Objective:To investigate the effects of allitridin on the expression of transcription factor T-bet of cytomegalovirus-induced myocarditis in mice and to analyze its role in anti-cytomegalovirus mechanisms. Methods: Si...Objective:To investigate the effects of allitridin on the expression of transcription factor T-bet of cytomegalovirus-induced myocarditis in mice and to analyze its role in anti-cytomegalovirus mechanisms. Methods: Sixty mice were randomly divided into allitridin therapy group, infected controls group and bland controls group. Allitridin therapy group were given to mice via the intraperitoneal (i.p.) route once a day with general dosege (25 mg·kg-1·d-1) at 24 h after infected MCMV; infected controls group were given with the same volume of 0.89% sodium chloride and bland controls group were only given with the same volume of 0.89% sodium chloride, without infected MCMV. All experimental mice were sacrificed on day 3, 5, 7 and 14 i.p. (n= 5 per time point). The expression levels of transcription factor T-bet were measured by RT-PCR. The expression levels of Th1 cytokine IFN-γ were measured by ELISA. Results: MCMV infection could markedly down-modulate the expression of IFN-γ and T-bet mRNA (P<0.01). Allitridin significantly up-regulated the expression of Th1 cytokines IFN-γ and Th1-specific transcription factor T-bet mRNA (P<0.01). Conclusion: Allitridin up-regulates the expression of transcription factor T-bet mRNA which is an important, but not the only factor to mediate the constitutive expression of Th1 cytokines IFN-γ.展开更多
文摘Objective:To investigate the effects of allitridin on the expression of transcription factor T-bet of cytomegalovirus-induced myocarditis in mice and to analyze its role in anti-cytomegalovirus mechanisms. Methods: Sixty mice were randomly divided into allitridin therapy group, infected controls group and bland controls group. Allitridin therapy group were given to mice via the intraperitoneal (i.p.) route once a day with general dosege (25 mg·kg-1·d-1) at 24 h after infected MCMV; infected controls group were given with the same volume of 0.89% sodium chloride and bland controls group were only given with the same volume of 0.89% sodium chloride, without infected MCMV. All experimental mice were sacrificed on day 3, 5, 7 and 14 i.p. (n= 5 per time point). The expression levels of transcription factor T-bet were measured by RT-PCR. The expression levels of Th1 cytokine IFN-γ were measured by ELISA. Results: MCMV infection could markedly down-modulate the expression of IFN-γ and T-bet mRNA (P<0.01). Allitridin significantly up-regulated the expression of Th1 cytokines IFN-γ and Th1-specific transcription factor T-bet mRNA (P<0.01). Conclusion: Allitridin up-regulates the expression of transcription factor T-bet mRNA which is an important, but not the only factor to mediate the constitutive expression of Th1 cytokines IFN-γ.
