7-Hydroxycoumarin prevents UVB-induced activation of NF-κB and subsequent overexpression of matrix metalloproteinases and inflammatory markers in human dermal fibroblast cells

Karthikeyan, R.; Kanimozhi, G.; Prasad, Nagarajan Rajendra; Balupillai, Agilan; Muthusamy, Ganesan; Shanmugam, Mohana; Gunaseelan, Srithar

doi:10.1016/j.jphotobiol.2016.04.027

Cited by 53 publications

(45 citation statements)

References 46 publications

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“…The observed result suggests that AY may act as a photoprotecting compound by diminishing the effects of UVB by maintaining the cellular antioxidant enzyme levels. The increased expression levels of SOD, catalase, GPx and reduced expression levels of LPO observed in the current study correlates well with the reports of Baek et al 21 and Karthikeyan et al 5 Baek et al 21 Cells pre-exposed with AY and then UVB exposed showed antioxidant enzymes level similar to that of control which infers that AY retained the level of antioxidants decreased upon UVB exposure. NAC was used as positive control.…”

Section: Antioxidant Enzyme Profile and The Protective Role Of Aysupporting

confidence: 92%

Asperyellone prevents HDF cells from UVB irradiation damages: An elaborated study

Santhakumaran

Shanuja

Narayanaswamy

et al. 2018

J of Cellular Biochemistry

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The current study explores the photo‐protective effect of asperyellone (AY) (a fungal secondary metabolite), assessed under in vitro condition using human dermal fibroblast cell line. AY was isolated from Aspergillus sp. during the resting phase and purified. The initial cytocompatibility assessment on concentrations of AY and the duration of exposure of UVB irradiations were studied respectively. N‐acetyl‐L‐cysteine (NAC) was used as positive control. Cells were then pretreated with optimized concentration of AY (2.0 μM) and NAC (1 mM) for 1 hour and then UVB irradiated (30 mJ/cm 2) for the period of 10 minutes. Results revealed that reactive oxygen species generated upon UVB irradiation found scavenged by the AY pretreatment at a significant level. Furthermore, an appreciable reduction in apoptotic cell count and DNA damages support the scavenging effect of AY. Assessments on the expression of enzymatic and nonenzymatic antioxidants evidently prove the protective role of AY. The reduced expression levels of inflammatory markers (TNF‐α and COX‐2), collagen degraders (MMP 2 and MMP 9), apoptotic protein expressions (Bax and Bcl‐2), and cell‐cycle arrest analyses substantiate the photo‐protective effect of AY similar to NAC (positive control). Thus, the observations made in the current study indicate the possible role of AY as a photo‐protective agent.

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Section: Antioxidant Enzyme Profile and The Protective Role Of Aysupporting

confidence: 92%

Asperyellone prevents HDF cells from UVB irradiation damages: An elaborated study

Santhakumaran

Shanuja

Narayanaswamy

et al. 2018

J of Cellular Biochemistry

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“…Enhanced ROS levels induce the production of matrix metalloproteinases (MMPs), which can degrade extracellular matrix components and inhibit collagen synthesis, causing skin relaxation, wrinkles, and erythema [9]. Additionally, excessive ROS levels can disrupt the balance of the oxidation/antioxidant system, resulting in the dysregulated secretion of antioxidants, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) [10-13]. Given the important role of ROS, reducing ROS accumulation is a future approach for skin photoprotection.…”

Section: Introductionmentioning

confidence: 99%

Rapamycin Protects Skin Fibroblasts from Ultraviolet B-Induced Photoaging by Suppressing the Production of Reactive Oxygen Species

