Linked Life Data

19420751

Source:http://linkedlifedata.com/resource/pubmed/id/19420751

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2009-5-7
pubmed:abstractText
Ultraviolet (UV)-induced DNA damage is a crucial molecular trigger for sunburn cell formation and skin cancer. Nucleotide excision repair (NER) is the main mechanism in repairing UVB-induced DNA damage to mammalian cells. The purpose of this study was to investigate the functional role of ginsenoside Rb1 in UV-induced DNA damage and apoptosis in HaCaT (keratinocyte cell line) cells, and Xpc(-) knockout mouse keratinocytes. Flow cytometry and Hoechst 33258 staining were performed in analyzing UV-induced apoptosis in keratinocytes treated with ginsenoside Rb1. The ImmunoDotBlot assay was used to detect cyclobutane pyrimidine dimers, the main sign of DNA damage. Western blot analysis was applied for analyzing Xeroderma pigmentosum-C (XPC) and excision repair cross-complementing 1 (ERCC1), two of the NER proteins. Ginsenoside Rb1 inhibited UV-induced apoptosis of keratinocytes and caused a notable reduction in UV-specific DNA lesions which was due to induction of DNA repair. This reduction was not observed in Xpc(-) knockout keratinocytes. Ginsenoside Rb1 induced the expression of specific components of the NER complex, such as XPC and ERCC1. Our results demonstrate that ginsenoside Rb1 can protect cells from apoptosis induced by UV radiation by inducing DNA repair.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0918-6158
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
837-41
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Ginsenoside Rb1 suppresses ultraviolet radiation-induced apoptosis by inducing DNA repair.
pubmed:affiliation
Department of Dermatology, First Affiliated Hospital of Nanjing Medical University, Nanjing, P.R. China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't