Multiple Protocols Combined with Hyperbaric Oxygen Therapy on the Maintenance of Ovarian Function in Patients After Ovarian Cystectomy.

Objective: This study aims to explore the effect of adjuvant hyperbaric oxygen therapy on ovarian function after laparoscopic ovarian cystectomy. Methods: A total of 60 patients with ovarian cysts treated at our hospital from January 2018 to August 2020 were enrolled. According to the different treatment modalities, the patients were divided into the control and observation groups. Patients in both groups underwent laparoscopic ovarian cystectomy with oral administration of Chinese patent medicine Kuntai capsules after surgery. Hyperbaric oxygen therapy was added to patients in the observation group in addition to the treatment in the control group. The anti-Müllerian hormone (AMH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), and antral follicle count (AFC) serum levels were detected in both groups before the operation and at the first and third menstrual cycles postoperatively to evaluate ovarian function. Results: At the first and third menstrual cycles after surgery, the AMH, E2, and AFC serum levels in the two groups were significantly lower than before surgery, and the FSH and LH serum levels were higher than before surgery. The differences were statistically significant (P < 0.05). After the operation, AMH, E2, and AFC serum levels in the observation group were significantly higher than in the control group. FSH and LH serum levels were significantly lower than in the control group, and the differences were statistically significant (P < 0.05). Conclusion: For patients undergoing laparoscopic ovarian cystectomy, the adjuvant hyperbaric oxygen therapy could significantly improve the postoperative ovarian reserve function with remarkable effects.

Exogenous insulin-like growth factor 1 attenuates sevoflurane anesthesia-induced cognitive dysfunction in aged rats.

Sevoflurane anesthesia is correlated with the generation of postoperative cognitive dysfunction. Insulin-like growth factor 1 (IGF-1) has important function in the nervous system development. Intravenously injected IGF-1 is reported to successfully pass the blood-brain barrier and perform neuroprotection effect in the brain. Memory and learning abilities were analyzed through Morris water maze task. Relative levels of protein were examined through Western blot and enzyme-linked immunosorbent assay (ELISA). Relative mRNA levels were shown through quantitative real-time polymerase chain reaction (qRT-PCR). IGF-1 expression in the plasma and hippocampus was downregulated in sevoflurane anesthesia-induced rats and rescued by intravenous IGF-1 injection. In aged rats, intravenous injection of IGF-1 alleviated sevoflurane-caused cognitive injuries and elevated TNF-α, IL-1ß, and IL-6 levels in the plasma and hippocampus and rescued sevoflurane-depressed Akt phosphorylation. In conclusion, the administration of IGF-1 through intravenous injection alleviates sevoflurane anesthesia-mediated neuroinflammation and cognitive impairment in rats. The effects of IGF-1 in this process may depend on its function in regulating the PI3K/Akt signaling pathway.NEW & NOTEWORTHY IGF-1 expression was downregulated by sevoflurane anesthesia in rats and could be rescued by intravenous IGF-1 injection, which alleviated sevoflurane-caused cognitive injuries and enhanced inflammatory responses in aged rats. Intravenous injection of IGF-1 rescued sevoflurane-depressed Akt phosphorylation in aged rats.

Amplification of lncRNA PVT1 promotes ovarian cancer proliferation by binding to miR-140.

Gene deletion or gene amplification acts as a driving factor of onset, progress, and metastasis in various cancers, including ovarian cancers. By mining the whole genome data of ovarian cancer patients, we identify the long noncoding RNA PVT1 as the most amplified gene. Knockdown of PVT1 was then achieved using a shRNA in two ovarian cancer cell lines, and cell viability was determined by trypan blue exclusion assay, cell metabolism by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, and cell cycle alteration by propidium iodide cell cycle analysis. Potential targeting microRNAs were predicted with starBase v2.0, and direct binding of miR-140 on PVT1 was confirmed by luciferase reporter assay and microRNA pull-down assay. Evolutionary conserved transcription factor-binding site was predicted via rVista 2.0. Our results show that PVT1 was the most amplified gene in ovarian cancer patients, and it was highly correlated with poor survival outcomes. Knockdown of PVT1 caused decreased cell viability, metabolic activity, and smaller proportion of S-phase cells. PVT1 directly bound to miR-140 and acted as a microRNA sponge, while transcription of PVT1 was regulated by the transcription factor FOXO4. In conclusion, viability, metabolism, and cell cycle of ovarian cancers are regulated by the FOXO4/PVT1/miR-140 signaling pathway.

A research on the protein expression of p53, p16, and MDM2 in endometriosis.

