Schisandrin B protects against solar irradiation-induced oxidative stress in rat skin tissue (original) (raw)
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Schisandrin B protects against solar irradiation-induced oxidative injury in BJ human fibroblasts
Fitoterapia, 2011
The effects of schisandrin B (Sch B) and its analogs on solar irradiation-induced oxidative injury were examined in BJ human fibroblasts. Sch B and schisandrin C (Sch C) increased cellular reduced glutathione (GSH) level and protected against solar irradiation-induced oxidative injury. The photoprotection was paralleled by decreases in the elastases-type protease activity and matrix-metalloproteinases-1 expression in solar-irradiated fibroblasts. The cytochrome P-450-mediated metabolism of Sch B or Sch C caused ROS production. The results suggest that by virtue of its pro-oxidant action and the subsequent glutathione antioxidant response, Sch B or Sch C may offer the prospect of preventing skin photo-aging.
Transcriptomics: Open Access, 2015
Generation of reactive oxygen species (ROS) is one of the important and early events after exposure to ionizing radiations and this ROS production is responsible for the degenerative changes ensuing irradiation. An attempt has been made to modulate the radiation induced-ROS by hesperidin (hesperitin-7-rhamnoglucoside), a bioflavonoid in the wounded skin of irradiated mouse. The lower half of the animals was shaved and the animals were orally administered or not with 100 mg/kg body weight of hesperidin before exposure to 6 Gy of partial body gamma-radiation. The activities of glutathione peroxidase, superoxide dismutase and glutathione concentration as well as lipid peroxidation were estimated in the skin of mouse at 0, 1.5, 3, 6, 12, 24 and 48 h post-irradiation. Irradiation of mouse to 6 Gy caused a significant depletion in the activities of glutathione peroxidase, superoxide dismutase as well as glutathione concentration. Exposure of mouse to 6 Gy resulted in a significant elevation in lipid peroxidation when compared to the base line levels of lipid peroxidation. Administration of hesperidin before hemi-body exposure to 6 Gy γ-rays significantly raised the activities of glutathione peroxidase, superoxide dismutase and glutathione concentration, whereas hesperidin pretreatment caused a significant reduction in the radiation induced lipid peroxidation. The present study demonstrates that hesperidin pretreatment reduces the radiation induced oxidative stress in the irradiated wounds of mouse and may be useful paradigm to reduce the radiation-induced oxidative stress before or after surgery.
Journal of Photochemistry and Photobiology B: Biology, 2015
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Biomolecules & Therapeutics, 2016
Human skin cells undergo pathophysiological processes via generation of reactive oxygen species (ROS) upon excessive exposure to ultraviolet B (UVB) radiation. This study investigated the ability of hesperidin (C28H34O15) to prevent apoptosis due to oxidative stress generated through UVB-induced ROS. Hesperidin significantly scavenged ROS generated by UVB radiation, attenuated the oxidation of cellular macromolecules, established mitochondrial membrane polarization, and prevented the release of cytochrome c into the cytosol. Hesperidin downregulated expression of caspase-9, caspase-3, and Bcl-2-associated X protein, and upregulated expression of B-cell lymphoma 2. Hesperidin absorbed wavelengths of light within the UVB range. In summary, hesperidin shielded human keratinocytes from UVB radiation-induced damage and apoptosis via its antioxidant and UVB absorption properties.
Natural Antioxidants: Multiple Mechanisms to Protect Skin From Solar Radiation
Frontiers in Pharmacology, 2018
Human skin exposed to solar ultraviolet radiation (UVR) results in a dramatic increase in the production of reactive oxygen species (ROS). The sudden increase in ROS shifts the natural balance toward a pro-oxidative state, resulting in oxidative stress. The detrimental effects of oxidative stress occur through multiple mechanisms that involve alterations to proteins and lipids, induction of inflammation, immunosuppression, DNA damage, and activation of signaling pathways that affect gene transcription, cell cycle, proliferation, and apoptosis. All of these alterations promote carcinogenesis and therefore, regulation of ROS levels is critical to the maintenance of normal skin homeostasis. Several botanical products have been found to exhibit potent antioxidant capacity and the ability to counteract UV-induced insults to the skin. These natural products exert their beneficial effects through multiple pathways, including some known to be negatively affected by solar UVR. Aging of the skin is also accelerated by UVR exposure, in particular UVA rays that penetrate deep into the epidermis and the dermis where it causes the degradation of collagen and elastin fibers via oxidative stress and activation of matrix metalloproteinases (MMPs). Because natural compounds are capable of attenuating some of the UV-induced aging effects in the skin, increased attention has been generated in the area of cosmetic sciences. The focus of this review is to cover the most prominent phytoproducts with potential to mitigate the deleterious effects of solar UVR and suitability for use in topical application.