摘要
The aim of this study is to investigate the effects of allitridin on the expression of transcription factor T-bet/GATA-3 in mice infected by murine cytomegalovirus. BALB/c mice model system of murine cytomegalovirus (MCMV) infection was established. In which 20 model mice were allocated randomly into allitridin treated group ( n =10) and infected control group ( n =10). Allitridin (25 mg·kg -1 ·d -1 ) was used in treated group at the 24 h by intraperitoneal route ( once/d ×14 d), and the same volume of saline solution was injected control mice. Normal control mice ( n =10), were only given with the same volume of 0.89% sodium chloride, without infection with MCMV. The expression levels of transcription factor T-bet/GATA-3 mRNA were measured by RT-PCR, and the expression levels of T helper 1(Th1) cytokine IFN-γ and Th2 cytokine IL-10 in supernatant of spleen cell culture were measured by ELISA. Experimental results showed MCMV infection could markedly down-modulate the expression of IFN-γ and T-bet, and significantly up-modulate the expression of IL-10 and GATA-3 mRNA. Allitridin could induce increased expression of transcription factor T-bet mRNA and Th1 cytokine IFN-γ significantly ( P <0.01), and decreased expression of transcription factor GATA-3 mRNA and Th2 cytokine IL-10 markedly ( P <0.01). It is concluded that MCMV infection leads to disequilibrium of Th1/Th2 cytokine expression: the level of Th1 cytokine IFN-γ decreases significantly and Th2 cytokine IL-10 overexpresses markedly. Allitridin can up-regulate the expression of T-bet and IFN-γ, and inhibit the expression of GATA-3 mRNA and IL-10 in MCMV infected mice, indicating a Th1 dominant state which should enhance the specific cellular immune reactions against CMV and be helpful for clearance of the cytomegalovirus in host.
The aim of this study is to investigate the effects of allitridin on the expression of transcription factor T-bet/GATA-3 in mice infected by murine cytomegalovirus. BALB/c mice model system of murine cytomegalovirus (MCMV) infection was established. In which 20 model mice were allocated randomly into allitridin treated group ( n =10) and infected control group ( n =10). Allitridin (25 mg·kg -1 ·d -1 ) was used in treated group at the 24 h by intraperitoneal route ( once/d ×14 d), and the same volume of saline solution was injected control mice. Normal control mice ( n =10), were only given with the same volume of 0.89% sodium chloride, without infection with MCMV. The expression levels of transcription factor T-bet/GATA-3 mRNA were measured by RT-PCR, and the expression levels of T helper 1(Th1) cytokine IFN-γ and Th2 cytokine IL-10 in supernatant of spleen cell culture were measured by ELISA. Experimental results showed MCMV infection could markedly down-modulate the expression of IFN-γ and T-bet, and significantly up-modulate the expression of IL-10 and GATA-3 mRNA. Allitridin could induce increased expression of transcription factor T-bet mRNA and Th1 cytokine IFN-γ significantly ( P <0.01), and decreased expression of transcription factor GATA-3 mRNA and Th2 cytokine IL-10 markedly ( P <0.01). It is concluded that MCMV infection leads to disequilibrium of Th1/Th2 cytokine expression: the level of Th1 cytokine IFN-γ decreases significantly and Th2 cytokine IL-10 overexpresses markedly. Allitridin can up-regulate the expression of T-bet and IFN-γ, and inhibit the expression of GATA-3 mRNA and IL-10 in MCMV infected mice, indicating a Th1 dominant state which should enhance the specific cellular immune reactions against CMV and be helpful for clearance of the cytomegalovirus in host.
