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Purpose: To verify whether there is lower incidence of adverse pregnancy outcomes after high-intensity focused ultrasound (HIFU) treatment than loop electrosurgical excision procedure (LEEP) in young women of childbearing age. Patients and Methods: This retrospective cohort study enrolled 46 patients treated with HIFU and 46 patients treated with LEEP. To compare the differences between the two groups, Fisher's exact test or the Kruskal–Wallis (K-W/H) test was used in the univariate analysis, while the logistic regression method was applied for further verification. Results: Basic characteristics showed no differences between the two groups (P > 0.05) except for parity (P < 0.001). Preterm birth rates were 6.52% and 0.00% in patients with cervical high-grade squamous intraepithelial lesions (HSIL) treated with LEEP and HIFU, respectively. The incidence rates of premature rupture of membranes (PROM) were respectively 15.22% and 21.74% in the two groups. There was no significant difference in pregnancy outcomes between the two groups (P > 0.05). Conclusion: This study is the first to compare the pregnancy outcomes of patients with cervical HSIL who treated with LEEP and HIFU procedures. Both HIFU treatment and LEEP are available options for patients of reproductive age with cervical HSIL. Therefore, it is necessary to conduct prospective single-center or multicenter randomized controlled studies. [ABSTRACT FROM AUTHOR]

Lappaol F (LAF), a natural lignan from Arctium lappa Linné (Asteraceae), inhibits tumor cell growth in vitro and in vivo. The underlying mechanism involves the suppression of the Yes-associated protein. However, the specific role of LAF in cell cycle regulation remains unknown. This study determined the molecular mechanism by which LAF regulates cell cycle progression. Various colon cancer cell lines (SW480, HCT15, and HCT116) were treated with LAF (25, 50, and 75 μmol/L) for 48 h. The effects of LAF on cell proliferation and cell cycle were determined using sulforhodamine B and flow cytometry assays. Differentially expressed proteins (DEPs) were identified using quantitative proteomics. Bioinformatic analysis of DEPs was conducted via Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Expression levels of DEPs in the cell cycle pathway were analyzed using RT-qPCR and western blotting. LAF suppressed the proliferation of SW480, HCT15, and HCT116 cells (IC50 47.1, 51.4, and 32.8 μmol/L, respectively) and induced cell cycle arrest at the S phase. A total of 6331 proteins were identified and quantified, of which 127 were differentially expressed between the LAF-treated and untreated groups. GO and KEGG enrichment analyses revealed that DEPs mainly participated in the cell cycle. CDKN1C/p57 showed the most significant differential expression, with the highest fold-change (3.155-fold). Knockdown of CDKN1C/p57 attenuated the S phase cell cycle arrest and proliferation inhibition induced by LAF. LAF exerts antitumor effects via S phase arrest by activating CDKN1C/p57 in colorectal cancer cells. [ABSTRACT FROM AUTHOR]

Objectives: Neuroprotective potential of 7‐methoxyflavanone (7MF) and its underlying mechanism was investigated. Methods: Inhibitory effects of 7MF on microglial activation and neuroinflammation were evaluated by employment of lipopolysaccharide (LPS)‐induced BV2 microglial cells. Changes in expression of genes and proteins of interest were investigated by RT‐qPCR analysis and Western blot analysis. Inhibitory effects of 7MF on microglial overactivation were verified in LPS‐treated C57BL/6J mice using ionized calcium‐binding adaptor molecule‐1 (Iba1) in the brain and interleukin‐6 (IL‐6) in serum as indicators. Key findings: In BV2 cells, pretreatment with 7MF antagonized LPS‐induced production of inflammatory factors IL‐6, tumour necrosis factor‐α (TNF‐α), cyclooxygenase‐2 (COX‐2), inducible nitric oxide synthase (iNOS), intercellular adhesion molecule‐1 (ICAM‐1) and monocyte chemoattractant protein‐1 (MCP‐1). Mechanistic studies revealed reduced expression of Toll‐like receptor 4 (TLR4), myeloid differentiation factor‐88 (MyD88), phosphorylated forms of c‐Jun N‐terminal kinase (p‐JNK) and extracellular signal‐regulated kinases 1/2 (p‐ERK) but increased nuclear accumulation of nuclear factor erythroid 2‐related factor 2 (Nrf2) and cellular expression of NAD(P)H quinone dehydrogenase‐1 (NQO‐1) by 7MF. In LPS‐treated mice, pretreatment with 7MF reduced the brain level of Iba1 and serum level of IL‐6. Conclusions: 7‐methoxyflavanone inhibited LPS‐stimulated TLR4/MyD88/MAPK signalling and activated Nrf2‐mediated transcription of antioxidant protein NQO‐1, showing antineuroinflammatory effect, so it is a potential neuroprotective agent. [ABSTRACT FROM AUTHOR]