Limits...
Resveratrol Derivative-Rich Melinjo Seed Extract Attenuates Skin Atrophy in Sod1-Deficient Mice.

Watanabe K, Shibuya S, Ozawa Y, Izuo N, Shimizu T - Oxid Med Cell Longev (2015)

Bottom Line: Since the loss of cytoplasmic SOD (SOD1) resulted in aging-like phenotypes in several types of murine tissue, SOD1 is essential for the maintenance of tissue homeostasis.MSE intake also exerts no adverse events in human study.In vitro experiments revealed that RSV significantly promoted the viability of Sod1 (-/-) fibroblasts.

View Article: PubMed Central - PubMed

Affiliation: Department of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.

ABSTRACT
The oxidative damages induced by a redox imbalance cause age-related changes in cells and tissues. Superoxide dismutase (SOD) enzymes play a pivotal role in the antioxidant system and they also catalyze superoxide radicals. Since the loss of cytoplasmic SOD (SOD1) resulted in aging-like phenotypes in several types of murine tissue, SOD1 is essential for the maintenance of tissue homeostasis. Melinjo (Gnetum gnemon Linn) seed extract (MSE) contains trans-resveratrol (RSV) and resveratrol derivatives, including gnetin C, gnemonoside A, and gnemonoside D. MSE intake also exerts no adverse events in human study. In the present studies, we investigated protective effects of MSE on age-related skin pathologies in mice. Orally MSE and RSV treatment reversed the skin thinning associated with increased oxidative damage in the Sod1 (-/-) mice. Furthermore, MSE and RSV normalized gene expression of Col1a1 and p53 and upregulated gene expression of Sirt1 in skin tissues. In vitro experiments revealed that RSV significantly promoted the viability of Sod1 (-/-) fibroblasts. These finding demonstrated that RSV in MSE stably suppressed an intrinsic superoxide generation in vivo and in vitro leading to protecting skin damages. RSV derivative-rich MSE may be a powerful food of treatment for age-related skin diseases caused by oxidative damages.

No MeSH data available.


Related in: MedlinePlus

RSV promotes fibroblasts outgrowth from Sod1−/− skin. (a and b) Number of outgrowth fibroblasts of Sod1+/+ and Sod1−/− mice in the skin disc culture treated with 10 μM RSV for 72 h (n = 8). Fibroblast number was counted on day 3. The statistical evaluations were performed using the two-tailed Student's t-test for unpaired values. These data indicate the mean ± SD; ∗P < 0.05. The scale bar represents 100 μM.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4477213&req=5

fig4: RSV promotes fibroblasts outgrowth from Sod1−/− skin. (a and b) Number of outgrowth fibroblasts of Sod1+/+ and Sod1−/− mice in the skin disc culture treated with 10 μM RSV for 72 h (n = 8). Fibroblast number was counted on day 3. The statistical evaluations were performed using the two-tailed Student's t-test for unpaired values. These data indicate the mean ± SD; ∗P < 0.05. The scale bar represents 100 μM.

Mentions: We investigated whether the RSV treatment attenuated intracellular ROS production and promoted the proliferation of Sod1−/− fibroblasts in vitro. Preliminary experiments revealed that RSV treatment for 24 h with various concentrations of 30 to 100 μM slightly suppressed cell viability of Sod1+/+ fibroblasts. In contrast, 10 μM RSV treatment for 72 h showed no adverse effect of cell viability in Sod1+/+ fibroblasts. Therefore, we determined dose and duration of the RSV experiment in vitro. Flow cytometer analysis indicated that RSV treatment significantly decreased intracellular ROS generation in Sod1−/− fibroblasts (Figure 3(c)). Moreover, the organ culture experiments using skin discs revealed that the Sod1−/− fibroblasts showed marked suppression of their outgrowth capacity compared to that observed in the Sod1+/+ mice (Figure 4(a)). Treatment with 10 μM RSV significantly enhanced the fibroblasts outgrowth activity from the Sod1−/− skin discs (Figure 4(b)). These findings collectively suggested that the RSV promoted the migration and proliferation of Sod1−/− fibroblasts in vitro.


