Epigenetic Regulation of Nuclear Factor Erythroid-2-Related Factor 2 in Colorectal Cancer Cells Resistant to Ionizing Radiation.

γ-Radiation resistance is a major obstacle to the success of radiotherapy in colorectal cancer. Antioxidant-related factors contribute to resistance to radiation therapy and, therefore, are targets for improving the therapeutic response. In this study, we evaluated the molecular mechanisms underlying γ-radiation resistance using the colorectal cancer cell line SNUC5 and γ-radiation-resistant variant SNUC5/RR, including analyses of the role of nuclear factor erythroid 2-related factor 2 (NRF2), a transcription factor that regulates antioxidant enzymes, and related epigenetic regulators.

C-Peptide Ameliorates Particulate Matter 2.5-Induced Skin Cell Apoptosis by Inhibiting NADPH Oxidation.

Connecting peptide (C-peptide), a byproduct of insulin biosynthesis, has diverse cellular and biological functions. Particulate matter 2.5 (PM) adversely affects human skin, leading to skin thickening, wrinkle formation, skin aging, and inflammation.

Butin Protects Keratinocytes From Particulate Matter 2.5 and Ultraviolet B-Mediated Damages.

Background: Butin is a naturally occurring compound with a wide range of medicinal properties, including anti-inflammatory, anti-arthritic, and antioxidant properties. Particulate matter 2.5 (PM) and ultraviolet B (UVB) radiation contribute to skin cell damage via the induction of oxidative stress.

Shikonin protects skin cells against oxidative stress and cellular dysfunction induced by fine particulate matter.

Shikonin, an herbal naphthoquinone, demonstrates a broad spectrum of pharmacological properties. Owing to increasingly adverse environmental conditions, human skin is vulnerable to harmful influences from dust particles. This study explored the antioxidant capabilities of shikonin and its ability to protect human keratinocytes from oxidative stress induced by fine particulate matter (PM).

The inhibitory effect of chlorogenic acid on oxidative stress and apoptosis induced by PM in HaCaT keratinocytes.

Exposure to fine particulate matter with an aerodynamic diameter of less than 2.5 μm (PM) can cause oxidative damage and apoptosis in the human skin. Chlorogenic acid (CGA) is a bioactive polyphenolic compound with antioxidant, antifungal, and antiviral properties.

Inhibitory Action of 1,3,5-Trihydroxybenzene on UVB-Induced NADPH Oxidase 4 through AMPK and JNK Signaling Pathways.

Specific sensitivity of the skin to ultraviolet B (UVB) rays is one of the mechanisms responsible for widespread skin damage. This study tested whether 1,3,5-trihydroxybenzene (THB), a compound abundant in marine products, might inhibit UVB radiation-induced NADPH oxidase 4 (NOX4) in both human HaCaT keratinocytes and mouse dorsal skin and explore its cytoprotective mechanism. The mechanism of action was determined using western blotting, immunocytochemistry, NADP/NADPH assay, reactive oxygen species (ROS) detection, and cell viability assay.

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

Particulate matter 2.5 (PM) 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.

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

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 (HO)‑generated oxidative stress in lung fibroblasts. To examine the effects of luteolin against HO‑induced damages, cell viability, sub‑G cell population, nuclear staining with Hoechst 33342, lipid peroxidation and comet assays were performed.

Silver nanoparticle-induced cell damage via impaired mtROS-JNK/MnSOD signaling pathway.

This study investigated the mechanism of silver nanoparticle (AgNP) cytotoxicity from a mitochondrial perspective. The effect of AgNP on manganese superoxide dismutase (MnSOD), a mitochondrial antioxidant enzyme, against oxidative stress has not been studied in detail. We demonstrated that AgNP decreased MnSOD mRNA level, protein expression, and activity in human Chang liver cells in a time-dependent manner.

Oxidative Stress-Mediated RUNX3 Mislocalization Occurs Via Jun Activation Domain-Binding Protein 1 and Histone Modification.

Runt domain transcription factor 3 (RUNX3) suppresses many different cancer types and is disabled by mutations, epigenetic repression, or cytoplasmic mislocalization. In this study, we investigated whether oxidative stress is associated with RUNX3 accumulation from the nucleus to the cytoplasm in terms of histone modification. Oxidative stress elevated histone deacetylase (HDAC) level and lowered that of histone acetyltransferase.

Protective effect of 3-bromo-4,5-dihydroxybenzaldehyde against PM-induced cell cycle arrest and autophagy in keratinocytes.

Particulate matter 2.5 (PM) poses a serious threat to human health and is responsible for respiratory disorders, cardiovascular diseases, and skin disorders. 3-Bromo-4,5-dihydroxybenzaldehyde (3-BDB), abundant in marine red algae, exhibits anti-inflammatory, antioxidant, and antidiabetic activities.

