title: Salvia miltiorrhiza injection restores apoptosis of fibroblast-like synoviocytes cultured with serum from patients with rheumatoid arthritis.
abstract: Salvia miltiorrhiza injection (SMI) is a water‑soluble agent, derived from Salvia miltiorrhiza (SM), that is traditionally used to treat cardiovascular and cerebrovascular diseases. Furthermore it has been demonstrated to possess the ability to induce apoptosis of tumor cells. However, it remains unclear whether SMI can induce apoptosis of rheumatoid arthritis (RA) fibroblast‑like synoviocytes (FLS), which are hyperplastic in RA due to defective apoptosis. There is also evidence that allogenic serum may be associated with the induction of apoptosis. The aim of the present study was to investigate the involvement of serum during SMI‑induced apoptosis in RA FLS. The results demonstrated that SMI could induce apoptosis of RA FLS, cultured with fetal bovine serum (FBS), in a dose‑dependent manner. In addition, SMI decreased the expression of nuclear factor‑κB in RA FLS nuclear extracts and inhibited the secretion of tumor necrosis factor‑α. Fas ligand expression was not detected in RA FLS, in either the presence or absence of SMI. The pro‑apoptotic genes B‑cell lymphoma 2 (Bcl‑2) associated X protein (Bax) and Fas, were shown to be upregulated following SMI stimulation, whereas the expression levels of the anti‑apoptotic gene Bcl‑2, were downregulated. Upon replacement of FBS with normal human serum, the apoptotic rate and Bax mRNA expression levels following SMI stimulation, were unchanged. However, culturing RA FLS with patient' serum (RPS), restored the apoptotic rate and Bax mRNA expression levels following SMI stimulation. There may be numerous mechanisms by which SMI inhibits RA FLS proliferation. The present study demonstrated that SMI can restore apoptosis of RA FLS cultured with RPS. These results indicate that SMI may have a potential role in the treatment of synovial hyperplasia of RA.
authors.affiliation: Laboratory of Genetics, West China Institute of Women and Children's Health, West China Second Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
authors.forename: Qing-Song
authors.initials: QS
authors.lastname: Liu
authors.affiliation: Institute of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China.
authors.forename: Xiong-Yan
authors.initials: XY
authors.lastname: Luo
authors.affiliation: Institute of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China.
authors.forename: Hong
authors.initials: H
authors.lastname: Jiang
authors.affiliation: Department of Clinical Laboratory, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Xing
authors.affiliation: Institute of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China.
authors.forename: Ming-Hui
authors.initials: MH
authors.lastname: Yang
authors.affiliation: Institute of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China.
authors.forename: Guo-Hua
authors.initials: GH
authors.lastname: Yuan
authors.affiliation: Department of Clinical Laboratory, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China.
authors.forename: Zhong
authors.initials: Z
authors.lastname: Tang
authors.affiliation: Laboratory of Genetics, West China Institute of Women and Children's Health, West China Second Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
authors.forename: He
authors.initials: H
authors.lastname: Wang
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000187:drug effects*; D001172:Arthritis, Rheumatoid / Q000378:metabolism / Q000473:pathology; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D016328:NF-kappa B / Q000378:metabolism; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D027561:Salvia miltiorrhiza / Q000737:chemistry* / Q000378:metabolism; D013582:Synovial Fluid / Q000166:cytology* / Q000187:drug effects* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism; D019014:fas Receptor / Q000378:metabolism
chemical_list: C491901:FAS protein, human; D016328:NF-kappa B; D010936:Plant Extracts; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein; D019014:fas Receptor