Protective properties of ginsenoside Rb3 against UV-B radiation-induced oxidative stress in HaCaT keratinocytes

Oh, Sun‐Joo; Oh, Yuri; Ryu, In Wang; Kim, Kyunghoon; Lim, Chang‐Jin

doi:10.1080/09168451.2015.1075862

Cited by 36 publications

(23 citation statements)

References 46 publications

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“…Here we report that the ROS contents has been suppressed, and the GSH and SOD activities have been increased by Rb1 in osteoblasts with AlCl3. The similar anti-oxidative effect of Rb1 has been found in UV-B-irradiated HaCaT cells (Oh et al, 2015) and in the H2O2-treated embryonic chick cardiomyocytes (Li et al 2012b). These evidences support our results.…”

Section: Discussionsupporting

confidence: 91%

Ginsenoside Rb1 alleviates aluminum chloride-induced rat osteoblasts dysfunction

Zhu

Zheng

et al. 2016

Toxicology

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Osteoblasts dysfunction, induced by aluminum (Al), plays a critical role in the osteoporosis etiology. Ginsenoside Rb1 (Rb1) has the therapeutic properties for osteoporosis. This study aimed to assess the efficiency of Rb1 in ameliorating Al-induced osteoblasts dysfunction. The osteoblasts were divided into four groups: Rb1-treated group (RG, 0.0145mg/mL Rb1), control group (CG, 0), AlCl-treated group (AG, 0.126mg/mL AlCl·6HO), AlCl+Rb1-treated group (ARG, 0.0145mg/mL Rb1 and 0.126mg/mL AlCl·6HO). After 24h of culture, the osteoblasts viability, the transforming growth factor-β1 (TGF-), bone morphogenetic protein-2 (BMP-2), the insulin-like growth factor I (IGF-I), core-binding factor α1 (Cbfα1) mRNA expressions, glutathione perioxidase (GSH-P and superoxide dismutase (SOD) activities, and reactive oxygen species (ROS) concentration were determined. The osteoblasts ultrastructural features were also observed. In the ARG, the osteoblasts viability, TGF-, BMP-2, IGF-I and Cbfα1 mRNA expressions and the GSH-P and SOD activities were significantly increased, the ROS concentration was significantly decreased, and osteoblasts histology lesion was attenuated compared with the AG. These results demonstrated that Rb1 could significantly reverse osteoblasts viability and osteoblasts growth regulation factor, inhibit oxidative stress, and attenuate histology lesion in the osteoblasts with AlCl. These results indicate that Rb1 can effectively alleviate the AlCl-induced osteoblasts dysfunction.

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Section: Discussionsupporting

confidence: 91%

Ginsenoside Rb1 alleviates aluminum chloride-induced rat osteoblasts dysfunction

Zhu

Zheng

et al. 2016

Toxicology

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“…Ginsenosides are the active molecular components of ginseng2829, and they have been widely used for their anti-aging, anti-cancer, and immunomodulatory functions3031. In addition, ginsenosides hold promise as natural antioxidants that reduce ROS production323334. Moreover, ginsenosides have been shown to up-regulate the GR35, which is responsible for GC sensitivity.…”

mentioning

confidence: 99%

Ginsenoside Rg1 attenuates ultraviolet B-induced glucocortisides resistance in keratinocytes via Nrf2/HDAC2 signalling

