Background: Oxidative stress induces the production of reactive oxygen species (ROS), which play important causative roles in various pathological conditions. Black ginseng (BG), a type of steam-processed ginseng, has drawn significant attention due to its biological activity, and is more potent tha...
Background: Oxidative stress induces the production of reactive oxygen species (ROS), which play important causative roles in various pathological conditions. Black ginseng (BG), a type of steam-processed ginseng, has drawn significant attention due to its biological activity, and is more potent than white ginseng (WG) or red ginseng (RG). Methods: We evaluated the protective effects of BG extract (BGE) against oxidative stress-induced cellular damage, in comparison with WG extract (WGE) and RG extract (RGE) in a cell culture model. Ethanolic extracts of WG, RG, and BG were used to evaluate ginsenoside profiles, total polyphenols, flavonoid contents, and antioxidant activity. Using AML-12 cells treated with $H_2O_2$, the protective effects of WGE, RGE, and BGE on cellular redox status, DNA, protein, lipid damage, and apoptosis levels were investigated. Results: BGE exhibited significantly enhanced antioxidant potential, as well as total flavonoid and polyphenol contents. ATP levels were significantly higher in BGE-treated cells than in control; ROS generation and glutathione disulfide levels were lower but glutathione (GSH) and NADPH levels were higher in BGE-treated cells than in other groups. Pretreatment with BGE inhibited apoptosis and therefore protected cells from oxidative stress-induced cellular damage, probably through ROS scavenging. Conclusion: Collectively, our results demonstrate that BGE protects AML-12 cells from oxidative stress-induced cellular damages more effectively than WGE or RGE, through ROS scavenging, maintenance of redox status, and activation of the antioxidant defense system.
Background: Oxidative stress induces the production of reactive oxygen species (ROS), which play important causative roles in various pathological conditions. Black ginseng (BG), a type of steam-processed ginseng, has drawn significant attention due to its biological activity, and is more potent than white ginseng (WG) or red ginseng (RG). Methods: We evaluated the protective effects of BG extract (BGE) against oxidative stress-induced cellular damage, in comparison with WG extract (WGE) and RG extract (RGE) in a cell culture model. Ethanolic extracts of WG, RG, and BG were used to evaluate ginsenoside profiles, total polyphenols, flavonoid contents, and antioxidant activity. Using AML-12 cells treated with $H_2O_2$, the protective effects of WGE, RGE, and BGE on cellular redox status, DNA, protein, lipid damage, and apoptosis levels were investigated. Results: BGE exhibited significantly enhanced antioxidant potential, as well as total flavonoid and polyphenol contents. ATP levels were significantly higher in BGE-treated cells than in control; ROS generation and glutathione disulfide levels were lower but glutathione (GSH) and NADPH levels were higher in BGE-treated cells than in other groups. Pretreatment with BGE inhibited apoptosis and therefore protected cells from oxidative stress-induced cellular damage, probably through ROS scavenging. Conclusion: Collectively, our results demonstrate that BGE protects AML-12 cells from oxidative stress-induced cellular damages more effectively than WGE or RGE, through ROS scavenging, maintenance of redox status, and activation of the antioxidant defense system.
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문제 정의
BGE functioned as a ROS scavenger and maintained the oxidative balance in AML-12 cells during oxidative stress, significantly preventing cellular damage and protecting against the apoptosis-induced cell death compared with RGE and WGE. To best of our knowledge, in this study, we report for the first time the modulatory role of BGE in oxidative stress-induced liver cell damage. However, further studies are required using in vivo model to determine the optimal conditions of administration.
가설 설정
(A) Level of lipid peroxidation measured using anti-HNE antibody and counterstained with DAB. (B) Protein carbonyl contents were measured using a DNP-specific antibody. (C) 8-OH-dG levels were analyzed using avidin-conjugated TRITC and fluorescence microscopy, and (D) the fluorescence intensity was quantified using the ImageJ software.
제안 방법
S2 in the supplemental information online). To further investigate whether BGE has a cytoprotective effect against H2O2 , apoptosis was detected using the TUNEL assay. H2O2 induce apoptotic cell death.
There were two main goals of this present study. The first was to determine whether WGE, RGE, and BGE exert comparable antioxidant potential and protection against H2O2-induced cellular damage. The second was to evaluate maintenance of cellular redox status and prevention of cellular damage (lipids, proteins, and DNA) specific to oxidative stress.
대상 데이터
AML-12 cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA). AML-12 cells were cultured according to supplier instructions and were maintained in a humidified incubator with 5% CO2 at 37℃.
데이터처리
Statistically significant differences between groups were determined using one-way analysis of variance using SAS software for Windows release 9.2 (SAS Institute Inc., Cary, NC, USA) on the W32_VSHOME platform. The least-squares means option using a Tukeye-Kramer adjustment was used for the multiple comparisons among the treatment groups.
이론/모형
Cell viability was assessed using an MTT assay as described previously [24]. Terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) staining was conducted according to the instruction manual provided by the manufacturer.
성능/효과
In conclusion, BGE supplementation might be useful for the protection against oxidative stress-induced liver damage by suppression of oxidative stress and maintenance of cellular redox status. BGE may be a potential natural agent for cellular defense in liver cells.
후속연구
To best of our knowledge, in this study, we report for the first time the modulatory role of BGE in oxidative stress-induced liver cell damage. However, further studies are required using in vivo model to determine the optimal conditions of administration.
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