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BACKGROUND Sedation with propofol injections is associated with a risk of addiction, but remimazolam benzenesulfonate is a comparable anesthetic with a short elimination half-life and independence from cell P450 enzyme metabolism. Compared to remimazolam, remimazolam benzenesulfonate has a faster effect, is more quickly metabolized, produces inactive metabolites and has weak drug interactions. Thus, remimazolam benzenesulfonate has good effectiveness and safety for diagnostic and operational sedation. AIM To investigate the clinical value of remimazolam benzenesulfonate in cardiac surgery patients under general anesthesia. METHODS A total of 80 patients who underwent surgery in the Department of Cardiothoracic Surgery from August 2020 to April 2021 were included in the study. Using a random number table, patients were divided into two anesthesia induction groups of 40 patients each: remimazolam (0.3 mg/kg remimazolam benzenesulfonate) and propofol (1.5 mg/kg propofol). Hemodynamic parameters, inflammatory stress response indices, respiratory function indices, perioperative indices and adverse reactions in the two groups were monitored over time for comparison. RESULTS At pre-anesthesia induction, the remimazolam and propofol groups did not differ regarding heart rate, mean arterial pressure, cardiac index or volume per wave index. After endotracheal intubation and when the sternum was cut off, mean arterial pressure and volume per wave index were significantly higher in the remimazolam group than in the propofol group (P < 0.05). After endotracheal intubation, the oxygenation index and the respiratory index did not differ between the groups. After endotracheal intubation and when the sternum was cut off, the oxygenation index values were significantly higher in the remimazolam group than in the propofol group (P < 0.05). Serum interleukin-6 and tumor necrosis factor-α levels 12 h after surgery were significantly higher than before surgery in both groups (P < 0.05). The observation indices were re-examined 2 h after surgery, and the epinephrine, cortisol and blood glucose levels were significantly higher in the remimazolam group than in the propofol group (P < 0.05). The recovery and extubation times were significantly lower in the remimazolam group than in the propofol group (P < 0.05); there were significantly fewer adverse reactions in the remimazolam group (10.00%) than in the propofol group (30.00%; P < 0.05). CONCLUSION Compared with propofol, remimazolam benzenesulfonate benefited cardiac surgery patients under general anesthesia by reducing hemodynamic fluctuations. Remimazolam benzenesulfonate influenced the surgical stress response and respiratory function, thereby reducing anesthesia-related adverse reactions.

The widespread use of therapeutic glucocorticoids has increased the incidences of glucocorticoid-induced osteoporosis (GIOP). Oxidative stress and mitochondrial dysfunction are major causes of GIOP; therefore, alleviation of excess oxidative stress in osteoblasts is a potential therapeutic strategy for osteoporosis. Exosomes derived from ADSCs (ADSCs-Exos), as novel cell-free therapeutics, can modulate various biological processes, such as immunomodulation, reduce oxidative damage, and promote tissue repair as well as regeneration. In this study, ADSCs-Exos restored the viability and osteogenic potential of MC3T3-E1 cells by attenuating apoptosis, oxidative damage, intracellular ROS generation, and mitochondrial dysfunction. Moreover, after pretreatment with ADSCs-Exos, Nrf2 expressions were upregulated in Dex-stimulated osteoblasts. Inhibitory assays showed that silencing Nrf2 partially eliminated the protective effects of ADSCs-Exos. The rat model assays confirmed that ADSCs-Exos alleviated the Dex-induced increase in oxidation levels, restored bone mass of the distal femur, and increased the expressions of Nrf2 and osteogenic markers in bone tissues. Thus, ADSCs-Exos alleviated apoptosis and oxidative stress by regulating Nrf2/HO-1 expressions after Dex and prevented the development of GIOP in vivo.

