Malvidin and cyanidin derivatives from açai fruit ( Euterpe oleracea Mart. ) counteract UV-A-induced oxidative stress in immortalized fibroblasts

Petruk, Ganna; Illiano, Anna; Giudice, Rita Del; Raiola, Assunta; Amoresano, Angela; Rigano, Maria Manuela; Piccoli, Renata; Monti, Daria Maria

doi:10.1016/j.jphotobiol.2017.05.013

Cited by 42 publications

(32 citation statements)

References 54 publications

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“…By removing the initially damaged mitochondria, aggregated proteins, and ROS, autophagy can provide an effective antioxidant strategy independent of the initiating mechanism. Excessive formation of ROS enhances lipid peroxidation, which results in a decrease in enzymatic and nonenzymatic antioxidants [49]. Our results confirmed that RAPA reduced ROS accumulation by restoring the activity of antioxidants, such as SOD, GPx, and CAT, after UVB irradiation.…”

Section: Discussionsupporting

confidence: 81%

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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Section: Discussionsupporting

confidence: 81%

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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“…The body has a natural defense against free radicals such as enzymatic antioxidants including superoxide dismutase and catalase as well as non-enzymatic antioxidants such as glutathione, vitamin C and E. Natural phytochemicals, among them polyphenols and carotenoids, also play important roles in ROS scavenging due to their ability to act as hydrogen donors, and reducing agents. Hence, nutraceuticals with antioxidant properties have received considerable interest because of their potential to modulate oxidative stress and ROS related health conditions [ 4 , 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Senna singueana: Antioxidant, Hepatoprotective, Antiapoptotic Properties and Phytochemical Profiling of a Methanol Bark Extract

et al. 2017

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Natural products are considered as an important source for the discovery of new drugs to treat aging-related degenerative diseases and liver injury. The present study profiled the chemical constituents of a methanol extract from Senna singueana bark using HPLC-PDA-ESI-MS/MS and 36 secondary metabolites were identified. Proanthocyanidins dominated the extract. Monomers, dimers, trimers of (epi)catechin, (epi)gallocatechin, (epi)guibourtinidol, (ent)cassiaflavan, and (epi)afzelechin represented the major constituents. The extract demonstrated notable antioxidant activities in vitro: In DPPH (EC50 of 20.8 µg/mL), FRAP (18.16 mM FeSO4/mg extract) assays, and total phenolic content amounted 474 mg gallic acid equivalent (GAE)/g extract determined with the Folin-Ciocalteu method. Also, in an in vivo model, the extract increased the survival rate of Caenorhabditis elegans worms pretreated with the pro-oxidant juglone from 43 to 64%, decreased intracellular ROS inside the wild-type nematodes by 47.90%, and induced nuclear translocation of the transcription factor DAF-16 in the transgenic strain TJ356. Additionally, the extract showed a remarkable hepatoprotective activity against d-galactosamine (d-GalN) induced hepatic injury in rats. It significantly reduced elevated AST (aspartate aminotransferase), and total bilirubin. Moreover, the extract induced a strong cytoplasmic Bcl-2 expression indicating suppression of apoptosis. In conclusion, the bark extract of S. sengueana represents an interesting candidate for further research in antioxidants and liver protection.

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“…Energy calculations of UVA exposure show that the amount of UVA radiation in Paris is less than that observed in Asian cities, such as Beijing, Tokyo, and Seoul, on any given day . UVA can penetrate the skin to the dermis, and because fibroblasts are the primary component of the dermal cortex, we used primary human dermal fibroblasts (HDFs) in this investigation. In our previous study, we showed that UVA radiation can cause apoptosis in primary HDFs by increasing the formation of reactive oxygen species (ROS) .…”

Section: Introductionmentioning

confidence: 99%

Cyanidin‐3‐o‐glucoside inhibits UVA‐induced human dermal fibroblast injury by upregulating autophagy

Bai

et al. 2019

Photoderm Photoimm Photomed

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Background/Purpose Ultraviolet (UV) A (315‐400 nm) is the UV light that most frequently reaches the Earth's surface and can penetrate the epidermis through to the dermis, causing various issues, including skin aging and skin cancer. The results of our previous studies have shown that the flavonoid monomer cyanidin‐3‐o‐glucoside (C3G) can effectively inhibit primary human dermal fibroblast (HDF) oxidative damage and apoptosis caused by UVA radiation. Many flavonoids can regulate the level of autophagy. However, whether C3G inhibits UVA‐induced oxidative damage to primary HDFs by regulating autophagy levels remains unclear. Methods and Results In this study, we used different doses (0‐12 J/cm2) of UVA to irradiate cells and showed that the expression levels of autophagy‐related gene 5 (Atg5) and microtubule‐associated protein 1 light chain 3 (LC3)‐II in primary HDFs first increased and then decreased. The expression of Atg5 and LC3‐II was significantly decreased under 12 J/cm2 (light‐damage model). C3G increased the levels of Atg5 and LC3‐II. Primary HDFs were pretreated with C3G, followed by treatment with the autophagy inhibitor 3‐methyladenine (3‐MA) after 12 J/cm2 UVA irradiation. The inhibitory effects of C3G on morphological changes, oxidative damage, and apoptosis in primary HDFs induced by UVA were significantly decreased. Conclusion C3G can inhibit UVA‐induced damage to primary HDFs by inducing autophagy. These results provide a theoretical basis for the application of natural compounds to resist light damage to the skin in the future.

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Malvidin and cyanidin derivatives from açai fruit ( Euterpe oleracea Mart. ) counteract UV-A-induced oxidative stress in immortalized fibroblasts

Cited by 42 publications

References 54 publications

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

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

Senna singueana: Antioxidant, Hepatoprotective, Antiapoptotic Properties and Phytochemical Profiling of a Methanol Bark Extract

Cyanidin‐3‐o‐glucoside inhibits UVA‐induced human dermal fibroblast injury by upregulating autophagy

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