Hesperidin Exhibits Protective Effects against PM2.5-Mediated Mitochondrial Damage, Cell Cycle Arrest, and Cellular Senescence in Human HaCaT Keratinocytes

Herath, Herath Mudiyanselage Udari Lakmini; Piao, Mei Jing; Kang, Kyoung Ah; Zhen, Ao Xuan; Fernando, Pincha Devage Sameera Madushan; Kang, Hee Kyoung; Yi, Joo Mi; Hyun, Jin‐Won

doi:10.3390/molecules27154800

Cited by 23 publications

(12 citation statements)

References 48 publications

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“…These results indicated that ATX suppressed PM 2.5 -induced ROS generation through the activation of the NRF2-antioxidant enzyme pathways. PM 2.5 -induced oxidative stress causes DNA damage, which leads to cell cycle arrest in skin cells (26). The data of the present study revealed that ATX decreased base modification or breakage of DNA damage in PM 2.5 -treated cells Figure 6.…”

Section: Discussionsupporting

confidence: 49%

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Protective effects of astaxanthin on particulate matter 2.5‑induced senescence in HaCaT keratinocytes via maintenance of redox homeostasis

Zhen,

Kang,

Piao

et al. 2024

Exp Ther Med

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Particulate matter 2.5 (PM 2.5 ) imposes a heavy burden on the skin and respiratory system of human beings, causing side effects such as aging, inflammation and cancer. Astaxanthin (ATX) is a well-known antioxidant widely used for its anti-inflammatory and anti-aging properties. However, few studies have investigated the protective effects of ATX against PM 2.5 -induced senescence in HaCaT cells. In the present study, the levels of reactive oxygen species (ROS) and antioxidant enzymes were measured after treatment with PM 2.5 . The results revealed that PM 2.5 generated excessive ROS and reduced the translocation of nuclear factor erythroid 2-related factor 2 (NRF2), subsequently reducing the expression of antioxidant enzymes. However, pretreatment with ATX reversed the ROS levels as well as the expression of antioxidant enzymes. In addition, ATX protected cells from PM 2.5 -induced DNA damage and rescued PM 2.5 -induced cell cycle arrest. The levels of senescence-associated phenotype markers, such as interleukin-1β, matrix metalloproteinases, and β-galactosidase, were increased by exposure to PM 2.5 , however these effects were reversed by ATX. After interfering with NRF2 mRNA expression and exposing cells to PM 2.5 , the levels of ROS and β-galactosidase were higher compared with siControl RNA cells exposed to PM 2.5 . However, ATX inhibited ROS and β-galactosidase levels in both the siControl RNA and the siNRF2 RNA groups. Thus, ATX protects HaCaT keratinocytes from PM 2.5 -induced senescence by partially inhibiting excessive ROS generation via the NRF2 signaling pathway.

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Section: Discussionsupporting

confidence: 49%

“…3D). A previous study revealed that PM 2.5 induces MMPs via the AP-1 signaling pathway through ROS generation (26). In addition, ROS increase the secretion of pro-inflammatory cytokines to high levels in most senescent cells (28).…”

Section: Discussionmentioning

confidence: 96%

Protective effects of astaxanthin on particulate matter 2.5‑induced senescence in HaCaT keratinocytes via maintenance of redox homeostasis

Zhen,

Kang,

Piao

et al. 2024

Exp Ther Med

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“…4A ). Furthermore, evaluation of phospho-H2A.X, a marker for DNA double-strand breaks ( 25 ), showed that luteolin pretreatment diminished expression levels of phospho-H2A.X in H 2 O 2 -exposed cells ( Fig. 4B ).…”

Section: Resultsmentioning

confidence: 93%

Protective effect of luteolin against oxidative stress‑mediated cell injury via enhancing antioxidant systems

