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Ameliorating Effect of Akebia quinata Fruit Extracts on Skin Aging Induced by Advanced Glycation End Products.

Shin S, Son D, Kim M, Lee S, Roh KB, Ryu D, Lee J, Jung E, Park D - Nutrients (2015)

Bottom Line: We also found that AQFE inhibits glycation reaction between BSA and glucose.AQFE reduced CML expression and stimulated fibrillin-1 expression in comparison to the methyglyoxal treatment.The overall results suggest that AQFE may work as an anti-skin aging agent by preventing oxidative stress and other complications associated with AGEs formation.

View Article: PubMed Central - PubMed

Affiliation: Biospectrum Life Science Institute, Eines Platz 11th FL, 442-13 Sangdaewon Dong, Seoungnam City, Gyunggi Do 462-807, Korea. biost@biospectrum.com.

ABSTRACT
The accumulation of free radicals and advanced glycation end products (AGEs) in the skin plays a very important role in skin aging. Both are known to interact with each other. Therefore, natural compounds or extracts that possess both antioxidant and antiglycation activities might have great antiageing potential. Akebia quinata fruit extract (AQFE) has been used to treat urinary tract inflammatory disease in traditional Korean and Chinese medicines. In the present study, AQFE was demonstrated to possess antioxidant and antiglycation activity. AQFE protects human dermal fibroblasts (HDFs) from oxidative stress and inhibits cellular senescence induced by oxidative stress. We also found that AQFE inhibits glycation reaction between BSA and glucose. The antiglycation activity of AQFE was dose-dependent. In addition, the antiglycation activity of AQFE was confirmed in a human skin explant model. AQFE reduced CML expression and stimulated fibrillin-1 expression in comparison to the methyglyoxal treatment. In addition, the possibility of the extract as an anti-skin aging agent has also been clinically validated. Our analysis of the crow's feet wrinkle showed that there was a decrease in the depth of deep furrows in RI treated with AQFE cream over an eight-week period. The overall results suggest that AQFE may work as an anti-skin aging agent by preventing oxidative stress and other complications associated with AGEs formation.

No MeSH data available.


Related in: MedlinePlus

Effect of AQFE treatment on viability against premature senescence induced by oxidative stress to HDFs. AQFE inhibited (A) rotenone or (B) H2O2-induced cytotoxicity measured with MTT assays. (C) SA-β-gal staining of human dermal fibroblast cells after exposure to rotenone on untreated control, cells treated with rotenone and cells treated with rotenone + AQFE 100 µg/mL. The number of SA-β-gal positive cells per field was calculated using Image J software. Data are mean ± standard deviation. §p < 0.01 compared with the vehicle-treated group; ##p < 0.01 compared with the rotenone or H2O2-treated group (n = 3). (D) SA-β-gal staining of human dermal fibroblast cells after exposure to advanced glycation end products on untreated batch, treated with BSA, treated with AGE-BSA, treated with AGE-BSA + AQFE 20 µg/mL, treated with AGE-BSA + AQFE 50 µg/mL and treated with AGE-BSA + AQFE 100 µg/mL. Data are mean ± standard deviation. §p < 0.01 compared with the vehicle-treated group; #p < 0.05 compared with the MG-treated group (n = 3). The results were confirmed by eight independent experiments.
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nutrients-07-05478-f005: Effect of AQFE treatment on viability against premature senescence induced by oxidative stress to HDFs. AQFE inhibited (A) rotenone or (B) H2O2-induced cytotoxicity measured with MTT assays. (C) SA-β-gal staining of human dermal fibroblast cells after exposure to rotenone on untreated control, cells treated with rotenone and cells treated with rotenone + AQFE 100 µg/mL. The number of SA-β-gal positive cells per field was calculated using Image J software. Data are mean ± standard deviation. §p < 0.01 compared with the vehicle-treated group; ##p < 0.01 compared with the rotenone or H2O2-treated group (n = 3). (D) SA-β-gal staining of human dermal fibroblast cells after exposure to advanced glycation end products on untreated batch, treated with BSA, treated with AGE-BSA, treated with AGE-BSA + AQFE 20 µg/mL, treated with AGE-BSA + AQFE 50 µg/mL and treated with AGE-BSA + AQFE 100 µg/mL. Data are mean ± standard deviation. §p < 0.01 compared with the vehicle-treated group; #p < 0.05 compared with the MG-treated group (n = 3). The results were confirmed by eight independent experiments.

