ABSTRACT
To investigate the therapeutic effect of peroxiredoxin-6(PRDX6)on ultraviolet-induced corneal injury in rats and explore the mechanism.The rat model of corneal injury was established by exposing to ultravio-let.Male wister rats were randomly divided into control groups,dexamethasone (DXM)groups and PRDX6 groups,the rats were administered four times a day and for 12 days.The corneal opacity was observed with a slit-lamp microscope.Histopathologic changes were observed with light microscopy.The content of corneal malonalde-hyde(MDA)was determined by thiobarbituric acid test and the total antioxidative capacity(TAOC)was detected by chemical colorimetric test.P38 MAPK signal pathway was detected with the method of Western blot and the gene expression of cytokines were measured by RT-PCR method.Compared with the control group,PRDX6 treat-ment significantly reduced corneal opacity,improved corneal pathology injury,decreased the MDA content and in-creased the TAOC.In the PRDX6 group the level of phosphorylated p38 protein was significantly lower than that in the control group.The gene expression of cytokine were different between control and PRDX6 groups(P <0.05).PRDX6 showed therapeutic effect in the rat model of ultraviolet-induced corneal injury.This maybe be concerned with that it could alleviated the oxidative damage,suppressed p38 MAPK phosphorylation and regulate the gene expression of cytokine.
ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of chromomycin A(2) in inducing apoptosis of HepG2 cells and explore the molecular mechanism.</p><p><b>METHODS</b>HepG2, MCF-7, A549, and 7901 cells were exposed to chromomycin A(2) and the changes in the cell viability were detected using MTT assay. The changes in the chromatins were observed with laser scanning confocal microscope after incubation of the cells with chromomycin A(2) (60 nmol/L) for 24 h. The changes in cell morphology were examined with a phase-contrast microscope, and the apoptotic cell populations, fluorescent intensity of reactive oxygen species (ROS) and mitochondrial membrane potential were determined using flow cytometry.</p><p><b>RESULTS</b>Chromomycin A(2) significantly inhibited the proliferation of the cells in a time- and dose-dependent manner, and caused changes in the cell morphology and cell apoptosis. Exposure of the cells to chromomycin A(2) resulted in chromatin condensation, ROS generation, and reduction of the mitochondrial membrane potential.</p><p><b>CONCLUSION</b>Increased ROS and mitochondria damage may importantly contribute to chromomycin A(2)-induced apoptosis in HepG2 cells.</p>
Subject(s)
Humans , Apoptosis , Cell Survival , Hep G2 Cells , Membrane Potential, Mitochondrial , Mitochondria , Pathology , Plicamycin , Pharmacology , Reactive Oxygen Species , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To study the expression and regulation of heat shock protein 90β (HSP90β) in the testis, epididymis and sperms of mice.</p><p><b>METHODS</b>The localization and expression of HSP90β mRNA and protein were investigated in the testis, epididymis and sperms of mice, and the regulation of HSP90β in the male reproductive system was explored.</p><p><b>RESULTS</b>HSP90β was expressed at a higher level in the epididymis than in the testis. In the sperms of the mice, HSP90β was localized in the acrosome area. The expression of HSP90β in mouse epididymis decreased after castration and recovered the normal level after testosterone treatment. HSP90β expression in the testis and epididymis also underwent changes during the postnatal development of the mice.</p><p><b>CONCLUSION</b>HSP90β may play an important role in spermiogenesis and fertilization, and its expression pattern in the epididymis after castration and during the postnatal development suggests its regulation by hormones and development.</p>