RESUMO
Objective@#To analyze the effect of human papillomavirus (HPV) detection and cervical cell basal fluid on the early diagnosis of cervical precancerous lesions.@*Methods@#From January 2016 to January 2017, 223 patients in the Maternal and Child Health Care Hospital of Yongkang who received gynecological cervical cancer precancerous lesions screening were selected.All patients into the outpatient screening categories were given cervical liquid-based cytology (TCT) examination and HPV detection, 61 patients with test results of double positive received colposcopy cervical biopsy histopathological examination, the final diagnosis of 49 patients with epithelial cell changes.The accuracy and sensitivity of different detection methods were compared.@*Results@#The detection rates of high risk HPV infection in cervicitis, CINⅠ, CINⅡ-CINⅢ and cervical cancer patients were 16.22%, 39.29%, 71.43% and 100.00% in 223 cases of this study.The total positive rate of TCT was 28.57%.The total positive rate was 44.44% in HPV group and 75.51% in combination test.The positive rate of combined detection was higher than TCT (χ2=21.63, P=0.000) and HPV (χ2=25.51, P=0.000), the difference was statistically significant.For ASC patients, the sensitivity of TCT, HPV and combined detection was 57.14%, 64.29% and 85.71%, respectively.The accuracy of TCT, HPV and combined detection was 64.29%, 71.43% and 92.86%, respectively.The sensitivity of combined detection was similar to TCT (χ2=2.13, P=0.140) and HPV (χ2=1.25, P=0.260). The accuracy of combined detection was similar to TCT (χ2=2.33, P=0.130) and HPV (χ2=1.39, P=0.240). For LISIL patients, the sensitivity of TCT, HPV and combined detection was 56.25%, 62.50% and 87.50%, respectively, the accuracy was 68.75%, 75.00% and 93.75%, respectively.The sensitivity of the combined test group was higher than that of TCT (χ2=3.86, P=0.049) and HPV (χ2=4.57, P=0.033), and the accuracy of combined test was higher than that of TCT (χ2=3.902, P=0.048) and that of HPV (χ2=4.13, P=0.034). For HISIL typing patients, the sensitivity of TCT, HPV and combined detection was 57.89%, 63.16% and 89.43%, respectively, and the accuracy was 73.68%, 78.95% and 94.74%, respectively.The sensitivity of the combined test group was higher than that of TCT (χ2=4.89, P=0.027) and that of HPV (χ2=3.99, P=0.047), and the accuracy of combined test was higher than that of TCT (χ2=3.99, P=0.048) and that of HPV (χ2=5.34, P=0.027).@*Conclusion@#High-risk HPV detection combined with TCT in the screen of cervical cancer precancerous lesions is simple and efficient, taking into account the accuracy and sensitivity, it can reduce the rate of missed diagnosis, has a positive effect on prevention and control of cervical cancer.
RESUMO
Aim To investigate Jaridonin′s selective killing of cancer cells and explore the related molecular mechanism. Methods After treatment by Jaridonin for 24 h, the effect of Jaridonin on the cell viability was examined using MTT assay. The effect of Jaridonin on cytomorphology and mitochondrial membrane poten-tial (Δψm) was observed by a fluorescence microsco-py. The apoptosis of cell lines treated with Jaridonin, as well as the level of reactive oxygen species ( ROS ) was analyzed by flow cytometry. Expression of the pro-teins related with mitochondria apoptosis pathways was detected by Western blot. Results Jaridonin caused strong antiproliferative and apoptotic effects on MGC-803 cells, but there were not remarkable effects on GES-1 cells. Furthermore, the expression of Bax was up-regulated, and the release of cytochrome c from mi-tochondria to cytosol was also promoted in MGC-803 cells treated by Jaridonin. The cleavage of caspase-3 in MGC-803 cells was also observed. Jaridonin increased persistently intracellular levels of ROS in MGC-803 cells, whereas the level of ROS in GES-1 rose in the first stage, and then decreased, and dropped to the basic level after 6 h. More interestingly, Jaridonin-in-duced ROS accumulation and the inhibition of MGC-803 cell proliferation were almost completely attenuated in the presence of GSH. Conclusions Jaridonin se-lectively kills cancer cells and induces apoptosis in MGC-803 through ROS-mediated mitochondrial dam-age.
RESUMO
<p><b>OBJECTIVE</b>The aim of this study was to explore the molecular mechanism of apoptosis in esophageal cancer cells induced by Isodon rubescens.</p><p><b>METHODS</b>The DNA-damage effect of Jaridonin was detected by single cell gel electrophoresis (SCGE). The p53 protein was determined by Western blot. GSH assay kit was employed to determine the GSH content in human esophageal cancer EC-1 cells. Intracellular levels of hydrogen peroxide (H2O2) or superoxide (O(2).-) were determined using the redox-sensitive probes 2', 7'-dichlorodihydrofluorescein diacetate (DCF) or dihydroethidium (DHE), and the fluorescence signal was assayed by fluorescence microscopy and by flow cytometry.</p><p><b>RESULTS</b>Jaridonin induced DNA damage in EC-1 cells remarkably. The olive tail moments (OTM) of control and 20, 40 µmol/L Jaridonin were 3.2, 45.2 and 89.0, respectively. Compared with the control, the differences were significant (P < 0.01 for both). Jaridonin resulted in extensive p53 up-regulation in the EC-1 cells. More importantly, the p53 up-regulation occurred as early as 2 h after Jaridonin incubation, and in a time-dependent manner (P < 0.05). p53 siRNA transfection inhibited apoptosis in the EC-1 cells, and the Jaridonin-induced apoptosis rate was reduced from 38.5% to 8.8%. Intracellular level of H2O2 was increased by Jaridonin, whereas the level of O(2).- was barely changed. The GSH content in EC-1 cells was reduced from (10.3 ± 1.6) nmol/mg protein to (4.6 ± 2.1) nmol/mg protein after 20 µmol/L Jaridonin incubation for 8 h, and it was further reduced with the increase of Jaridonin concentration. Jaridonin induced DNA damage, H2O2 accumulation and apoptosis were significantly attenuated in the presence of GSH, but Jaridonin showed little effect on normal human liver L-02 cells.</p><p><b>CONCLUSIONS</b>Jaridonin selectively induces apoptosis in esophageal cancer EC-1 cells through H2O2-mediated DNA damage by depleting GSH.</p>