Naringin, a Natural Flavonoid, Modulates UVB Radiation-Induced DNA Damage and Photoaging by Modulating NER Repair and MMPS Expression in Mouse Embryonic Fibroblast Cells

Das, Roopa NilamberLal; Balupillai, Agilan; Ernest, David; Santhoshkumar, Murali; Sridevi, M

doi:10.1615/jenvironpatholtoxicoloncol.2020031914

Cited by 8 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Numerous studies have shown that DNA damage plays a crucial role in the mechanism of UV‐induced photoaging. 26 , 27 Firstly, DNA damage triggers mitochondrial dysfunction. 28 Secondly, UV‐induced DNA damage causes functional degeneration and depletion of stem cells.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies have shown that DNA damage plays a crucial role in the mechanism of UV‐induced photoaging 26,27 . Firstly, DNA damage triggers mitochondrial dysfunction 28 .…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence suggests that the DNA-repairing capacity can be enhanced to realize an anti-photoaging effect. 27,33,34 Chen et al revealed that metformin reduced DNA damage and protected cells from UVA-induced photoaging by activating the PI3K/AKT/mTOR pathway. 35 However, there are some shortcomings in this experiment.…”

Section: Con Clus Ionmentioning

confidence: 99%

See 2 more Smart Citations

5‐aminolevulinic acid photodynamic therapy protects against UVB‐induced skin photoaging: A DNA‐repairing mechanism involving the BER signalling pathway

Wang,

Gu,

Shi

et al. 2024

J Cellular Molecular Medi

View full text Add to dashboard Cite

Low‐dose 5‐aminolevulinic acid photodynamic therapy (ALA‐PDT) has been used to cope with skin photoaging, and is thought to involve DNA damage repair responses. However, it is still unknown how low‐dose ALA‐PDT regulates DNA damage repair to curb skin photoaging. We established a photoaging model using human dermal fibroblasts (HDFs) and rat skin. RNA‐sequencing (RNA‐seq) analysis was conducted to identify differentially expressed genes (DEGs) in HDFs before and after low‐dose ALA‐PDT treatment, followed by bioinformatics analysis. Senescence‐associated β‐galactosidase (SA‐β‐gal) staining was employed to assess skin aging‐related manifestations and Western blotting to evaluate the expression of associated proteins. A comet assay was used to detect cellular DNA damage, while immunofluorescence to examine the expression of 8‐hydroxy‐2′‐deoxyguanosine (8‐oxo‐dG) in cells and skin tissues. In both in vivo and in vitro models, low‐dose ALA‐PDT alleviated the manifestations of ultraviolet B (UVB)‐induced skin photoaging. Low‐dose ALA‐PDT significantly reduced DNA damage in photoaged HDFs. Furthermore, low‐dose ALA‐PDT accelerated the clearance of the photoproduct 8‐oxo‐dG in photoaged HDFs and superficial dermis of photoaged rat skin. RNA‐seq analysis suggested that low‐dose ALA‐PDT upregulated the expression of key genes in the base excision repair (BER) pathway. Further functional validation showed that inhibition on BER expression by using UPF1069 significantly suppressed SA‐β‐gal activity, G2/M phase ratio, expression of aging‐associated proteins P16, P21, P53, and MUTYH proteins, as well as clearance of the photoproduct 8‐oxo‐dG in photoaged HDFs. Low‐dose ALA‐PDT exerts anti‐photoaging effects by activating the BER signalling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Numerous studies have shown that DNA damage plays a crucial role in the mechanism of UV‐induced photoaging 26,27 . Firstly, DNA damage triggers mitochondrial dysfunction 28 .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

5‐aminolevulinic acid photodynamic therapy protects against UVB‐induced skin photoaging: A DNA‐repairing mechanism involving the BER signalling pathway

Wang,

Gu,

Shi

et al. 2024

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Manna et al [47] demonstrated that pretreatment with naringin significantly prevented γ-radiation (6Gy)-induced intracellular ROS-mediated oxidative DNA damage; inhibited radiation-induced G 1 /S-phase cell cycle arrest by modulating p53-dependent p21/WAF1, cyclin E, and cyclin dependent kinase 2 (CDK2) activation; and reversed the inflammation through downregulating nuclear factor kappa B (NF-kB) signaling pathways and balancing the expression of C-reactive protein, monocyte chemoattractant protein-1 (MCP-1), and iNOS2 at sites of inflammation in murine splenocytes. Besides, naringin pretreatment could effectively deter UVB-mediated DNA damage, alter apoptotic marker expression (Bax, BCl-2, caspase-9, and caspase-3), and potentially modulate NER gene (XPC, TFIIH, XPE, ERCC1, and GAPDH) expression, thereby augmenting DNA repair [48].…”

Section: Polyphenolic Phytochemicalsmentioning

confidence: 99%

Radioprotectors, Radiomitigators, and Radiosensitizers

Montoro,

Obrador,

Mistry

et al. 2023

Radiobiology Textbook

View full text Add to dashboard Cite

This chapter gives an overview of molecules and mechanisms able to intervene with the biological effects of ionizing radiation (IR), either related to their clinical use in radiotherapy or in the field of radiation protection in case of an accidental exposure to radiation and/or nuclear emergencies. According to the National Cancer Institute, “radiomodifiers” can be classified into (a) radioprotectors (protect molecules and tissues from direct and indirect damage induced by IR) or (b) radiomitigators (reduce and help to repair damage), depending on whether they are administered pre- or post-IR exposure, respectively. Most of them are free radical scavengers and antioxidants (or enhancers of the antioxidant defenses), increase DNA repair mechanisms, have anti-inflammatory properties, and/or prevent cell death. On the other hand, (c) radiosensitizers directly or indirectly enhance DNA damage and ROS production, increasing IR toxicity on tumor cells, thus they are used to increase radiotherapy efficacy in cancer patients. The section “Radionuclides and methods to treat contaminated individuals” describes the medical consequences and treatment modalities of internal contamination by radionuclides. Overall, the chapter discusses the effects of most currently known radiomodifiers, their specific properties, and their mechanisms of action, by emphasizing results obtained in recent preclinical and clinical trials.

show abstract

“…Naringin decreases oxidative UVB radiation damage in NIH-3T3 cells and the associated inflammatory response by modulating PPAR-γ expression. As such, it can effectively prevent UVB-mediated DNA damage, photoaging, and apoptosis[83]. In another in vitro assay, fresh and oven-dried grapefruit peel extracts dis-played strong cytoprotective properties in SH-SY5Y neuroblastoma cell cultures at concentrations ranging from 0.1 -0.25 mg/ml [72].…”

mentioning

confidence: 99%

Vitamin C, Grape Seed Extract and Citrus Bioflavonoids Protect the Skin against Photoaging: A Review

West¹,

Deng²,

Palu³

2020

JBM

View full text Add to dashboard Cite

Naringin, a Natural Flavonoid, Modulates UVB Radiation-Induced DNA Damage and Photoaging by Modulating NER Repair and MMPS Expression in Mouse Embryonic Fibroblast Cells

Cited by 8 publications

References 0 publications

5‐aminolevulinic acid photodynamic therapy protects against UVB‐induced skin photoaging: A DNA‐repairing mechanism involving the BER signalling pathway

5‐aminolevulinic acid photodynamic therapy protects against UVB‐induced skin photoaging: A DNA‐repairing mechanism involving the BER signalling pathway

Radioprotectors, Radiomitigators, and Radiosensitizers

Vitamin C, Grape Seed Extract and Citrus Bioflavonoids Protect the Skin against Photoaging: A Review

Contact Info

Product

Resources

About