Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0849640 (skin damage)
 1,516 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Silibinin (SB), a flavonoid isolated from the milk thistle, Silybum marianum, has been shown to exhibit protective effects against skin damage. The objective of the present study was to investigate the effect of topical application of SB on levels of stromelysine 1 (STM1) gene expression, acetyl hexoseamines and collagen production during skin wound healing. Full-thickness skin wounds were topically treated with 10% and 20% SB extract in acetonitril:olive oil (AOO) (4:1) for 30 days, and expression level of STM1 transcript, n-acetyl glucoseamine (NAGLA), n-acetyl galactoseamine (NAGAA) and collagen contents were analyzed on the 10th, 20th and 30th days post wounding. SB in dose- and time-dependent manner accelerated wound closure time and increased levels of STM1 mRNA, hydroxyproline, NAGLA and NAGAA compared to the untreated and vehicle (AOO)-treated rats. The current study provides evidence that SB, by increasing STM1 gene expression and extracellular matrix constituents including glycosaminoglycans and collagen contents, promotes a faster wound healing process and can be used as a healing agent in future.
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PMID:Silibinin regulates matrix metalloproteinase 3 (stromelysine1) gene expression, hexoseamines and collagen production during rat skin wound healing. 2297 3

Ultraviolet B (UVB) in the sun light is a major cause of skin damage, which accompanies complex alterations in irradiated skin cells, including DNA lesions, oxidative stress, inflammation and caspase activation. The protection against UVB damage requires multiple interruptions such as repair of the DNA lesions, scavenging of the reactive oxygen species (ROS), repression of the inflammation and others. Silibinin is suggested as an anti-UVB reagent, but the underlying mechanisms have not been fully elucidated. In this study, we found a role of autophagy in the anti-UVB effect of silibinin in A431 cells. Autophagy was reduced after UVB-irradiation while restored by silibinin through the suppression of the IGF-1R signalling pathway. The protective effect of silibinin in UVB-irradiated A431 cells was further enhanced by pre-treatment with an autophagy inducer, rapamycin, while it was reversed by an autophagy inhibitor, wortmannin, indicating that elevated autophagy contributed to the cell survival. Consistently, cell apoptosis was augmented by siRNAs targeting Beclin 1 and Atg5, supporting the hypothesis that autophagy induced by silibinin plays a protective role against UVB-induced epidermal apoptosis.
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PMID:Autophagy induced by silibinin protects human epidermoid carcinoma A431 cells from UVB-induced apoptosis. 2360 70

Ultraviolet B (UVB) is a major cause of skin inflammation, leading to skin damage. Our previous in vivo study revealed that a natural flavonoid silibinin had marked anti-inflammatory effect on UVB-exposed murine skin. UVB exposure caused reduced autophagy in epidermis while it promoted autophagy in dermis. Nevertheless, silibinin inhibited the inflammatory flux in the skin epidermis as well as dermis through the modulation of autophagy. In order to elucidate the underlying protective mechanisms of silibinin for UVB damage on skin, separate studies on epidermis and dermis are helpful. Derived from the normal tissue of the mouse, L929 cells are capable of representing some characteristics of dermal cells. UVB irradiation caused L929 cell apoptosis in a time- and dose-dependent manner. Ataxia-telangiectasia-mutated (ATM) protein and p53 were activated to cause cell apoptosis, accompanying upregulation of the autophagic flux. The pharmacological inhibition of ATM, p53 and autophagy or the transfection with autophagy-associated protein-targeted small interfering RNAs showed that the UVB-activated ATM-p53 axis and autophagy formed a positive feedback loop, which synergistically promoted cell apoptosis. Silibinin treatment simultaneously repressed the activation of ATM-p53 and autophagy and thereby protected UVB-irradiated L929 cells from apoptotic death.
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PMID:Silibinin protects murine fibroblast L929 cells from UVB-induced apoptosis through the simultaneous inhibition of ATM-p53 pathway and autophagy. 2382 51