Liu

et al. 2016

Sci Rep

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Oxidative stress, which occurs after ultraviolet (UV) radiation, usually results in Glucocorticoid (GC) resistance and the subsequent development of skin inflammation. One approach to protecting the skin against UV radiation is the use of antioxidants. The ginsenoside Rg1 is a novel natural antioxidant isolated from the medicinal plant Panax ginseng C.A. Mey. We demonstrated that UVB exposure exacerbated inflammation and reduced both the level of the glucocorticoid receptor (GR) and the efficacy of dexamethasone (Dex) in human keratinocytes (HaCaT cells). Pretreatment with Rg1 increased the expression of GR and restored Dex responsiveness to inflammation in UVB-irradiated HaCaT cells. Mechanistically, Rg1 rescued UVB-induced HDAC2 degradation. HDAC2 knockdown partially abolished the Rg1-induced up-regulation of GR and the enhancement of GC sensitivity. In addition, Rg1 reduced the production of reactive oxygen species (ROS), which preceded the up-regulation of HDAC2, and consequent sensitization of cells to Dex. Moreover, Rg1 treatment promoted the translocation and activation of Nrf2. Nrf2 knockdown partially abolished the Rg1-induced decrease of ROS production and increase of HDAC2. Rg1 also potentiated the anti-inflammatory effects of Dex in UVB-irradiated mouse skin. In conclusion, we demonstrated that Rg1 attenuated UVB-induced GC insensitivity. Notably, these effects were partially mediated by the Nrf2/HDAC2 pathway.

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“…Ginsenosidase type‐I could hydrolyze Rb3 via the pathway: Rb3→C‐Mx1→C‐Mx→C‐K . Among them, Rb3 can produce the metabolite ginsenoside C‐Mx under the action of an enzymatic reaction, yielding strong anti‐oxidative activity, clearance of free radicals and an antiaging effect based on dermatology research . C‐K as the final metabolite offers an antiphotoaging effect and increases both skin moisture levels and melanin synthesis .…”

Section: Discussionmentioning

confidence: 99%

“…Treatment with 20 lM C-Mx decreased levels of p-ERK, p-JNK and p-38 by 49. 25,45.68, and 52.28%, respectively.…”

Section: C-mx Inhibited Uvb-induced Activation Of the P38/mapk Signalmentioning

confidence: 95%

Ginsenoside C‐Mx Isolated from Notoginseng Stem‐leaf Ginsenosides Attenuates Ultraviolet B‐mediated Photoaging in Human Dermal Fibroblasts

Liu

Hwang

Park

et al. 2018

Photochem & Photobiology

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Notoginseng is a traditional herbal medicine widely used for medicinal therapy in Asia, as it contains numerous ginsenosides with pharmacological effects. In this study, we submitted Notoginseng stem-leaf (NGL) ginsenosides to an enzyme to create a reaction with the monomer products of ginsenoside C-Mx and then investigated the ability of ginsenoside C-Mx to protect the skin against ultraviolet B-induced injury in normal human dermal fibroblasts (NHDFs). Ginsenoside C-Mx alleviated UVB-induced intracellular reactive oxygen species (ROS), MMP-1 and IL-6 expression while accelerating TGF-β and procollagen type I secretion. In addition, ginsenoside C-Mx reversed UVB-induced procollagen type I reduction by regulating the TGF-β/Smad signaling pathway. Moreover, ginsenoside C-Mx inhibited activation of AP-1 transcription factor, an inducer of MMPs. Ginsenoside C-Mx displayed an outstanding antioxidant capacity, increasing expression of cytoprotective antioxidants such as HO-1 and NQO-1 expression by enhancing the nuclear accumulation of Nrf2. Interestingly, application of ginsenoside C-Mx treatment (1, 10, 20 μm) significantly diminished UVB-induced suppressed NF-κB expression, decreasing the over-released inflammatory cytokines. Taken together, our findings indicated that ginsenoside C-Mx may act as a promising natural cosmetic ingredient for prevention and treatment of UVB-induced skin damage.

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Protective properties of ginsenoside Rb3 against UV-B radiation-induced oxidative stress in HaCaT keratinocytes

Cited by 36 publications

References 46 publications

Ginsenoside Rb1 alleviates aluminum chloride-induced rat osteoblasts dysfunction

Ginsenoside Rb1 alleviates aluminum chloride-induced rat osteoblasts dysfunction

Ginsenoside Rg1 attenuates ultraviolet B-induced glucocortisides resistance in keratinocytes via Nrf2/HDAC2 signalling

Ginsenoside C‐Mx Isolated from Notoginseng Stem‐leaf Ginsenosides Attenuates Ultraviolet B‐mediated Photoaging in Human Dermal Fibroblasts

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