AI Article Synopsis
- Acute UV-B radiation causes significant photodamage to cells, and the study focuses on how polysaccharides from Lindl. (DNPs) can help protect HaCaT keratinocytes from this harm.
- DNPs were found to enhance cell viability and proliferation after UVB exposure by scavenging harmful reactive oxygen species, boosting antioxidant enzyme activities, and reducing malondialdehyde levels.
- The protective effects of DNPs involve regulating specific signaling pathways that prevent cell cycle arrest and apoptosis, suggesting their potential as therapeutic agents against UVB-induced damage.
Article Abstract
Acute ultraviolet (UV)-B radiation is the major external factor causing photodamage. In this study, we aimed to determine the effects of Lindl. polysaccharides (DNPs) on photodamage in HaCaT keratinocytes after UVB irradiation and the underlying mechanisms. We found that DNPs significantly attenuated the decline in the viability and proliferation of HaCaT cells after UVB irradiation. Moreover, DNPs scavenged reactive oxygen species (ROS), improved the activities of endogenous antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase, and reduced the levels of malondialdehyde, while partially attenuating cell cycle arrest, suggesting their antioxidant and anti-apoptotic properties. The mitogen-activated protein kinase () pathway was found to be important for the attenuation of UVB-induced photodamage in the HaCaT cells. Furthermore, DNPs exerted cytoprotective effects by downregulating UVB-induced ROS-mediated phosphorylation of MAPKs, including p38, c-Jun N-terminal kinase, and extracellular signal-regulated kinase, and by inhibiting p53 expression as well as the apoptotic cascade response. Therefore, DNPs ameliorated UVB-induced oxidative damage and apoptosis in HaCaT cells via the regulation of . Our findings thus highlight the Lindl polysaccharides as promising therapeutic candidates for UVB-induced photodamage.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10094248 | PMC |
| http://dx.doi.org/10.3390/ijms24076120 | DOI Listing |
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