Qin

Ren

Jia

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ultraviolet B (UVB) irradiation alters multiple molecular pathways in the skin, thereby inducing skin photoaging. Murine dermal fibroblasts (MDFs) were subjected to a series of 4 sub-cytotoxic UVB doses (120 mJ/cm²), resulting in changes in cell shape, DNA damage, cell cycle arrest, extracellular matrix variations, reactive oxygen species (ROS) generation, and alterations in major intracellular antioxidant and cellular autophagy levels. Rapamycin (RAPA) is a new macrolide immunosuppressive agent that is primarily used in oncology, cardiology, and transplantation medicine and has been found to extend the lifespan of genetically heterogeneous mice. Several studies have shown that RAPA may have anti-aging effects in cells and organisms. Thus, in this study, we explored the effects and mechanisms of RAPA against the photoaging process using a well-established cellular photoaging model. Methods: We developed a stress-induced premature senescence (SIPS) model through repeated exposure of MDFs to ultraviolet B (UVB) irradiation. The cells were cultured in the absence or presence of RAPA for 48 h. Senescent phenotypes were assessed by examining cell viability, cell morphology, senescence-associated β-galactosidase (SA-β-gal) expression, cell cycle progression, intracellular ROS production, matrix metalloproteinase (MMP) synthesis and degradation, extracellular matrix (ECM) component protein expression, alterations in major intracellular antioxidant levels, and the cellular autophagy level. Results: Compared with the UVB group, pretreatment with RAPA (5 µM) significantly decreased the staining intensity and percentage of SA-β-gal-positive cells and preserved the elongated cell shape. Moreover, cells pretreated with RAPA showed inhibition of the reduction in the type I collagen content by blocking the UVB-induced upregulation of MMP expression. RAPA also decreased photoaging cell cycle arrest and downregulated p53 and p21 expression. RAPA application significantly attenuated irradiation-induced ROS release by modulating intracellular antioxidants and increasing the autophagy level. Conclusions: Our study demonstrated that RAPA elicited oxidative damage in vitro by reducing ROS accumulation in photoaged fibroblasts. The anti-aging effect can be attributed to the maintenance of normal antioxidant and cellular autophagy levels. However, determination of the definitive mechanism requires further study.

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“…It is proposed that the use of antioxidant derivatives may prevent premature skin ageing and other skin adverse effects [17]. Several natural antioxidants exhibit beneficial effects against UVB radiation induced cellular and molecular changes [12,18]. Melatonin, a natural defense system, present in the skin possesses anti-apoptotic and anti-carcinogenic effects by protecting nuclear and/or mitochondrial DNA from UVB-induced oxidative damage or acting as electrons donor(s) to selected proteins [19–20].…”

Section: Introductionmentioning

confidence: 99%

Linalool prevents oxidative stress activated protein kinases in single UVB-exposed human skin cells

et al. 2017

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Ultraviolet-B radiation (285–320 nm) elicits a number of cellular signaling elements. We investigated the preventive effect of linalool, a natural monoterpene, against UVB-induced oxidative imbalance, activation of mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling in HDFa cells. We observed that linalool treatment (30 μM) prevented acute UVB-irradiation (20 mJ/cm2) mediated loss of activities of antioxidant enzymes in HDFa cells. The comet assay results illustrate that linalool significantly prevents UVB-mediated 8-deoxy guanosine formation (oxidative DNA damage) rather than UVB-induced cyclobutane pyrimidine (CPD) formation. This might be due to its ability to prevent UVB-induced ROS formation and to restore the oxidative imbalance of cells. This has been reflected in UVB-induced overexpression of MAPK and NF-κB signaling. We observed that linalool inhibited UVB-induced phosphorylation of ERK1, JNK and p38 proteins of MAPK family. Linalool inhibited UVB-induced activation of NF-κB/p65 by activating IκBa. We further observed that UVB-induced expression of TNF-α, IL6, IL-10, MMP-2 and MMP-9 was modulated by linalool treatment in HDFa cells. Thus, linalool protects the human skin cells from the oxidative damages of UVB radiation and modulates MAPK and NF-κB signaling in HDFa cells. The present findings substantiate that linalool may act as a photoprotective agent against UVB-induced skin damages.

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7-Hydroxycoumarin prevents UVB-induced activation of NF-κB and subsequent overexpression of matrix metalloproteinases and inflammatory markers in human dermal fibroblast cells

Cited by 53 publications

References 46 publications

Asperyellone prevents HDF cells from UVB irradiation damages: An elaborated study

Asperyellone prevents HDF cells from UVB irradiation damages: An elaborated study

Rapamycin Protects Skin Fibroblasts from Ultraviolet B-Induced Photoaging by Suppressing the Production of Reactive Oxygen Species

Linalool prevents oxidative stress activated protein kinases in single UVB-exposed human skin cells

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