Psychological factors increase the risk of ovarian cancer.

This study evaluated whether psychological stress increases the incidence of ovarian cancer. A literature search of the electronic databases PubMed and Web of Science from the date of inception to August 2022 was undertaken. Studies with data on psychosocial factors associated with ovarian cancer incidence were included in this study. A random-effect model meta-analysis was undertaken to estimate these data. We used subgroup analysis to adjust for heterogeneity. A total of 4 articles, 10 sets of data, 8 cohort studies, and 2 case-control studies from 682 records were included in this review. Meta-analyses of the included cohort study subgroups suggested that psychological factors increase the risk of ovarian cancer (effect size = 1.37, 95% CI: 1.20-1.53); the subgroup of case-control studies suggested that psychological factors did not increase ovarian cancer risk (effect size = 0.84, 95% CI: 0.70-0.98). These findings indicate that psychological stress is a possible new risk factor for ovarian cancer.Prospero registration number: CRD42022357983IMPACT STATEMENTWhat is already known on this subject? Psychological stress has been shown to increase the risk of many diseases. The relationship between psychological stress and the incidence of ovarian cancer has not been confirmed.What do the results of this study add? The effect of psychological stress on the risk of ovarian cancer was estimated using meta-analysis as an overall ratio.What are the implications of these findings for clinical practice and/or further research? Relaxing psychological stress and appropriate psychotherapy in clinical settings can help reduce the risk of ovarian cancer.

Astragaloside IV inhibits adenovirus replication and apoptosis in A549 cells in vitro.

OBJECTIVES: Astragaloside IV, purified from the Chinese medical herb Astragalus membranaceus (Fisch) Bge and Astragalus caspicus Bieb, is an important natural product with multiple pharmacological actions. This study investigated the anti-ADVs effect of astragaloside IV on HAdV-3 (human adenovirus type 3) in A549 cell. METHODS: CPE, MTT, quantitative real-time PCR (qPCR), flow cytometry (FCM) and Western blot were apply to detect the cytotoxicity, the inhibition and the mechanisms of astragaloside IV on HAdV-3. KEY FINDINGS: TC(0 ) of astragaloside IV was 116.8 µm, the virus inhibition rate from 15.98% to 65.68% positively was correlated with the concentration of astragaloside IV from 1.25 µm to 80 µm, IC50 (the medium inhibitory concentration) was 23.85 µm, LC50 (lethal dose 50% concentration) was 865.26 µm and the TI (therapeutic index) was 36.28. qPCR result showed astragaloside IV inhibited the replication of HAdV-3. Flow FCM analysis demonstrated that the anti-HAdV-3 effect was associated with apoptosis. Astragaloside IV was further detected to reduce the protein expressions of Bax and Caspase-3 and increasing the protein expressions of Bcl-2 using western blotting, which improved the anti-apoptosis mechanism of astragaloside IV on HAdV-3. CONCLUSIONS: Our findings suggested that astragaloside IV possessed anti-HAdV-3 capabilities and the underlying mechanisms might involve inhibiting HAdV-3 replication and HAdV-3-induced apoptosis.

Anti-adenovirus activities of shikonin, a component of Chinese herbal medicine in vitro.

Radix Lithosperm eyrthrorhizon is a common prescription compound in traditional Chinese medicine. Shikonin is a major component of Radix Lithospermi and has various biological activities. We have investigated the inhibitory effect of shikonin on the growth of adenovirus type 3 (AdV3) in vitro. The antiviral function of shikonin against AdV3 and its virus inhibition ratio were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method (MTT). The expression of hexon protein in AdV3 was determined by immunofluorescence assay using laser scanning confocal microscopy (LSCM) and Western blot analysis. In addition, the rate of apoptosis in cells infected by AdV3 was determined by flow cytometry. Shikonin (0.0156-1 µM) inhibited growth of AdV3 in a concentration-dependent manner with a virus inhibition rate of 23.8-69.1%. Expression of hexon protein in AdV3 was higher in the virus control group than in the shikonin-treated groups as determined by immunofluorescence assay and Western blotting (p<0.05). The rate of shikonin-treated HeLa cell apoptosis had a statistically significant decrease with increasing concentration of drug (p<0.05). Our data demonstrate that shikonin possesses anti-AdV3 capabilities and that the potential antiviral mechanism might involve inhibiting the degree of apoptosis and hexon protein expression of AdV.