Protective Effect of Fermented Sea Tangle Extract on Skin Cell Damage Caused by Particulate Matter.

The skin is directly exposed to atmospheric pollutants, especially particulate matter 2.5 (PM) in the air, which poses significant harm to skin health. However, limited research has been performed to identify molecules that can confer resistance to such substances.

Rosmarinic Acid Protects Skin Keratinocytes from Particulate Matter 2.5-Induced Apoptosis.

The exposure of the human skin to particulate matter 2.5 (PM) results in adverse health outcomes, such as skin aging, wrinkle formation, pigment spots, and atopic dermatitis. It has previously been shown that rosmarinic acid (RA) can protect keratinocytes from ultraviolet B radiation by enhancing cellular antioxidant systems and reducing oxidative damage; however, its protective action against the adverse effects of PM on skin cells remains unclear.

Naringenin Induces Cellular Apoptosis in Melanoma Cells Intracellular ROS Generation.

Background/aim: Melanoma is a prevalent malignant tumor that arises from melanocytes. The treatment of malignant melanoma has become challenging due to the development of drug resistance. It is, therefore, imperative to identify novel therapeutic drug candidates for controlling malignant melanoma.

Rosmarinic Acid Inhibits Ultraviolet B-Mediated Oxidative Damage via the AKT/ERK-NRF2-GSH Pathway and .

Rosmarinic acid (RA) is a phenolic ester that protects human keratinocytes against oxidative damage induced by ultraviolet B (UVB) exposure, however, the mechanisms underlying its effects remain unclear. This study aimed to elucidate the cell signaling mechanisms that regulate the antioxidant activity of RA and confirm its cyto-protective role. To explore the signaling mechanisms, we used the human keratinocyte cell line HaCaT and SKH1 hairless mouse skin.

Correction: Kang et al. Anticolon Cancer Effect of Korean Red Ginseng via Autophagy- and Apoptosis-Mediated Cell Death. 2022, , 3558.

In the original publication [...

Korean Red Ginseng Attenuates Particulate Matter-Induced Senescence of Skin Keratinocytes.

Skin is a direct target of fine particulate matter (PM), as it is constantly exposed. Herein, we investigate whether Korean red ginseng (KRG) can inhibit PM-induced senescence in skin keratinocytes. PM-treated human keratinocyte cell lines and normal human epidermal keratinocytes showed characteristics of cellular senescence, including flat and enlarged forms; however, KRG suppressed them in both cell types.

Baicalein Inhibits α-Melanocyte-stimulating Hormone-stimulated Melanogenesis via p38 Mitogen-activated Protein Kinase Pathway in B16F10 Mouse Melanoma Cells.

Excessive UVB exposure causes development of both malignant and non-malignant melanoma via the secretion of α-melanocyte-stimulating hormone (α-MSH). We investigated whether baicalein (5,6,7-trihydroxyflavone) could inhibit α-MSH-stimulated melanogenesis. Baicalein prevented UVB- and α-MSH-induced melanin production and attenuated α-MSH-stimulated tyrosinase (monophenol monooxygenase) activity, and expression of tyrosinase and tyrosine-related protein-2.

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

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 (PM)-induced skin cell damage in vitro and in vivo.

Hesperidin Protects SH-SY5Y Neuronal Cells against High Glucose-Induced Apoptosis via Regulation of MAPK Signaling.

Neurodegenerative diseases are associated with neuronal cell death through apoptosis. Apoptosis is tightly associated with the overproduction of reactive oxygen species (ROS), and high glucose levels contribute to higher oxidative stress in diabetic patients. Hesperidin, a natural active compound, has been reported to scavenge free radicals.

Anticolon Cancer Effect of Korean Red Ginseng via Autophagy- and Apoptosis-Mediated Cell Death.

Ginseng ( Meyer) has been used in East Asian traditional medicine for a long time. Korean red ginseng (KRG) is effective against several disorders, including cancer. The cytotoxic effects of KRG extract in terms of autophagy- and apoptosis-mediated cell death and its mechanisms were investigated using human colorectal cancer lines.

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

Particulate matter 2.5 (PM) exposure can trigger adverse health outcomes in the human skin, such as skin aging, wrinkles, pigment spots, and atopic dermatitis. PM is associated with mitochondrial damage and the generation of reactive oxygen species (ROS).

Hesperidin Protects Human HaCaT Keratinocytes from Particulate Matter 2.5-Induced Apoptosis via the Inhibition of Oxidative Stress and Autophagy.

Numerous epidemiological studies have reported that particulate matter 2.5 (PM) causes skin aging and skin inflammation and impairs skin homeostasis. Hesperidin, a bioflavonoid that is abundant in citrus species, reportedly has anti-inflammatory properties.