title: [Effect of Bugu Mixture on all-trans retinoic acid-induced apoptosis of bone marrow stromal cells].
abstract: OBJECTIVE
  We used the SD rat's bone marrow stromal cells (BMSCs) cultured in vitro to observe the effects of Bugu Mixture on the apoptosis and to explore the molecular biologic mechanism of the treatment of osteoporosis with Bugu Mixture.
  
  
  METHODS
  BMSCs were separated from the bones of the extremities of SD rats in vitro. The morphologic changes, the apoptosis cell cycles, the mitochondrion membrane potential changes, and the Bcl-2 and Bax gene expression were observed, and the effects of Bugu Mixture on the course of cell apoptosis were evaluated.
  
  
  RESULTS
  The earlier use of Bugu Mixture could decrease the cells blocked in G0/G1 phase, and promote their synthesis of DNA in S phase. The expression of Bcl-2 was higher in the Bugu Mixture group than that in the all-trans retinoic acid (ATRA) induced group, and the expression of Bax was lower in the Bugu Mixture group than that in the ATRA induced group. The mitochondrion membrane potential descended significantly in the Bugu Mixture group than that in the ATRA induced group.
  
  
  CONCLUSIONS
  The mechanism of the treatment of osteoporosis with Bugu Mixture is that the earlier use of Bugu Mixture can decrease the amount of apoptostic cells induced by ATRA, thus promoting the cell mitosis and restraining the apoptosis. It can also act as a protector to Bcl-2 located on the mitochondrion membrane. By preventing the transferring of the Bax protein from cell-plasma to mitochondrion membrane, it takes the advantage of Bcl-2 in forming Bcl-2/Bax homodimer so as to prevent the opening of the permeability transition pore to avoid the changing of mitochondrion membrane potential and the destruction of biosynthesis caused by the mitochondrion release of apoptosis inducing factors and to reach the objective of restraining apoptosis.
authors.affiliation: Department of Orthopedics and Traumatology, Fujian Traditional Chinese Medical College, Fuzhou, Fujian Province 350003, China. linan000@tom.com
authors.forename: Nan
authors.initials: N
authors.lastname: Li
authors.forename: He-Ming
authors.initials: HM
authors.lastname: Wang
authors.forename: Xu
authors.initials: X
authors.lastname: Lin
authors.forename: Liang-Pu
authors.initials: LP
authors.lastname: Zheng
authors.forename: Lin
authors.initials: L
authors.lastname: Shen
authors.forename: Yi-Ping
authors.initials: YP
authors.lastname: Lin
authors.forename: Lin-Ying
authors.initials: LY
authors.lastname: Zhou
authors.forename: Xiu-Rong
authors.initials: XR
authors.lastname: Zhong
authors.forename: Fang
authors.initials: F
authors.lastname: Lin
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001854:Bone Marrow Cells / Q000187:drug effects* / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D005434:Flow Cytometry; D007150:Immunohistochemistry; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017154:Stromal Cells / Q000187:drug effects* / Q000378:metabolism; D014212:Tretinoin / Q000633:toxicity; D051028:bcl-2-Associated X Protein
chemical_list: C494828:Bax protein, rat; D004365:Drugs, Chinese Herbal; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D051028:bcl-2-Associated X Protein; D014212:Tretinoin