[Gambogic acid induces apoptosis of Jurkat cell through the MAPK signal pathway].

The aim of this study was to investigate the apoptosis-inducing effect of gambogic acid (GA) on Jurkat cells and its underlying signaling pathway. Apoptosis induced by GA and some inhibitors was assayed by Annexin V/PI doubling staining. The levels of caspase 3, caspase 8 and caspase 9 activated in living Jurkat cells were measured by flow cytometry. The expressions of caspase 3, caspase 9, p-JNK and P38 were detected by Western blot. The results showed that GA induced apoptosis of Jurkat cells in a dose-dependent manner. The positive cell number of activated caspase 3, caspase 8, caspase 9 and the levels of activated caspase 3, caspase 9, p-JNK, P38 increased after Jurkat cells were treated with GA. ROS, CaMKII, caspase 3, caspase 9, MAPKK, JNK1/2 and P38 inhibitors had some significant effect on GA-induced apoptosis. ROS, CaMKII, MAPKK, JNK1/2 and P38 inhibitors decreased the levels of activated caspase 3, caspase 9 by GA.ROS, CaMKII, MAPKK, JNK1/2 inhibitors decreased the levels of p-JNK by GA. ROS, CaMKII, MAPKK, P38 inhibitors decreased the levels of P38 by GA. It is concluded that GA induced apoptosis of Jurkat cells by activated caspases through activating of ROS-CaMKII-MAPKK-JNK/P38 pathway.

[The relationship between polymorphism of genes XPA, XPC, XPD, XRCC1 and susceptibility to acute lymphoblastic leukemia].

OBJECTIVE: To study the relationship between polymorphism of genes XPA, XPC, XPD, XRCC1 and susceptibility to acute lymphoblastic leukemia (ALL) in a Chinese population. METHODS: Polymorphism were determined by a case-control study through matrix-assisted laser desorption/ionization tandem time-of-flight mass spectrometry method of Mass-ASSAY platform in 114 confirmed ALL cases and 169 age- and sex-matched controls, so as to compare the relationship between different genotypes and ALL risk. RESULTS: Multivariate logistic regression analysis revealed that individuals carrying at least one 23G variant allele (AG/GG genotypes) had a significantly increased risk for ALL (adjusted OR 2.02; 95%CI 1.08 - 3.78) compared with the wild-type genotype (23AA), and evidence that positive interactions between the polymorphisms in XPC C499T and XPA A23G might occur. Furthermore, individuals with both putative risk genotypes had a significantly higher risk (adjusted OR 5.60; 95%CI 1.57 - 19.90), compared with those with both wild-genotypes. By contrast, no significant association was observed between the XPD T751G, XRCC1 G399A, C194T polymorphism and ALL risk. CONCLUSIONS: XPA A23G and XPC C499T polymorphism may contribute to the risk of developing ALL. There are significant combinations between XPC C499T and XPA A23G.