A b s t r a c tIntroduction: Ovarian cancer is one of the leading causes of cancer-related deaths in women. Treatments for ovarian cancer include surgery followed by chemotherapy. However, the survival rate for ovarian cancer is still not satisfactory. Moreover, the current chemotherapy has numerous associated side effects. Therefore there is an urgent need to look for novel and more viable treatment options. Against this backdrop the present study was designed to evaluate the anticancer activity of sugiol against ovarian cancer cells. Material and methods: Cell viability was assessed by CCK8 assay, apoptosis by DAPI, AO/ER and annexin V/PI staining. Mitochondrial membrane potential and cell cycle analysis was performed by flow cytometry. Cell migration was investigated by wound healing assay. Protein expression was monitored by western blotting. Results: The results of the present study indicated that sugiol exerts significant (p < 0.0001) anticancer effects on SKOV3 cancer cells with an IC 50 of 25 μM. However, sugiol exhibited less cytotoxicity against normal ovarian cells with an IC 50 of 62.5 μM. The anticancer effects of sugiol were found to be due to G0/G1 cell cycle arrest and mitochondrial apoptosis. Sugiol also inhibited cell migration of SKOV3 cells dose dependently. Moreover, the results showed that sugiol could inhibit the RAF/MEK/ERK signalling pathway in a dose-dependent manner. Conclusions:The results of the present study indicate that sugiol exerts potent anticancer effects on SKOV3 cells via induction of cell cycle arrest, mitochondrial apoptosis and inhibition of the RAF/MEK/ERK signalling pathway.
Objective: The purpose of the study was to investigate the association between macrophage migration inhibitory factor (MIF) gene polymorphisms and gestational diabetes mellitus (GDM) in Han Chinese women. Methods: In this study, 915 unrelated pregnant women were recruited, among whom 430 had GDM and 485 served as controls. The rs755622 in the MIF gene (MIF-173G/C) was detected by the polymerase chain reaction Tm-shift genotyping method with fluorescence melting curve analysis. The associations of rs755622 in MIF variants with plasma glucose and insulin levels in the oral glucose tolerance test (OGTT) as well as with with blood fat levels were investigated. Results: The frequencies of genotypes and allele types of rs755622 in MIF were significantly different between women of the GDM and control groups (all p < 0.001). Moreover, the single nucleotide polymorphism (SNP) was significantly associated with increased glucose levels at 0, 60 and 120 min during the OGTT (all p < 0.0038) and with the increased homeostasis model assessment of insulin resistance (p < 0.001) in the GDM group. Conclusion: Genetic polymorphism of rs755622 in MIF is associated with increased risk of GDM and insulin resistance in Han Chinese women.
<b><i>Background:</i></b>The estrogen receptor α (ERα) gene is a potential candidate gene of gestational diabetes mellitus (GDM). <b><i>Objectives:</i></b> The purpose of the study was to investigate the relationship of ERα gene polymorphism (single nucleotide polymorphism [SNP]) and its expression in placental tissues with the development of GDM. <b><i>Methods:</i></b> The SNPs of PvuII and Xba I in the ERα gene of 175 pregnant women with GDM and 240 healthy pregnant women were detected by polymerase chain reaction-restriction fragment length polymorphism. Immunohistochemistry and western blotting were used to analyze the expression of the ERα gene in placental tissues. <b><i>Results:</i></b> The results showed that the frequency of the CC + CT genotype and the C allele frequency of PvuII in the GDM group was significantly higher than that of the control group (<i>p</i> < 0.05). There was no significant difference in the genotype distribution and allele frequency of Xba I between the GDM group and control group. The expression of ERα in placental tissues of pregnant women with GDM was higher than that in the control group (<i>p</i> < 0.05). The participants with the PvuII CC + CT genotype had elevated levels of fasting blood glucose, homeostasis model assessment of insulin resistance (IR), and ERα expression in placental tissues compared with those with the TT genotype in the GDM group (<i>p</i> < 0.05). The SNP of Xba I of ERα gene had no correlation with clinical biochemical indicators of GDM and the expression of ERα in placental tissues (<i>p</i> > 0.05). <b><i>Conclusions:</i></b> This study suggested that SNP of the ERα gene and abnormal expression of ERα in placenta tissues were associated with GDM. The C allele of PvuII may be associated with GDM. In addition, SNP of the PvuII site in pregnant women with GDM was related to the degree of IR and to the upregulation of ERα expression in placental tissues, which may play an important role in the pathogenesis of GDM.
Introduction: The environment of the operating room (OR) is closely related to the postoperative complications of patients, and it is necessary to study, to what extent, the stringent management of the OR can reduce postoperative complications. Methodology: 426 patients who underwent surgery between January 2016 and December 2017 were selected from two class-100 laminar flow ORs of equivalent area, and were divided into an experimental group and a control group. Results: The experimental group had significantly lower total air-borne bacterial count in the OR than the control group 10 minutes before surgery (6.21 ± 4.14 vs. 11.58 ± 5.36 CFU/cm3), 10 minutes (15.67 ± 6.21 vs. 20.83 ± 5.78 CFU/cm3), 30 minutes (27.34 ± 8.18 vs. 39.56 ± 7.86 CFU/cm3) and 60 minutes (43.62 ± 7.66 vs. 51.63 ± 8.43 CFU/cm3) into surgery, and at the end of surgery (57.34 ± 7.67 vs. 69.33 ± 9.41 CFU/cm3) (all p < 0.05). The incidence rates of increased body temperature and leukocyte count 3 days post-surgery, and the duration of antibiotic therapy and hospital stay were significantly reduced in the experimental group compared to the control group (all p < 0.05). Furthermore, the total number of pathogens in the incision at 2 hours into surgery was also significantly lower in the experimental group than in the control group (p < 0.05). Conclusion: Stringent application of the infection control pathway is an efficacious measure for improving the air cleanliness of the neurosurgery OR, decreasing the incidence rates of postoperative complications and infection, as well as controlling pathogen transmission.
Insulin-like growth factor II (IGF-II) can stimulate myogenesis and is critically involved in skeletal muscle differentiation. The presence of negative regulators of this process, however, is not well explored. Here, we showed that in myoblast cells, IGF-II negatively regulated peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) mRNA expression, while constitutive expression of PGC-1α induced myoblast differentiation. These results suggest that the negative regulation of PGC-1α by IGF-II may act as a negative feedback mechanism in IGF-II-induced myogenic differentiation. Reporter assays demonstrated that IGF-II suppresses the basal PGC-1α promoter activity. Blocking the IGF-II signaling pathway increased the endogenous PGC-1α levels. In addition, pharmacological inhibition of PI3 kinase activity prevented the downregulation of PGC-1α but the activation of mTOR was not required for this process. Importantly, further analysis showed that forkhead transcription factor FoxO1 contributes to mediating the effects of IGF-II on PGC-1 promoter activity. These findings indicate that IGF-II reduces PGC-1α expression in skeletal muscle cells through a mechanism involving PI3K-Akt-FoxO1 but not p38 MAPK or Erk1/2 MAPK pathways.
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