Ginsenoside Rb1 Suppresses Ultraviolet Radiation-Induced Apoptosis by Inducing DNA Repair
Ginsenoside Rb1 Suppresses Ultraviolet Radiation-Induced Apoptosis by Inducing DNA Repair
复制标题
人参皂苷 Rb1 通过诱导 DNA 修复抑制紫外线辐射诱导的细胞凋亡
DOI：
10.1248/bpb.32.837
复制
发表时间：
2009-05-01
影响因子：
2
通讯作者：
Gao, Jie
中科院分区：
文献类型：
--
作者：
Cai, Bao-Xiang;Jin, Song-Liang;Gao, Jie
紫外线（UV）诱导的DNA损伤是晒伤细胞形成和皮肤癌的关键分子触发因素。核苷酸切除修复（NER）是UVB诱导的哺乳动物细胞DNA损伤的主要修复机制。本研究的目的是探讨在紫外线诱导的HaCaT（角质形成细胞系）细胞和Xpc（-）敲除小鼠角质形成细胞的DNA损伤和细胞凋亡中，Rb 1的功能作用。流式细胞术和Hoechst 33258染色分析UV诱导角质形成细胞凋亡与抗辐射Rb 1。免疫斑点分析用于检测环丁烷嘧啶二聚体，DNA损伤的主要标志。Western blot分析用于分析着色性干皮病-C（XPC）和切除修复交叉互补I（ERCC I），两个NER蛋白。人参皂苷Rb1可抑制紫外线诱导的角质形成细胞凋亡，并通过诱导DNA修复，显著减少紫外线特异性DNA损伤。在Xpc（-）敲除角质形成细胞中未观察到这种减少。人参皂苷Rb1诱导NER复合物的特定组分如XPC和ERCC1的表达。我们的研究结果表明，抗辐射Rb 1可以保护细胞免受紫外线辐射诱导的细胞凋亡诱导的DNA修复。
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 I (ERCC I), 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.