Fernando,

Ko,

Piao

et al. 2024

Mol Med Rep

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Physiological stress such as excessive reactive oxygen species (ROS) production may contribute normal fibroblasts activation into cancer-associated fibroblasts, which serve a crucial role in certain types of cancer such as pancreatic, breast, liver and lung cancer. The present study aimed to examine the cytoprotective effects of luteolin (3′,4′,5,7-tetrahydroxyflavone) against hydrogen peroxide (H 2 O 2 )-generated oxidative stress in lung fibroblasts. To examine the effects of luteolin against H 2 O 2 -induced damages, cell viability, sub-G 1 cell population, nuclear staining with Hoechst 33342, lipid peroxidation and comet assays were performed. To evaluate the effects of luteolin on the protein expression level of apoptosis, western blot assay was performed. To assess the antioxidant effects of luteolin, detection of ROS using H 2 DCFDA staining, O 2 − and ·OH using electron spin resonance spectrometer and antioxidant enzyme activity was performed. In a cell-free chemical system, luteolin scavenges superoxide anion and hydroxyl radical generated by xanthine/xanthine oxidase and the Fenton reaction (FeSO 4 /H 2 O 2 ). Furthermore, Chinese hamster lung fibroblasts (V79-4) treated with H 2 O 2 showed a significant increase in cellular ROS. Intracellular ROS levels and damage to cellular components such as lipids and DNA in H 2 O 2 -treated cells were significantly decreased by luteolin pretreatment. Luteolin increased cell viability, which was impaired following H 2 O 2 treatment and prevented H 2 O 2 -mediated apoptosis. Luteolin suppressed active caspase-9 and caspase-3 levels while increasing Bcl-2 expression and decreasing Bax protein levels. Additionally, luteolin restored levels of glutathione that was reduced in response to H 2 O 2 . Moreover, luteolin enhanced the activity and protein expressions of superoxide dismutase, catalase, glutathione peroxidase, and heme oxygenase-1. Overall, these results indicated that luteolin inhibits H 2 O 2 -mediated cellular damage by upregulating antioxidant enzymes.

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“…Oxidative stress leads to DNA oxidation and mutation, cancer, and senescence [ 29 ]. PM 2.5 -induced oxidative stress causes DNA damage, which leads to cell cycle arrest in skin cells [ 44 ]. In this study, we noted less DNA damage in the 3-BDB and PM 2.5 groups than in the PM 2.5 group ( Figure 3 ).…”

Section: Discussionmentioning

confidence: 99%

3-Bromo-4,5-dihydroxybenzaldehyde Protects Keratinocytes from Particulate Matter 2.5-Induced Damages

Zhen,

Piao,

Kang

et al. 2023

Antioxidants

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Cellular senescence can be activated by several stimuli, including ultraviolet radiation and air pollutants. This study aimed to evaluate the protective effect of marine algae compound 3-bromo-4,5-dihydroxybenzaldehyde (3-BDB) on particulate matter 2.5 (PM2.5)-induced skin cell damage in vitro and in vivo. The human HaCaT keratinocyte was pre-treated with 3-BDB and then with PM2.5. PM2.5-induced reactive oxygen species (ROS) generation, lipid peroxidation, mitochondrial dysfunction, DNA damage, cell cycle arrest, apoptotic protein expression, and cellular senescence were measured using confocal microscopy, flow cytometry, and Western blot. The present study exhibited PM2.5-generated ROS, DNA damage, inflammation, and senescence. However, 3-BDB ameliorated PM2.5-induced ROS generation, mitochondria dysfunction, and DNA damage. Furthermore, 3-BDB reversed the PM2.5-induced cell cycle arrest and apoptosis, reduced cellular inflammation, and mitigated cellular senescence in vitro and in vivo. Moreover, the mitogen-activated protein kinase signaling pathway and activator protein 1 activated by PM2.5 were inhibited by 3-BDB. Thus, 3-BDB suppressed skin damage induced by PM2.5.

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Hesperidin Exhibits Protective Effects against PM2.5-Mediated Mitochondrial Damage, Cell Cycle Arrest, and Cellular Senescence in Human HaCaT Keratinocytes

Cited by 23 publications

References 48 publications

Protective effects of astaxanthin on particulate matter 2.5‑induced senescence in HaCaT keratinocytes via maintenance of redox homeostasis

Protective effects of astaxanthin on particulate matter 2.5‑induced senescence in HaCaT keratinocytes via maintenance of redox homeostasis

Protective effect of luteolin against oxidative stress‑mediated cell injury via enhancing antioxidant systems

3-Bromo-4,5-dihydroxybenzaldehyde Protects Keratinocytes from Particulate Matter 2.5-Induced Damages

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