Effect of tetramethylpyrazine on lipopolysaccharides induced macrophage cyclo-oxidase-2 expression and apoptosis of cardiac myocytes.
- Author:
Jing-yuan WAN
1
;
Du-yun YE
;
Ping WU
;
Li ZHANG
;
Xia GONG
;
Yunfeng HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Apoptosis; drug effects; Cells, Cultured; Cyclooxygenase 2; Isoenzymes; biosynthesis; genetics; Lipopolysaccharides; Macrophages; enzymology; Mice; Myocytes, Cardiac; cytology; Prostaglandin-Endoperoxide Synthases; biosynthesis; genetics; Pyrazines; pharmacology; RNA, Messenger; biosynthesis; genetics; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction
- From: Chinese Journal of Integrated Traditional and Western Medicine 2004;24(10):906-911
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of tetramethylpyrazine (TMP) on lipopolysaccharides (LPS) induced macrophage cyclo-oxidase-2 (COX-2) gene expression and activity in RAW264.7 mice, and to further investigate the effect and mechanism of TMP on LPS induced apoptosis of cardiac myocytes in suckling mice.
METHODSRT-PCR and Western Blot (WB) were used to investigate the macrophage COX-2 gene expression, ELISA was used to measure its activity, fluorescence microscopy was used to determine the apoptosis of murine neonatal cardiac myocyte, and fluorescence spectrophotometry was used to detect the concentration of intracellular calcium ion (Ca2+).
RESULTSTMP of 10(-6) mol/L could significantly reduce the COX-2 mRNA and protein expression (P < 0.05), in 10(-5) mol/L and 10(-4) mol/L could significantly decrease the COX-2 expression (P < 0.01) stimulated by LPS, but couldn't influence the activity of COX-2 by different TMP concentration. TMP in 10(-5) mol/L could significantly lower the concentration of intracellular Ca2+ in cardiac myocyte, and antagonize the LPS induced apoptosis of cardiac myocyte in suckling mice (P < 0.05).
CONCLUSIONTMP has the pharmacological effect in inhibiting LPS induced macrophage COX-2 expression and apoptosis of cardiac myocyte in suckling mice.
