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1.  Study on the Apoptosis Mechanism Induced by T-2 Toxin 
PLoS ONE  2013;8(12):e83105.
T-2 toxin is known to induce apoptosis in mammalian cells. The mechanism of apoptosis induced by T-2 toxin has been proposed to be linked with oxidative stress and mitochondrial pathway. In the current study, the toxic effect of T-2 on Hela, Bel-7402, and Chang liver cells was examined in dose-dependent and time-dependent manner by MTT assay. Caspase-3 was found to be up-regulated under T-2 toxin stress, which suggested that T-2 toxin induced cell apoptosis. Endogenous GSH and MDA levels in all three cell lines were found down- and up-regulated respectively, which indicated the link between toxic effect of T-2 toxin and intracellular oxidative stress. It was also found by MTT assay that NAC, which maintained the level of GSH in cells, could protect cells from death. Western-blot result showed that the level of both activated Caspase-8 and Caspase-9 increased when cells were treated by T-2 toxin. Caspase-9 was found to be activated earlier than Caspase-8. It was also found that p53 was up-regulated under T-2 toxin stress in the study. These results implied that the effect of T-2 toxin on cells was apoptosis rather than necrosis, and it was probably induced through mitochondrial pathway. To the best of our knowledge, the present study is the first to show that JunD is down-regulated in T-2 toxin induced apoptosis. By construction of an over-expression vector for the JunD gene, we observed that the survival ratio of JunD over-expressed cells obviously increased under T-2 toxin stress. These results suggested that the mechanism of T-2 induced cell death was closely connected with oxidative stress, and that JunD plays an important role in the defensive process against T-2 toxin stress.
doi:10.1371/journal.pone.0083105
PMCID: PMC3873290  PMID: 24386148
2.  Thrombolytic effects of Douchi Fibrinolytic enzyme from Bacillus subtilis LD-8547 in vitro and in vivo 
BMC Biotechnology  2012;12:36.
Background
Today, thrombosis is one of the most widely occurring diseases in modern life. Drugs with thrombolytic functions are the most effective methods in the treatment of thrombosis. Among them, Douchi fibrinolytic enzyme (DFE) is a promising agent. DFE was isolated from Douchi, a typical and popular soybean-fermented food in China, and it can dissolve fibrin directly and efficiently. A strain, Bacillus subtilis LD-8547 produced DFE with high fibrinolytic activity has been isolated in our lab previously.
Results
In the study, thrombolytic effect of DFE from Bacillus subtilis LD-8547 was studied in vitro and in vivo systematically. The results showed that DFE played a significant role in thrombolysis and anticoagulation in vitro. And the thrombolytic effects correlated with DFE in a dose-dependent manner. In vivo, the acute toxicity assay showed that DFE had no obvious acute toxicity to mice. Test of carrageenan-induced thrombosis in mice indicated that the DFE significantly prevented tail thrombosis, and arterial thrombosis model test indicated that Douchi fibrinolytic enzyme DFE had thrombolytic effect on carotid thrombosis of rabbits in vivo. Other results in vivo indicated that DFE could increase bleeding and clotting time obviously.
Conclusions
The DFE isolated from Bacillus subtilis LD-8547 has obvious thrombolytic effects in vitro and in vivo. This function demonstrates that this enzyme can be a useful tool for preventing and treating clinical thrombus.
doi:10.1186/1472-6750-12-36
PMCID: PMC3434014  PMID: 22748219
Thrombolytic effects; Douchi Fibrinolytic enzyme; in vitro; in vivo

Results 1-2 (2)