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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

MSE and RSV attenuate collagen decline in skin tissues of Sod1−/− mice. (a) Sirius red staining of the back skin of Sod1−/− and Sod1+/+ mice treated with the MSE or RSV. Relative mRNA expression of (b) Sirt1, (c) Col1a1, and (d) p53. Each of the mRNA expressions was determined by qRT-PCR (n = 8–12). 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, ∗∗P < 0.01. The scale bar represents 100 μm.
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fig2: MSE and RSV attenuate collagen decline in skin tissues of Sod1−/− mice. (a) Sirius red staining of the back skin of Sod1−/− and Sod1+/+ mice treated with the MSE or RSV. Relative mRNA expression of (b) Sirt1, (c) Col1a1, and (d) p53. Each of the mRNA expressions was determined by qRT-PCR (n = 8–12). 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, ∗∗P < 0.01. The scale bar represents 100 μm.

Mentions: In a preliminary experiment, MF diets containing 5% or 0.5% MSE were orally administrated to the Sod1+/+ and Sod1−/− mice daily for 12 weeks beginning at 4 weeks of age. The results showed that both MSE diets improved the skin thickness of Sod1−/− mice and there were no adverse effects of skin pathologies of Sod1+/+ mice (data not shown). Therefore, we selected the control diet containing 0.5% MSE to confirm antiatrophic effect on Sod1−/− skin. MSE and RSV were orally administered to the Sod1+/+ and Sod1−/− mice under the same conditions. As shown in Figure 1(a), the skin of Sod1−/− mice was significantly thinner compared to that of Sod1+/+ mice, confirming skin atrophy in Sod1−/− mice. The back skin of Sod1−/− that had been administrated with the MSE diets was significantly thicker compared to that of Sod1−/− mice treated with the control diet (Figures 1(b)–1(d)). RSV diet also improved skin atrophy of Sod1−/− mice compared to Sod1−/− mice treated with the control diet (Figures 1(b)–1(d)). To investigate the adverse effect of MSE and RSV diets, we similarly administered MSE and RSV to the Sod1+/+ mice. No significant difference in skin thickness and morphology was observed in Sod1+/+ mice treated with MSE and RSV (data not shown), indicating that MSE and RSV were safety food factors in skin during short-time treatment. In addition, Sirius red staining revealed that the skin of Sod1−/− mice was decreased in staining intensity compared to that observed in Sod1+/+ mice (Figure 2(a)), confirming dermal collagen decline in Sod1−/− mice. Notably, both MSE and RSV diets increased the Sirius red intensity in Sod1−/− dermis (Figure 2(a)), implying enhancement of collagen level in Sod1−/− skin.


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)

MSE and RSV attenuate collagen decline in skin tissues of Sod1−/− mice. (a) Sirius red staining of the back skin of Sod1−/− and Sod1+/+ mice treated with the MSE or RSV. Relative mRNA expression of (b) Sirt1, (c) Col1a1, and (d) p53. Each of the mRNA expressions was determined by qRT-PCR (n = 8–12). 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, ∗∗P < 0.01. The scale bar represents 100 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4477213&req=5

fig2: MSE and RSV attenuate collagen decline in skin tissues of Sod1−/− mice. (a) Sirius red staining of the back skin of Sod1−/− and Sod1+/+ mice treated with the MSE or RSV. Relative mRNA expression of (b) Sirt1, (c) Col1a1, and (d) p53. Each of the mRNA expressions was determined by qRT-PCR (n = 8–12). 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, ∗∗P < 0.01. The scale bar represents 100 μm.
Mentions: In a preliminary experiment, MF diets containing 5% or 0.5% MSE were orally administrated to the Sod1+/+ and Sod1−/− mice daily for 12 weeks beginning at 4 weeks of age. The results showed that both MSE diets improved the skin thickness of Sod1−/− mice and there were no adverse effects of skin pathologies of Sod1+/+ mice (data not shown). Therefore, we selected the control diet containing 0.5% MSE to confirm antiatrophic effect on Sod1−/− skin. MSE and RSV were orally administered to the Sod1+/+ and Sod1−/− mice under the same conditions. As shown in Figure 1(a), the skin of Sod1−/− mice was significantly thinner compared to that of Sod1+/+ mice, confirming skin atrophy in Sod1−/− mice. The back skin of Sod1−/− that had been administrated with the MSE diets was significantly thicker compared to that of Sod1−/− mice treated with the control diet (Figures 1(b)–1(d)). RSV diet also improved skin atrophy of Sod1−/− mice compared to Sod1−/− mice treated with the control diet (Figures 1(b)–1(d)). To investigate the adverse effect of MSE and RSV diets, we similarly administered MSE and RSV to the Sod1+/+ mice. No significant difference in skin thickness and morphology was observed in Sod1+/+ mice treated with MSE and RSV (data not shown), indicating that MSE and RSV were safety food factors in skin during short-time treatment. In addition, Sirius red staining revealed that the skin of Sod1−/− mice was decreased in staining intensity compared to that observed in Sod1+/+ mice (Figure 2(a)), confirming dermal collagen decline in Sod1−/− mice. Notably, both MSE and RSV diets increased the Sirius red intensity in Sod1−/− dermis (Figure 2(a)), implying enhancement of collagen level in Sod1−/− skin.

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