ABSTRACT
Aim To investigate the effect of progester-one ( PROG) in protecting the neurons against impair-ment induced by the Aβ1-42 activated astrocytes, and the underlying molecular mechanism. Methods The astrocytes were divided into 5 groups: control, Aβ, and Aβplus PROG groups treated with 3 different con-centrations of progesterone for 24h. Then, Aβand pro-gesterone were removed, and neurons were co-cultured with the treated astrocytes. MTT assay was used to e-valuate the viability of cultured neurons; ELISA was used to detect the levels of IL-1βand TNF-αin culture media of astrocytes; immunofluorescence and Western blot were performed to detect the activation of NF-κB in astrocytes. Results PROG dose dependently pro-tected against Aβ1-42 activated astrocytes induced via-bility decrease in co-cultured neurons. Aβ induced release of IL-1β and TNF-α from astrocytes, and in-crease of NF-κB activity was abolished by progesterone treatment. Conclusion PROG protects the neurons through inhibiting the reactivity of astrocytes, and the underlying mechanism involves the NF-κB signal trans-duction.
ABSTRACT
Objective To assess the value of CMV viral load test in the diagnosis and prognostic judgment of infantile cytomegalovirus infection with whole blood and urine specimens. Methods 50 infants with active CMV infection were selected, which pp65 antigen was positive in serological detection and either CMV-IgM positive or the titer of CMV-IgG ≥40. The viral load in whole blood and urine specimens was detected before and after a course of preemptive ganciclovir treatment and the pp65 antigen was determined after treatment. Results 98% patients were manifested as cytomegalovirus viral load quantitative measurement in whole blood positive before the treatment, while 14% after. The positive ratio of pp65 assay after therapy was 6%. And there was no significant difference between the results of the two kinds of detection methods measurement in urine before and after treatment was 98% and 90%, respectively. The results of urinary viral load quantitative detection did not coincide with clinical characteristics of CMV infection (P＜0.05,Sp＝0.11,PVP＝0.55, (Youden's index)＝0.09). Conclusions Good coincidence could be found between CMV-DNA quantitative measurement in whole blood and pp65 antigenemia assay. And the former could be used as a diagnostic index of CMV positive infection. While single urinary viral load quantitative detection had no significance for the distinction between active and latent CMV infection and dynamic monitoring of CMV treatment.