[Effect of Apigenin on proliferation, cell cycle and apoptosis of mouse T cells in vitro].

AIM: To study the effect of Apigenin (AP) on the proliferation, cell cycle and apoptosis of mouse T cells in vitro. METHODS: The lymphocytes were prepared from lymph nodes and thymus of mice. The effect of AP on the proliferation of T in response to ConA at different concentrations (25, 50, 100, 150, 200 micromol/L) was detected by MTT. Cell cycle was measured by PI staining and FCM. The effect of Apigenin and Apigenin with DEX on T cell apoptosis was measured by Annexin V-FITC/PI double staining and FCM. The effect of different concentrations of AP cytotoxicity to T cells was measured by MTT. RESULTS: 25-200 micromol/L of AP didn't have cytotoxicity to T cells, but it had some inhibitory effect on T cells in response to ConA(P<0.01), arresting cell cycle at G0/G1 in a dose-dependent manner. Different concentrations of AP inhibited the apoptosis of T cells, especially those induced by DEX(P<0.01). CONCLUSION: AP can inhibit the proliferation of mouse T cells in response to ConA, arrest cell cycle at G0/G1 and inhibit the apoptosis of T cells.

[Study on the mitochondrial inner membrane potential of apoptotic thymocytes at cell and organelle level].

In this study, dexamethasone was used to induce mouse thymocyte apoptosis. The PI and Annexin V/PI staining flowcytometry methods were adopted to detect late and early phases apoptosis. Inner mitochondrial membrane potential (deltapsim) was examined by JC-1 and DiOC6(3)/PI staining flowcytometry. Direct JC-1 staining technology was applied to test the of deltapsim abstracted pure mitochondria. Results showed: DEX could significantly induce late and early phase mouse thymocyte apoptosis; at cell level, DEX was observed to reduce staining ability of deltapsim dependant fluorescence, J-aggregate and DiOC6(3), to drop down mitochondria number, but to cause no significant change of cell membrane integrity. Results of pure mitochondria detection showed most of them maintained normal deltapsim. According to above results, we concluded DEX could reduce mitochondria number when inducing mouse thymocyte apoptosis; and the remaining ones maintain normal function to meet the energy need for apoptotic process.