Ginsenoside Rg3 attenuates skin disorders via down-regulation of MDM2/HIF1α signaling pathway

As one of the most common primary intraocular carcinomas, retinoblastoma generally stems from the inactivation of the retinoblastoma RB1 gene in retinal cells. Antisense non-coding RNA in the INK4 locus (ANRIL), a long non-coding RNA (lncRNA), has been reported to affect tumorigenesis and progression of various cancers, including gastric cancer and non-small cell lung cancer. However, limited investigations emphasized the role of ANRIL in human retinoblastoma. Hence, the current study was intended to investigate the effects of ANRIL on the proliferation, apoptosis, and invasion of retinoblastoma HXO-RB44 and Y79 cells. The lentivirus-based packaging system was designed to aid the up-regulation of ANRIL and ATM expressions or employed for the down-regulation of ANRIL in human retinoblastoma cells. Afterward, ANRIL expression, mRNA and protein expression of ATM and E2F1, and protein expression of INK4b, INK4a, alternate reading frame (ARF), p53 and retinoblastoma protein (pRB) were determined in order to elucidate the regulation effect associated with ANRIL on the ATM-E2F1 signaling pathway. In addition, cell viability, apoptosis, and invasion were detected accordingly. The results indicated that the down-regulation of ANRIL or up-regulation of ATM led to an increase in the expressions of ATM, E2F1, INK4b, INK4a, ARF, p53, and pRB. The silencing of ANRIL or up-regulation of ATM exerted an inhibitory effect on the proliferation and invasion while improving the apoptosis of HXO-RB44 and Y79 cells. In conclusion, the key observations of our study demonstrated that ANRIL depletion could act to suppress retinoblastoma progression by activating the ATM-E2F1 signaling pathway. These results provide a potentially promising basis for the targetted intervention treatment of human retinoblastoma.

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Ginsenoside Rg3 suppresses mast cell–mediated allergic inflammation via mitogen-activated protein kinase signaling pathway

Journal of Ginseng Research ◽

10.1016/j.jgr.2018.02.008 ◽

2019 ◽

Vol 43 (2) ◽

pp. 282-290 ◽

Cited By ~ 12

Author(s):

Ji-Ye Kee ◽

Seung-Heon Hong

Keyword(s):

Mast Cell ◽

Protein Kinase ◽

Signaling Pathway ◽

Allergic Inflammation ◽

Mitogen Activated Protein Kinase ◽

Kinase Signaling ◽

Ginsenoside Rg3 ◽

Mitogen Activated Protein ◽

Protein Kinase Signaling ◽

Kinase Signaling Pathway

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Transcriptional down-regulation by insulin of the beta 3-adrenergic receptor expression in 3T3-F442A adipocytes: a mechanism for repressing the cAMP signaling pathway.

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.91.12.5677 ◽

1994 ◽

Vol 91 (12) ◽

pp. 5677-5681 ◽

Cited By ~ 46

Author(s):

B. Feve ◽

K. Elhadri ◽

A. Quignard-Boulange ◽

J. Pairault

Keyword(s):

Signaling Pathway ◽

Adrenergic Receptor ◽

Receptor Expression ◽

Camp Signaling ◽

Down Regulation ◽

Camp Signaling Pathway

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A fish oil/pectin diet suppresses radiation‐enhanced colon carcinogenesis via down‐regulation of the β‐catenin signaling pathway

The FASEB Journal ◽

10.1096/fasebj.23.1_supplement.897.6 ◽

2009 ◽

Vol 23 (S1) ◽

Author(s):

Hyemee Kim ◽

Nancy D. Turner ◽

Stella S. Taddeo ◽

Laurie A. Davidson ◽

Naisyin Wang ◽

...

Keyword(s):

Fish Oil ◽

Signaling Pathway ◽

Colon Carcinogenesis ◽

Down Regulation

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Fermentation of Panax notoginseng root extract polysaccharides attenuates oxidative stress and promotes type I procollagen synthesis in human dermal fibroblast cells

BMC Complementary Medicine and Therapies ◽

10.1186/s12906-020-03197-8 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Shiquan You ◽

Xiuqin Shi ◽

Dan Yu ◽

Dan Zhao ◽

Quan An ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Activity ◽

Oxidative Damage ◽

Signaling Pathway ◽

Dermal Fibroblast ◽

Panax Notoginseng ◽

Human Dermal Fibroblast ◽

Down Regulation ◽

Smad Signaling ◽

Smad Signaling Pathway

Abstract Background Panax notoginseng is one of the most valuable traditional Chinese medicines. Polysaccharides in P. notoginseng has been shown to significantly reduce the incidence of human diseases. However the application of fermentation technology in Panax notoginseng is not common, and the mechanism of action of P. notoginseng polysaccharides produced by fermentation is still unclear. The specific biological mechanisms of fermented P. notoginseng polysaccharides (FPNP) suppresses H2O2-induced apoptosis in human dermal fibroblast (HDF) and the underlying mechanism are not well understood. Methods In this study, the effects of water extracted and fermentation on concentration of polysaccharides in P. notoginseng extracts were analyzed. After the H2O2-induced HDF model of oxidative damage was established, and then discussed by the expression of cell markers, including ROS, MDA, SOD, CAT, GSH-Px and MMP-1, COL-I, ELN, which were detected by related ELISA kits. The expression of TGF-β/Smad pathway markers were tested by qRT-PCR to determine whether FPNP exerted antioxidant activity through TGF-β signaling in HDF cells. Results The polysaccharide content of Panax notoginseng increased after Saccharomyces cerevisiae CGMCC 17452 fermentation. In the FPNP treatment group, ROS and MDA contents were decreased, reversed the down-regulation of the antioxidant activity and expression of antioxidant enzyme (CAT, GSH-Px and SOD) induced by H2O2. Furthermore, the up-regulation in expression of TGF-β, Smad2/3 and the down-regulation in the expression of Smad7 in FPNP treated groups revealed that FPNP can inhibit H2O2-induced collagen and elastin injury by activating TGF-β/Smad signaling pathway. Conclusion It was shown that FPNP could inhibit the damage of collagen and elastin induced by H2O2 by activating the TGF-β/Smad signaling pathway, thereby protecting against the oxidative damage induced by hydrogen peroxide. FPNP may be an effective attenuating healing agent that protects the skin from oxidative stress and wrinkles.

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