This study aims to examine the expression of p53, p16, and murine double minute 2 (MDM2) protein in normal endometrium and endometriosis, in order to discuss the role of p53, p16, and MDM2 protein and apoptosis in the pathogenesis and development of endometriosis, and provide a theoretical basis for clinical diagnosis and treatment.The immunohistochemical streptavidin-biotin peroxidase method was used to detect the expression of p53, p16, and MDM2 in tissue samples obtained from 30 women with pathologically confirmed ovarian endometriosis and 29 women with pathologically confirmed normal endometrium. The relationship between p53, p16, and MDM2 expression and apoptosis was analyzed.In normal endometrium, the positive rate of p53 in the secretory phase was higher than that in the proliferative phase (P < .05). Furthermore, the positive rate of p53 in normal endometrium was higher than that in ovarian endometriosis (P < .05). There was a significant difference between normal endometrium and ovarian endometriosis.The positive rate of p16 in normal endometrium was higher than that in ovarian endometriosis (P < .05). Furthermore, there was a significant difference between normal endometrium and ovarian endometriosis. The positive rate of MDM2 in normal endometrium was lower than that in ovarian endometriosis (P < .05).In ovarian endometriosis, the expression of p53 and p16 was positively correlated with each other (r = 0.611, P < .01). However, the expression of p53 and MDM2 was negatively correlated with each other (r = -0.541, P < .01). Furthermore, the expression of p16 and MDM2 might not be relevant in the endometriosis (r = 0.404, P > .05).As important apoptosis regulatory genes, p53, p16, and MDM2 might be involved in the pathogenesis and development of endometriosis.

Long noncoding RNA LINC00261 regulates endometrial carcinoma progression by modulating miRNA/FOXO1 expression.

Long noncoding RNA LINC00261 was reported to be downregulated in multiple cancers. LINC00261 overexpression inhibits cancer cell proliferation, migration, and invasion. But the expression and function of LIN00261 in endometrial carcinoma are still elusive. We found that LINC00261 mRNA levels were downregulated in endometrial carcinoma, and LINC00261 overexpression inhibited endometrial carcinoma cell proliferation, migration, and invasion. miRNAs, including miR-182, miR-183, miR-153, miR-27a, and miR-96, were predicted to bind LINC00261 and FOXO1, and functioned to attenuate expression of LINC00261 and FOXO1. Overexpressed LINC00261 lowered these dissociative miRNAs, resulting in increase of FOXO1 protein levels. The knockdown of FOXO1 eliminated the suppression effect of overexpressed LINC00261 on endometrial carcinoma cell aggressiveness. LINC00261 promotes FOXO1 expression through reducing FOXO1-targeted miRNAs to suppress endometrial carcinoma cell proliferation, migration, and invasion. SIGNIFICANCE OF THE STUDY: LINC00261 is downregulated in endometrial carcinoma and associated with metastasis of this cancer. LINC00261 elevates FOXO1 protein levels through reducing FOXO1-targeted miRNAs to suppress endometrial carcinoma cell proliferation, migration, and invasion.

A Mechanism Study Underlying the Protective Effects of Cyclosporine-A on Lung Ischemia-Reperfusion Injury.

AIM: This study is aimed at validating the hypothesis that administration of cyclosporine-A (CsA) would be protective in lung ischemia-reperfusion (I/R) injury and in exploring the underlying mechanism. METHODS: Rabbits were divided into 4 groups: the control, sham operation, I/R, and I/R with CsA treatment. Flow cytometry was used to measure the mitochondrial membrane potential. Laser scanning confocal microscope was used to analyze mitochondrion permeability transition pore (MPTP). The apoptotic cell was detected by the TUNEL staining. Western blot was performed to analyze the protein expression levels. RESULTS: CsA not only attenuated the histopathologic alterations in lung and mitochondria after I/R injury, but also attenuated I/R injury through increasing MPP and inhibiting MPTP opening. Besides, CsA attenuated I/R injury through suppressing the release of cytochrome-c (CytC), inhibiting cell apoptosis and decreasing the expression levels of cyclophilin-D (Cyp-D), adenine nucleotide translocase 1 (ANT1) and voltage-dependent anion channel 1 (VDAC1). Finally, we found that Cyp-D knockdown inhibits I/R injury-induced MPTP opening and cell apoptosis. CONCLUSION: Our study found that the protective role of CsA on lung I/R injury depends on the inhibition of MPTP and CytC release, suppression of the activation of mitochondrial apoptosis pathway and the expressions of apoptotic-related proteins, as well as the decreased expression levels of ANT1 and VDAC1.