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Protective effects of tetramethylpyrazine on rat myocardial cells infected by Coxsackie virus B3 and its signal transduction mechanism
QIAN Zhao-Xin, HUANG Han, LIN Xiao-Juan
Chinese Journal of Contemporary Pediatrics ›› 2009, Vol. 11 ›› Issue (08) : 687-690.
PDF(1118 KB)
PDF(1118 KB)
Protective effects of tetramethylpyrazine on rat myocardial cells infected by Coxsackie virus B3 and its signal transduction mechanism
OBJECTIVE: To study the protective effects of tetramethylpyrazine (TMPZ) on rat myocardial cells infected by Coxsackie virus B3 (CVB3) and its signal transduction mechanism. METHODS: The cultured myocardial cells of neonatal Sprague-Dawley rats were randomly treated with CVB3, CVB3+TMPZ (100 μmol/L), TMPZ (100 μmol/L) (negative control) or DMEM (blank control). After treatment, the beating rate of myocardial cells and the LDH activity in the culture fluid were measured. Cell viability was ascertained with MTT assay. Western blot was used to study the expression of nuclear factor kappa-B (NF-κB) protein in myocardial cells. RESULTS: The beating rate of myocardial cells in the untreated CVB3 infection group was significantly lower than that in the TMPZ-treated CVB3 infection group (32.0±3.6 bpm vs 84.3±3.5 bpm, P<0.01). The LDH activity and NF-κB expression in the TMPZ-treated CVB3 infection group was significantly reduced when compared with untreated CVB3 infection group (P<0.05, P<0.01, respectively). Cell viability 7 days after CVB3 infection in the TMPZ-treated group was higher than that in the untreated CVB3 infection group ［(86.7±2.7)％ vs (35.3±3.4)%; P<0.01］. CONCLUSIONS: TMPZ can provide protective effects on rat myocardial cells infected by CVB3, possibly by an inhibition of the activity of NF-κB in myocardial cells.［Chin J Contemp Pediatr, 2009, 11 (8):687-690］
Myocarditis / Coxsackie virus B3 / Nuclear factor kappa-B / Tetramethylpyrazine / Rats
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