Silymarin induces apoptosis primarily through a p53-dependent pathway involving Bcl-2/Bax, cytochrome c release, and caspase activation.
暂无分享,去创建一个
[1] T. Mosmann. Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays. , 1983, Journal of immunological methods.
[2] H. Mukhtar,et al. Essential role of caspases in epigallocatechin-3-gallate-mediated inhibition of nuclear factor kappaB and induction of apoptosis , 2004, Oncogene.
[3] Yoichi Taya,et al. DNA Damage-Induced Phosphorylation of p53 Alleviates Inhibition by MDM2 , 1997, Cell.
[4] S. Korsmeyer,et al. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death , 1993, Cell.
[5] S. Lowe,et al. p53-Dependent apoptosis suppresses tumor growth and progression in vivo , 1994, Cell.
[6] H. Wagner,et al. [On the chemistry of silymarin (silybin), the active principle of the fruits from Silybum marianum (L.) Gaertn. (Carduus marianus L.)]. , 1968, Arzneimittel-Forschung.
[7] S. Korsmeyer,et al. bax-deficiency promotes drug resistance and oncogenic transformation by attenuating p53-dependent apoptosis. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[8] D. Fisher. Apoptosis in cancer therapy: Crossing the threshold , 1994, Cell.
[9] R. Mohan,et al. A flavonoid antioxidant, silymarin, affords exceptionally high protection against tumor promotion in the SENCAR mouse skin tumorigenesis model. , 1999, Cancer research.
[10] B. Vogelstein,et al. Participation of p53 protein in the cellular response to DNA damage. , 1991, Cancer research.
[11] J. Larrick,et al. Inhibition of apoptosis as a mechanism of tumor promotion , 1994, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[12] B. Kaina. DNA damage-triggered apoptosis: critical role of DNA repair, double-strand breaks, cell proliferation and signaling. , 2003, Biochemical pharmacology.
[13] D. Green,et al. The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis , 1997, Science.
[14] H. Mannherz,et al. Premature keratinocyte death and expression of marker proteins of apoptosis in human skin after UVB exposure , 2003, Archives of Dermatological Research.
[15] S. Katiyar. Silymarin and skin cancer prevention: anti-inflammatory, antioxidant and immunomodulatory effects (Review). , 2005, International journal of oncology.
[16] R. Agarwal,et al. Inhibition of human carcinoma cell growth and DNA synthesis by silibinin, an active constituent of milk thistle: comparison with silymarin. , 1999, Cancer letters.
[17] R Montesano,et al. Database of p53 gene somatic mutations in human tumors and cell lines. , 1994, Nucleic acids research.
[18] C. Elmets,et al. Treatment of green tea polyphenols in hydrophilic cream prevents UVB-induced oxidation of lipids and proteins, depletion of antioxidant enzymes and phosphorylation of MAPK proteins in SKH-1 hairless mouse skin. , 2003, Carcinogenesis.
[19] K. Vousden,et al. Regulation and function of the p53 tumor suppressor protein. , 2001, Current opinion in cell biology.
[20] T. Cotter,et al. Control of mitochondrial integrity by Bcl-2 family members and caspase-independent cell death. , 2004, Biochimica et biophysica acta.
[21] A. Eastman,et al. Activation of programmed cell death (apoptosis) by cisplatin, other anticancer drugs, toxins and hyperthermia. , 1990, Biochemical pharmacology.
[22] H. Horvitz,et al. Mechanisms and functions of cell death. , 1991, Annual review of cell biology.
[23] R. Agarwal,et al. Protective effects of silymarin against photocarcinogenesis in a mouse skin model. , 1997, Journal of the National Cancer Institute.
[24] Weiya Ma,et al. Induction of apoptosis by caffeine is mediated by the p53, Bax, and caspase 3 pathways. , 2003, Cancer research.
[25] John Calvin Reed. Regulation of apoptosis by bcl-2 family proteins and its role in cancer and chemoresistance. , 1995, Current opinion in oncology.
[26] Weiya Ma,et al. Resveratrol suppresses cell transformation and induces apoptosis through a p53-dependent pathway. , 1999, Carcinogenesis.
[27] A. Wyllie,et al. Cell death: the significance of apoptosis. , 1980, International review of cytology.
[28] D. Meek,et al. Serine 15 phosphorylation stimulates p53 transactivation but does not directly influence interaction with HDM2 , 1999, The EMBO journal.
[29] S. Katiyar,et al. EGCG down-regulates telomerase in human breast carcinoma MCF-7 cells, leading to suppression of cell viability and induction of apoptosis. , 2004, International journal of oncology.
[30] Y Taya,et al. A role for ATR in the DNA damage-induced phosphorylation of p53. , 1999, Genes & development.
[31] N. Colburn,et al. Tumour promoter induces anchorage independence irreversibly , 1979, Nature.
[32] A. Levine,et al. The p53 proto-oncogene can act as a suppressor of transformation , 1989, Cell.
[33] J. Hickman,et al. Apoptosis induced by anticancer drugs , 1992, Cancer and Metastasis Reviews.
[34] C. Larsen. [The BCL2 gene, prototype of a gene family that controls programmed cell death (apoptosis)]. , 1994, Annales de genetique.
[35] D. Pinkel,et al. Retention of wild‐type p53 in tumors from p53 heterozygous mice: reduction of p53 dosage can promote cancer formation , 1998, The EMBO journal.
[36] Sung-ju Ahn,et al. Involvement of NF-κB and caspases in silibinin-induced apoptosis of endothelial cells , 2004 .
[37] P. O'Connor,et al. Induction of bax by genotoxic stress in human cells correlates with normal p53 status and apoptosis. , 1994, Oncogene.
[38] D. Housman,et al. Abrogation of oncogene-associated apoptosis allows transformation of p53-deficient cells. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[39] S. Korsmeyer,et al. Bax suppresses tumorigenesis and stimulates apoptosis in vivo , 1997, Nature.
[40] N. Colburn,et al. Transfer by pro gene transfection of tumor promoter-sensitive phenotype to promotion-insensitive JB6 cells. , 1988, Cancer research.
[41] Larsen Cj. [The BCL2 gene, prototype of a gene family that controls programmed cell death (apoptosis)]. , 1994 .
[42] B. Barres,et al. Programmed cell death and the control of cell survival: lessons from the nervous system. , 1993, Science.
[43] R. Agarwal,et al. Silibinin prevents ultraviolet radiation-caused skin damages in SKH-1 hairless mice via a decrease in thymine dimer positive cells and an up-regulation of p53-p21/Cip1 in epidermis. , 2004, Carcinogenesis.
[44] Dean P. Jones,et al. Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked , 1997, Science.
[45] L. Donehower,et al. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours , 1992, Nature.
[46] B. Hoffman,et al. Molecular controls of growth arrest and apoptosis: p53-dependent and independent pathways. , 1995, Oncogene.
[47] G. Stark,et al. Transgenic mice with p53‐responsive lacZ: p53 activity varies dramatically during normal development and determines radiation and drug sensitivity in vivo , 1997, The EMBO journal.
[48] S. Katiyar. Treatment of silymarin, a plant flavonoid, prevents ultraviolet light-induced immune suppression and oxidative stress in mouse skin. , 2002, International journal of oncology.