results indicate that catalpol extends lifespan and increases stress tolerance of C. elegans via DAF-16/FOXO and SKN-1/Nrf activation dependent on insulin/IGF signaling and JNK signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Oriental Pharmacy, College of Pharmacy, Woosuk University, Jeonbuk 565-701, Republic of Korea.

ABSTRACT
Catalpol is an effective component of rehmannia root and known to possess various pharmacological properties. The present study was aimed at investigating the potential effects of catalpol on the lifespan and stress tolerance using C. elegans model system. Herein, catalpol showed potent lifespan extension of wild-type nematode under normal culture condition. In addition, survival rate of catalpol-fed nematodes was significantly elevated compared to untreated control under heat and oxidative stress but not under hyperosmolality conditions. We also found that elevated antioxidant enzyme activities and expressions of stress resistance proteins were attributed to catalpol-mediated increased stress tolerance of nematode. We further investigated whether catalpol's longevity effect is related to aging-related factors including reproduction, food intake, and growth. Interestingly, catalpol exposure could attenuate pharyngeal pumping rate, indicating that catalpol may induce dietary restriction of nematode. Moreover, locomotory ability of aged nematode was significantly improved by catalpol treatment, while lipofuscin levels were attenuated, suggesting that catalpol may affect age-associated changes of nematode. Our mechanistic studies revealed that mek-1, daf-2, age-1, daf-16, and skn-1 are involved in catalpol-mediated longevity. These results indicate that catalpol extends lifespan and increases stress tolerance of C. elegans via DAF-16/FOXO and SKN-1/Nrf activation dependent on insulin/IGF signaling and JNK signaling.

No MeSH data available.


Related in: MedlinePlus

Effects of catalpol on the nuclear localization of DAF-16. The translocation of DAF-16 was visualized under fluorescence microscope using TJ356 strain which carries daf-16::gfp transgene. To induce heat-shock, worms were incubated at 36°C for 2 h. Worms were subjected to analyze GFP expression on the 4th day of adulthood.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4363898&req=5

fig7: Effects of catalpol on the nuclear localization of DAF-16. The translocation of DAF-16 was visualized under fluorescence microscope using TJ356 strain which carries daf-16::gfp transgene. To induce heat-shock, worms were incubated at 36°C for 2 h. Worms were subjected to analyze GFP expression on the 4th day of adulthood.

Mentions: The underlying mechanism of catalpol-mediated longevity was dissected using loss of function mutant worms relevant to aging [22]. We found that the mean lifespan of sir-2.1 mutants was significantly enhanced by catalpol exposure, indicating that SIR-2.1 is not responsible for catalpol's activity (Table 1). However, catalpol failed to increase the lifespan of mutants including mek-1, daf-2, age-1, daf-16, and skn-1. Thus, we estimated that these genes are involved in catalpol-induced lifespan regulation (Table 1). We double checked the involvement of daf-16 using TJ356 strain which carries daf-16::gfp transgene. As can be seen in Figure 7, heat shock triggers DAF-16 nuclear localization and catalpol-fed worms also exhibited similar phenotype, suggesting that catalpol activates the transcriptional activity of DAF-16.


Catalpol Modulates Lifespan via DAF-16/FOXO and SKN-1/Nrf2 Activation in Caenorhabditis elegans.

Seo HW, Cheon SM, Lee MH, Kim HJ, Jeon H, Cha DS - Evid Based Complement Alternat Med (2015)

Effects of catalpol on the nuclear localization of DAF-16. The translocation of DAF-16 was visualized under fluorescence microscope using TJ356 strain which carries daf-16::gfp transgene. To induce heat-shock, worms were incubated at 36°C for 2 h. Worms were subjected to analyze GFP expression on the 4th day of adulthood.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4363898&req=5

fig7: Effects of catalpol on the nuclear localization of DAF-16. The translocation of DAF-16 was visualized under fluorescence microscope using TJ356 strain which carries daf-16::gfp transgene. To induce heat-shock, worms were incubated at 36°C for 2 h. Worms were subjected to analyze GFP expression on the 4th day of adulthood.
Mentions: The underlying mechanism of catalpol-mediated longevity was dissected using loss of function mutant worms relevant to aging [22]. We found that the mean lifespan of sir-2.1 mutants was significantly enhanced by catalpol exposure, indicating that SIR-2.1 is not responsible for catalpol's activity (Table 1). However, catalpol failed to increase the lifespan of mutants including mek-1, daf-2, age-1, daf-16, and skn-1. Thus, we estimated that these genes are involved in catalpol-induced lifespan regulation (Table 1). We double checked the involvement of daf-16 using TJ356 strain which carries daf-16::gfp transgene. As can be seen in Figure 7, heat shock triggers DAF-16 nuclear localization and catalpol-fed worms also exhibited similar phenotype, suggesting that catalpol activates the transcriptional activity of DAF-16.

Bottom Line: We also found that elevated antioxidant enzyme activities and expressions of stress resistance proteins were attributed to catalpol-mediated increased stress tolerance of nematode.Moreover, locomotory ability of aged nematode was significantly improved by catalpol treatment, while lipofuscin levels were attenuated, suggesting that catalpol may affect age-associated changes of nematode.These results indicate that catalpol extends lifespan and increases stress tolerance of C. elegans via DAF-16/FOXO and SKN-1/Nrf activation dependent on insulin/IGF signaling and JNK signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Oriental Pharmacy, College of Pharmacy, Woosuk University, Jeonbuk 565-701, Republic of Korea.

ABSTRACT
Catalpol is an effective component of rehmannia root and known to possess various pharmacological properties. The present study was aimed at investigating the potential effects of catalpol on the lifespan and stress tolerance using C. elegans model system. Herein, catalpol showed potent lifespan extension of wild-type nematode under normal culture condition. In addition, survival rate of catalpol-fed nematodes was significantly elevated compared to untreated control under heat and oxidative stress but not under hyperosmolality conditions. We also found that elevated antioxidant enzyme activities and expressions of stress resistance proteins were attributed to catalpol-mediated increased stress tolerance of nematode. We further investigated whether catalpol's longevity effect is related to aging-related factors including reproduction, food intake, and growth. Interestingly, catalpol exposure could attenuate pharyngeal pumping rate, indicating that catalpol may induce dietary restriction of nematode. Moreover, locomotory ability of aged nematode was significantly improved by catalpol treatment, while lipofuscin levels were attenuated, suggesting that catalpol may affect age-associated changes of nematode. Our mechanistic studies revealed that mek-1, daf-2, age-1, daf-16, and skn-1 are involved in catalpol-mediated longevity. These results indicate that catalpol extends lifespan and increases stress tolerance of C. elegans via DAF-16/FOXO and SKN-1/Nrf activation dependent on insulin/IGF signaling and JNK signaling.

No MeSH data available.


Related in: MedlinePlus