Mentions: Oxidative stress is the main cause of cellular senescence. Rotenone was chosen as a senescence-inducing agent because it acts on mitochondrial complex I, leading to increased levels of intracellular ROS and mimicking the physiological process of ROS induced damage that is hypothesized to underlie the aging process [34,35]. Cellular senescence induced by H2O2 has also been widely used to evaluate the antiaging effects of test materials [36]. H2O2 can induce oxidative stress in cells, which may involve the overproduction and accumulation of oxygen free radicals [37]. Figure 5A,B show the effect of AQFE on cell viability under premature senescence in HDFs following rotenone or H2O2 treatment. HDFs were pretreated with 100 μg/mL AQFE for 2 h and then stimulated with 1 μM rotenone or 250 μM H2O2. Cell viability was analyzed after 72 h. As expected, AQFE pretreatment attenuated both the rotenone and H2O2-induced decrease in cell viability. Rotenone and H2O2-treated cells showed a 29.17% ± 7.47% and 20.71% ± 2.11% reduction in cell viability compared with untreated cells, respectively. However, AQFE pretreated cells showed only 8.95% ± 5.28% and 5.97% ± 4.78% reductions compared with untreated cells, respectively. The present study also assayed for the presence of SA-β-galactosidase activity to investigate whether AQFE affects oxidative stress-induced senescence, which would contribute to its protective effect against ROS-mediated cell damage. Rotenone treatment increased the number of SA-β-galactosidase-positive cells to 76.33% ± 4.51% compared with the control. However, only 43.00% ± 1.73% of the cells pretreated with AQFE were SA-β-galactosidase-positive following treatment with Rotenone (Figure 5C). These data indicated that AQFE has the potential to inhibit cellular senescence by oxidative stress in HDF cells.


Ameliorating Effect of Akebia quinata Fruit Extracts on Skin Aging Induced by Advanced Glycation End Products.

Shin S, Son D, Kim M, Lee S, Roh KB, Ryu D, Lee J, Jung E, Park D - Nutrients (2015)

Effect of AQFE treatment on viability against premature senescence induced by oxidative stress to HDFs. AQFE inhibited (A) rotenone or (B) H2O2-induced cytotoxicity measured with MTT assays. (C) SA-β-gal staining of human dermal fibroblast cells after exposure to rotenone on untreated control, cells treated with rotenone and cells treated with rotenone + AQFE 100 µg/mL. The number of SA-β-gal positive cells per field was calculated using Image J software. Data are mean ± standard deviation. §p < 0.01 compared with the vehicle-treated group; ##p < 0.01 compared with the rotenone or H2O2-treated group (n = 3). (D) SA-β-gal staining of human dermal fibroblast cells after exposure to advanced glycation end products on untreated batch, treated with BSA, treated with AGE-BSA, treated with AGE-BSA + AQFE 20 µg/mL, treated with AGE-BSA + AQFE 50 µg/mL and treated with AGE-BSA + AQFE 100 µg/mL. Data are mean ± standard deviation. §p < 0.01 compared with the vehicle-treated group; #p < 0.05 compared with the MG-treated group (n = 3). The results were confirmed by eight independent experiments.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4663606&req=5

