1.Impact of flash glucose monitoring system on glycemic control in pregnant women with type 2 diabetes mellitus
Zhaoyan ZHANG ; Xiuqing LOU ; Xuefang WANG ; Yue ZHAO ; Xudong SU
Chinese Journal of Diabetes 2024;32(6):418-422
Objective To evaluate the impact of flash glucose monitoring(FGM)system on glycemic control and adverse pregnancy outcome in pregnant women with type 2 diabetes mellitus(T2DM).Methods This prospective,open-label,randomized,controlled clinical trial involved 109 women with T2DM at 16~18 weeks of gestation who visited Liaocheng People's hospital and Liaocheng Women and Children Hospital from June 2018 to June 2022.They were randomly assigned to FGM group(54 cases)and control group(55 cases).The FGM group wore FGM at 20,24,28 and 32 weeks of pregnancy respectively.The Con group underwent self-monitoring of blood glucose(SMBG).Both groups adjusted insulin doses based on blood glucose monitoring results.HbA1c was measured at 18 weeks and 36 weeks of pregnancy.Information related to adverse pregnancy outcomes was compared between the two groups.Results Fasting and postprandial glucose and HbA1c were significantly lower in FGM group compared with con group(P<0.05).Neonatal hypoglycemia was significantly lower in FGM group(P<0.05).There was no difference between the two groups in terms of BMI,insulin dose,gestational week of delivery,Apgar score,neonatal weight and the incidence of preeclampsia,premature delivery,polyhydramnios,cesarean section,SGA,macrosomia and postpartum hemorrhage(P>0.05).Time in range(TIR),time below range(TBR),time above range(TAR),and mean amplitude of glucose excursion(MAGE)were significantly improved at 32 weeks compared to 20 weeks in FGM group(P<0.05).Conclusions Repeated intermittent use of FGM in pregnant women with T2DM could reduce the blood glucose level and the incidence of neonatal hypoglycemia.
2.Effect of dexmedetomidine on ERK/Na +-K +-ATPase signaling pathway in lung tissues of rats with mechanical ventilation-induced lung injury
Min QU ; Wenbo SUN ; Zhongyan YAO ; Xiuqing ZHANG ; Ning LOU ; Cuili JIAO ; Lihua SU ; Shuhua LI ; Zilong QI ; Lei CHEN ; Peng CHEN
Chinese Journal of Anesthesiology 2020;40(6):687-690
Objective:To evaluate the effect of dexmedetomidine on the extracellular signal-regulated kinase(ERK)/sodium-potassium ATPase(Na + -K + -ATPase)signaing pathway in lung tissues of rats with mechanical ventilation-induced lung injury (VILI). Methods:Forty-eighty clean-grade male Sprague-Dawley rats, weighing 270-320 g, aged 4-5 months, were divided into 4 groups ( n=12 each) using a random number table method: control group (group C), VILI (alpha2-adrenergic receptor antagonist) group (group V), dexmedetomidine group (group D), and dexmedetomidine plus yohimbine group (group DY). Group C underwent no mechanical ventilation and breathed air spontaneously for 4 h. Mechanical ventilation (respiratory rate 40 breaths/min, tidal volume 40 ml/kg, inspiratory/expiratory ratio 1∶1, PEEP 0, fraction of inspired oxygen 21%) lasted 4 h in group V. Dexmedetomidine was infused intravenously in a dose of 5.0 μg/kg at 20 min before ventilation followed by an infusion of 5.0 μg·kg -1· h -1 throughout ventilation in group D. In group DY, yohimbine 0.1 mg/kg was injected intravenously at 10 min before dexmedetomidine, and the other treatments were similar to these previously described in group D. Blood samples and lung tissues were taken at 4 h of mechanical ventilation to determine the wet/dry weight ratio (W/D ratio), lung permeability index (LPI), alveolar fluid clearance rate (AFC), and expression of extracellular signal-regulated kinase (ERK), phosphorylated extracellular signal-regulated kinase (p-ERK), and Na + -K + -ATPase in lung tissues (by Western blot) and to observe pathological changes of lung tissues. Results:Compared with group C, LPI and W/D ratio were significantly increased, AFC was decreased, p-ERK expression was up-regulated, and Na + -K + -ATPase expression was down-regulated in group V and group DY ( P<0.05), and no significant change was found in the incidence of the parameters mentioned above in group D ( P>0.05). Compared with group V, LPI and W/D ratio were significantly decreased, AFC was increased, p-ERK expression was down-regulated, Na + -K + -ATPase expression was up-regulated ( P<0.05), and the pathological changes of lung tissues were significantly attenuated in group D, and no significant change was found in the incidence of the parameters mentioned above in group DY ( P>0.05). Compared with group D, LPI and W/D ratio were significantly increased, AFC was decreased, p-ERK expression was up-regulated, Na + -K + -ATPase expression was down-regulated ( P<0.05), and the pathological changes of lung tissues were accentuated in group DY. Conclusion:The mechanism by which dexmedetomidine alleviates VILI may be related to activating alpha2-adrenergic receptors and inhibiting ERK/Na + -K + -ATPase signaling pathway in rats.
3.Glutathione depletion inhibits angiotensinⅡ-induced activation of c-Jun/ATF-2 and NF-?B in cultured macrophages
Ning LOU ; Xueqing YU ; Shenglang ZHU ; Xiuqing DONG
Chinese Journal of Pathophysiology 2000;0(10):-
AIM: The aim of this study was to reveal the regulatory role of glutathione (GSH) in the transcriptional activity of activating transcription factor-2 (c-Jun/ATF-2) and nuclear factor-?B (NF-?B) of macrophages induced by angiotensin Ⅱ(AngⅡ). METHODS: Macrophage intracellular GSH was determined by fluorophotometry, and buthionine-[S,R]-sulfoximine(BSO)was used for depletion of intracellular GSH. The phosphorylation of c-Jun/ATF-2 and expression of NF-?B p65 were determined by immunoblot, and the activity of NF-?B was determined by electrophoresis mobility shift assay (EMSA). The c-Jun/ATF-2 was also determined by Immunohistochemical staining. RESULTS: The GSH content in the macrophage was decreased in cells that were lipid-peroxidized with AngⅡ (1.0 (?mol/L)) for 30 min and 60 min, respectively, followed by an adaptive GSH increase in the presence of AngⅡ (1.0 (?mol/L)) for longer time. In parallel, exposure to AngⅡfor 60 min also decreased macrophage GSH content in a dose-dependent manner. The GSH of RAW 264.7 cells were depleted by BSO, a specific inhibitor of GSH synthesis, and incubation for 18 h with 0.5 mmol/L BSO was sufficient for complete depletion of intracellular GSH. The phosphorylation of c-Jun/ATF-2 could be induced by the AngⅡ (1.0 (?mol/L)), whereas it did not occur in glutathione-depleted RAW 264.7 macrophages. The activation of NF-?B could also be induced by the AngⅡ (1.0 (?mol/L)), but it did not occur in glutathione-depleted RAW 264.7 macrophages. CONCLUSION: These data provide evidences that the intracellular glutathione redox may participate in the regulation of transcription activity of c-Jun/ATF-2 and NF-?B in macrophages. [

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