摘要
<p><b>OBJECTIVE</b>Cheongseoikki-tang (CIT, Korean), also called Qingshu Yiqi decoction () and Seisho-ekki-to (Japanese), is well known as an effective traditional combination of herbs for treating cardiovascular diseases. This study was to research its effects on bone marrow-derived mast cell (BMMC)-mediated allergy and inflammation mechanisms.</p><p><b>METHODS</b>In this study, the biological effect of Cheongseoikki-tang ethanol extract (CITE) was evaluated, focusing on its effects on the production of allergic mediators by phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187 (A23187)-stimulated BMMCs. These allergic mediators included interleukin-6 (IL-6), prostaglandin D2 (PGD2), leukotriene C4 (LTC4), and β-hexosaminidase (β-hex).</p><p><b>RESULTS</b>Our data revealed that CITE inhibited the production of IL-6, PGD2, LTC4, and β-hex induced by PMA plus A23187 (P<0.05).</p><p><b>CONCLUSION</b>These findings indicate that CITE has the potential for use in the treatment of allergy.</p>
Subject(s)
Animals , Male , Mice , Anti-Inflammatory Agents , Pharmacology , Therapeutic Uses , Bone Marrow Cells , Pathology , Calcimycin , Pharmacology , Cell Degranulation , Cell Survival , Drugs, Chinese Herbal , Pharmacology , Therapeutic Uses , Hypersensitivity , Drug Therapy , Pathology , Interleukin-6 , Bodily Secretions , Leukotriene C4 , Pharmacology , Mast Cells , Pathology , Physiology , Mice, Inbred BALB C , Prostaglandin D2 , Tetradecanoylphorbol Acetate , Pharmacology , beta-N-Acetylhexosaminidases , Metabolism摘要
Polymorphisms of the prion protein gene (PRNP) havebeen detected in several cervid species. In order toconfirm the genetic variations, this study examined theDNA sequences of the PRNP obtained from 33 captivesika deer (Cervus nippon laiouanus) in Korea. A total ofthree single-nucleotide polymorphisms (SNPs) at codons100, 136 and 226 in the PRNP of the sika deer wereidentified. The polymorphic site located at codon 100 hasnot been reported. The SNPs detected at codons 100 and226 induced amino acid substitutions. The SNP at codon136 was a silent mutation that does not induce any aminoacid change. The genotype and allele frequencies weredetermined for each of the SNPs.