[Effect of dihydroartemisinin on the expression of BCR/ABL fusion gene in leukemia K562 cells].

OBJECTIVE: To investigate the effect of dihydroartemisinin (DHA) on the BCR/ABL fusion gene in leukemia K562 cell. METHODS: K562 cells were cultured in vitro. The rate of proliferation inhibition of cells treated with various concentrations of DHA were determined by using [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT) method. Expression of BCR/ABL fusion gene was analyzed by reverse transcription(RT-PCR) before and after DHA treatment. Apoptosis of K562 cells was detected by flow cytometry. RESULTS: The growth of K562 cells was inhibited when the concentrations of DHA were 10-160 umol/L. With the added dose of DHA, the growth inhibition was remarkable, with the rate of inhibition risen from 52.76% to 94.65%. The expression of BCR/ABL fusion gene, as detected by RT-PCR after incubating the K562 cells with 20 umol/L DHA, measured as ΔCt = 4.45 ± 0.25 after 12 h and ΔCt = 5.23 ± 0.21 after 24 h, which was significantly lower compared with that of the control ( ΔCt = 4.23 ± 0.21, P < 0.05). CONCLUSION: DHA can inhibit the proliferation of leukemia K562 cells and facilitate the induction of apoptosis by downregulating the expression of BCR/ABL fusion gene.

Detection of human herpes virus 6B in patients with mesial temporal lobe epilepsy in West China and the possible association with elevated NF-κB expression.

BACKGROUND: There has been a long-standing suspicion that an association exists between mesial temporal lobe epilepsy (MTLE) and the herpes virus. Evidence for HHV-6B involvement has been reported. However, no investigation has been performed in China. METHODS: We used nested PCR and immunohistochemistry to detect viral DNA of human herpes virus (HHV)-6B, HHV-6A, herpes simplex virus (HSV)-1 and HSV-2 in resected brain tissues from patients with MTLE and control. A principal transcription factor, NF-κB, that is associated with the inflammatory response was also investigated by real-time PCR, western blotting and immunohistochemistry. RESULTS: HHV-6B DNA was detected in hippocampal samples from 9 out of 32 (28.1%) patients with MTLE and in 1 of 12 (8.3%) control samples. Immunoreactivity for HHV-6B was consistently present in MTLE patients positive for HHV-6 detected by PCR. Significant staining for HHV-6B antigen was distributed mainly around or in the nucleus of cells that morphologically resembled astrocytes and microglia. HHV-6B positivity was related to febrile convulsion history of patients with MTLE. The expression of NF-κB was up-regulated and distributed in the nucleus of glial cells in MTLE patients positive for HHV-6B. CONCLUSION: This study was first to find HHV-6B in MTLE patients from West China and demonstrate a possible association between HHV-6B positivity and activation of NF-κB. The detailed role of HHV-6B and its association with NF-κB in the development of chronic MTLE requires further investigation.