Background Propofol is an intravenous anesthetic agent that commonly induces significant neuroapoptosis. MicroRNAs (miRNAs) have been reported to participate in the regulation of propofol exposure-mediated neurotoxicity. MiR-215, as one of miRNAs, was found to regulate nerve cell survival. However, the mechanism through which miRNAs regulate propofol exposure-mediated neurotoxicity is still unclear. Methods Real-time PCR was used to detect miR-215 expression level. Cell viability was measured using MTT assay. Cell apoptosis was examined via flow cytometry analysis. ROS, MDA, LDH and SOD levels were assayed through ELISA kits. Dual luciferase reporter assay identified the interaction between miR-215 and large tumor suppressor 2 (LATS2). Protein level was detected using western blot analysis. Results MiR-215 expression was downregulated in propofol-treated rat hippocampal neurons. MiR-215 mimics promoted cell viability and reduced apoptosis in propofol-treated neonatal rat hippocampal neuron. MiR-215 mimics also caused inhibition of oxidative stress as evidenced by suppression of ROS, MDA and LDH levels as well as increase of SOD level. In addition, we found that large tumor suppressor 2 (LATS2) is a target of miR-215 and miR-215 mimics decreased LATS2 level in propofol-treated neonatal rat hippocampal neuron. Further, LATS2 overexpression suppressed the effect of miR-215 on propofol-induced apoptosis and oxidative stress in neonatal rat hippocampal neuron. Conclusion Taken together, we demonstrate that miR-215 attenuates propofol-induced apoptosis and oxidative stress in neonatal rat hippocampal neuron by targeting LATS2, suggesting that miR-215 may provide a new candidate for the treatment of propofol exposure-induced neurotoxicity.

Objective: To study the correlation of Doppler ultrasound parameters with angiogenesis and cancer cell growth in endometrial cancer. Methods: Patients with endometrial cancer and fibroids who accepted surgical resection in the Central Hospital of Enshi Autonomous Prefecture between March 2015 and June 2017 were selected as the research subjects and enrolled in the observation group and control group of the study respectively. The preoperative pelvic Doppler ultrasonography was done to determine the blood flow parameters resistance index (RI) and pulsatility index (PI) of the endometrial lesions; after surgical resection, the endometrial cancer lesion tissue was collected from the observation group and normal endometrial tissue was collected from the control group to determine the contents of proproliferation molecules, pro-invasion molecules and angiogenesis molecules. Results: PI and RI levels in endometrial cancer lesion of observation group were significantly lower than those of control group, and cIAP1, cIAP2, RLIP76, p-Pak4ser474, EFEMP2, CXCR4, CXCR7, Snail, Septin-9, β-arrestin2 and SOX2 protein levels in endometrial cancer lesion were significantly higher than those of control group; PI and RI levels in endometrial cancer lesion were negatively correlated with cIAP1, cIAP2, RLIP76, p-Pak4ser474, EFEMP2, CXCR4, CXCR7, Snail, Septin-9, β-arrestin2 and SOX2 protein levels. Conclusion: The Doppler ultrasound parameters of endometrial carcinoma lesion are closely related to the angiogenesis and cancer cell growth in the lesion.

Objective: To measure the contrast-enhanced ultrasound parameters of endometrial benign and malignant lesions and investigate their correlation with malignant molecule expression. Methods: A total of 118 patients who were examined and diagnosed with endometrial benign hyperplasia in the hospital between December 2012 and January 2017 were collected as endometrial hyperplasia group, and 67 patients with endometrial carcinoma were collected as endometrial cancer group. The differences in the levels of uterine contrast-enhanced ultrasound parameters as well as the expression of proliferation, apoptosis and invasion genes in endometrial lesion tissue were compared between the two groups. Pearson test was used to evaluate the correlation between uterine contrast-enhanced ultrasound parameters and malignant molecule expression in the lesions. Results: Contrast-enhanced ultrasound parameter TTP level of endometrial cancer group was lower than that of endometrial hyperplasia group whereas PI level was higher than that of endometrial hyperplasia group. Proliferation gene EFEMP2 mRNA expression in lesion tissue of endometrial cancer group was lower than that of endometrial hyperplasia group whereas RRM2 and DJ-1 mRNA expression were higher than those of endometrial hyperplasia group; apoptosis genes P53, c-myc and Livin mRNA expression were higher than those of endometrial hyperplasia group whereas Caspase-3 and Bid mRNA expression were lower than those of endometrial hyperplasia group; invasion gene DKK1 mRNA expression was lower than that of endometrial hyperplasia group whereas HMGB1, EZH2 and Snail mRNA expression were higher than those of endometrial hyperplasia group. Pearson test showed that the contrast-enhanced ultrasound parameter levels of endometrial cancer were directly correlated with the malignant molecule expression in the lesion tissues. Conclusion: contrast-enhanced ultrasound parameter levels can be used to identify endometrial benign and malignant lesions and are directly correlated with the severity of the lesion.