The effect of Xuebijing on the activation-induced cell death (AICD) of T lymphocyte
10.3760/cma.j.issn.0254-5101.2009.11.001
- VernacularTitle:血必净对活化诱导T细胞凋亡的调节
- Author:
Wenxiu CHANG
;
Shuhua CAO
;
Hongmei GAO
;
Yongqiang WANG
- Publication Type:Journal Article
- Keywords:
Activation-induction;
T lymphocyte;
Apoptotic related gene
- From:
Chinese Journal of Microbiology and Immunology
2009;29(11):965-970
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the influence of Xuebijing injection on apoptosis, apoptotic related gene mRNA levels and activity of caspase3 in activated T lymphocyte. Methods The T lymphocytes were obtained from the spleens of BALB/c mice and be induced to be activated and apoptotic by cultured with Con A + IL-2. Apoptosis was investigated by flow cytometry. RT-PCR was used to detect the expression of Fas, FasL, Bcl-2, Bax, IL-2 mRNA, and the activity of caspase3 in T lymphocyte was also detected by spectrophotometric method. In the mean time, the effect of Xuebijing injection on those parameters was observed. Results After the induction, T lymphocyte apoptosis raised at 18 h. At 6 h after the induction, there was no expression of FasL, Bax mRNA, and no change in the expression of Fas and Bcl-2 mRNA. At 18 h, the expressions of Fas, FasL, Bax mRNA rised and the expression of Bcl-2 mRNA lessened. The activity of caspase3 also ascended. Xuebijing injection can cut down the apoptosis induced by induction, make the expression of Fas, FasL, Bax mRNA decreased and Bcl-2 mRNA improved. The activity of caspase3 also fallen after the Xuebijing injection treated. It can promote the expressions of IL-2 mRNA at early phase of AICD (6 h) and depress the expressions at the late period (18 h). Conclusion The apoptosis of T lymphocyte induced by activation was regulated by the change of Fas, FasL, Bcl-2, Bax mRNA expression. Xuebijing injection can ameliorate the apoptosis through regulating the expression of IL-2 and apoptotic related gene mRNA, improve the proliferation activity of T lymphocyte.