Resveratrol Derivative-Rich Melinjo Seed Extract Attenuates Skin Atrophy in Sod1-Deficient Mice.

Watanabe K, Shibuya S, Ozawa Y, Izuo N, Shimizu T - Oxid Med Cell Longev (2015)

RSV promotes fibroblasts outgrowth from Sod1−/− skin. (a and b) Number of outgrowth fibroblasts of Sod1+/+ and Sod1−/− mice in the skin disc culture treated with 10 μM RSV for 72 h (n = 8). Fibroblast number was counted on day 3. The statistical evaluations were performed using the two-tailed Student's t-test for unpaired values. These data indicate the mean ± SD; ∗P < 0.05. The scale bar represents 100 μM.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4477213&req=5

fig4: RSV promotes fibroblasts outgrowth from Sod1−/− skin. (a and b) Number of outgrowth fibroblasts of Sod1+/+ and Sod1−/− mice in the skin disc culture treated with 10 μM RSV for 72 h (n = 8). Fibroblast number was counted on day 3. The statistical evaluations were performed using the two-tailed Student's t-test for unpaired values. These data indicate the mean ± SD; ∗P < 0.05. The scale bar represents 100 μM.
Mentions: We investigated whether the RSV treatment attenuated intracellular ROS production and promoted the proliferation of Sod1−/− fibroblasts in vitro. Preliminary experiments revealed that RSV treatment for 24 h with various concentrations of 30 to 100 μM slightly suppressed cell viability of Sod1+/+ fibroblasts. In contrast, 10 μM RSV treatment for 72 h showed no adverse effect of cell viability in Sod1+/+ fibroblasts. Therefore, we determined dose and duration of the RSV experiment in vitro. Flow cytometer analysis indicated that RSV treatment significantly decreased intracellular ROS generation in Sod1−/− fibroblasts (Figure 3(c)). Moreover, the organ culture experiments using skin discs revealed that the Sod1−/− fibroblasts showed marked suppression of their outgrowth capacity compared to that observed in the Sod1+/+ mice (Figure 4(a)). Treatment with 10 μM RSV significantly enhanced the fibroblasts outgrowth activity from the Sod1−/− skin discs (Figure 4(b)). These findings collectively suggested that the RSV promoted the migration and proliferation of Sod1−/− fibroblasts in vitro.

Bottom Line: Since the loss of cytoplasmic SOD (SOD1) resulted in aging-like phenotypes in several types of murine tissue, SOD1 is essential for the maintenance of tissue homeostasis.MSE intake also exerts no adverse events in human study.In vitro experiments revealed that RSV significantly promoted the viability of Sod1 (-/-) fibroblasts.

View Article: PubMed Central - PubMed

Affiliation: Department of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.

ABSTRACT
The oxidative damages induced by a redox imbalance cause age-related changes in cells and tissues. Superoxide dismutase (SOD) enzymes play a pivotal role in the antioxidant system and they also catalyze superoxide radicals. Since the loss of cytoplasmic SOD (SOD1) resulted in aging-like phenotypes in several types of murine tissue, SOD1 is essential for the maintenance of tissue homeostasis. Melinjo (Gnetum gnemon Linn) seed extract (MSE) contains trans-resveratrol (RSV) and resveratrol derivatives, including gnetin C, gnemonoside A, and gnemonoside D. MSE intake also exerts no adverse events in human study. In the present studies, we investigated protective effects of MSE on age-related skin pathologies in mice. Orally MSE and RSV treatment reversed the skin thinning associated with increased oxidative damage in the Sod1 (-/-) mice. Furthermore, MSE and RSV normalized gene expression of Col1a1 and p53 and upregulated gene expression of Sirt1 in skin tissues. In vitro experiments revealed that RSV significantly promoted the viability of Sod1 (-/-) fibroblasts. These finding demonstrated that RSV in MSE stably suppressed an intrinsic superoxide generation in vivo and in vitro leading to protecting skin damages. RSV derivative-rich MSE may be a powerful food of treatment for age-related skin diseases caused by oxidative damages.

No MeSH data available.


Related in: MedlinePlus