nutrients-07-05478-f005: Effect of AQFE treatment on viability against premature senescence induced by oxidative stress to HDFs. AQFE inhibited (A) rotenone or (B) H2O2-induced cytotoxicity measured with MTT assays. (C) SA-β-gal staining of human dermal fibroblast cells after exposure to rotenone on untreated control, cells treated with rotenone and cells treated with rotenone + AQFE 100 µg/mL. The number of SA-β-gal positive cells per field was calculated using Image J software. Data are mean ± standard deviation. §p < 0.01 compared with the vehicle-treated group; ##p < 0.01 compared with the rotenone or H2O2-treated group (n = 3). (D) SA-β-gal staining of human dermal fibroblast cells after exposure to advanced glycation end products on untreated batch, treated with BSA, treated with AGE-BSA, treated with AGE-BSA + AQFE 20 µg/mL, treated with AGE-BSA + AQFE 50 µg/mL and treated with AGE-BSA + AQFE 100 µg/mL. Data are mean ± standard deviation. §p < 0.01 compared with the vehicle-treated group; #p < 0.05 compared with the MG-treated group (n = 3). The results were confirmed by eight independent experiments.
Mentions: Oxidative stress is the main cause of cellular senescence. Rotenone was chosen as a senescence-inducing agent because it acts on mitochondrial complex I, leading to increased levels of intracellular ROS and mimicking the physiological process of ROS induced damage that is hypothesized to underlie the aging process [34,35]. Cellular senescence induced by H2O2 has also been widely used to evaluate the antiaging effects of test materials [36]. H2O2 can induce oxidative stress in cells, which may involve the overproduction and accumulation of oxygen free radicals [37]. Figure 5A,B show the effect of AQFE on cell viability under premature senescence in HDFs following rotenone or H2O2 treatment. HDFs were pretreated with 100 μg/mL AQFE for 2 h and then stimulated with 1 μM rotenone or 250 μM H2O2. Cell viability was analyzed after 72 h. As expected, AQFE pretreatment attenuated both the rotenone and H2O2-induced decrease in cell viability. Rotenone and H2O2-treated cells showed a 29.17% ± 7.47% and 20.71% ± 2.11% reduction in cell viability compared with untreated cells, respectively. However, AQFE pretreated cells showed only 8.95% ± 5.28% and 5.97% ± 4.78% reductions compared with untreated cells, respectively. The present study also assayed for the presence of SA-β-galactosidase activity to investigate whether AQFE affects oxidative stress-induced senescence, which would contribute to its protective effect against ROS-mediated cell damage. Rotenone treatment increased the number of SA-β-galactosidase-positive cells to 76.33% ± 4.51% compared with the control. However, only 43.00% ± 1.73% of the cells pretreated with AQFE were SA-β-galactosidase-positive following treatment with Rotenone (Figure 5C). These data indicated that AQFE has the potential to inhibit cellular senescence by oxidative stress in HDF cells.

Bottom Line: We also found that AQFE inhibits glycation reaction between BSA and glucose.AQFE reduced CML expression and stimulated fibrillin-1 expression in comparison to the methyglyoxal treatment.The overall results suggest that AQFE may work as an anti-skin aging agent by preventing oxidative stress and other complications associated with AGEs formation.

View Article: PubMed Central - PubMed

Affiliation: Biospectrum Life Science Institute, Eines Platz 11th FL, 442-13 Sangdaewon Dong, Seoungnam City, Gyunggi Do 462-807, Korea. biost@biospectrum.com.

ABSTRACT
The accumulation of free radicals and advanced glycation end products (AGEs) in the skin plays a very important role in skin aging. Both are known to interact with each other. Therefore, natural compounds or extracts that possess both antioxidant and antiglycation activities might have great antiageing potential. Akebia quinata fruit extract (AQFE) has been used to treat urinary tract inflammatory disease in traditional Korean and Chinese medicines. In the present study, AQFE was demonstrated to possess antioxidant and antiglycation activity. AQFE protects human dermal fibroblasts (HDFs) from oxidative stress and inhibits cellular senescence induced by oxidative stress. We also found that AQFE inhibits glycation reaction between BSA and glucose. The antiglycation activity of AQFE was dose-dependent. In addition, the antiglycation activity of AQFE was confirmed in a human skin explant model. AQFE reduced CML expression and stimulated fibrillin-1 expression in comparison to the methyglyoxal treatment. In addition, the possibility of the extract as an anti-skin aging agent has also been clinically validated. Our analysis of the crow's feet wrinkle showed that there was a decrease in the depth of deep furrows in RI treated with AQFE cream over an eight-week period. The overall results suggest that AQFE may work as an anti-skin aging agent by preventing oxidative stress and other complications associated with AGEs formation.

No MeSH data available.


Related in: MedlinePlus