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Background Previous studies have confirmed that nicotine exposure is an independent risk factor for miscarriage, but it is not clear whether nicotine causes unexplained recurrent spontaneous abortion (URSA) through oxidative stress. Objective To explore potential mediating effect of oxidative stress on the relationship between nicotine exposure and URSA. Methods Using a 1∶1 matched case-control study, 88 patients with URSA visiting Beijing Obstetrics and Gynecology Hospital affiliated to Capital Medical University from April to October in 2018 were selected as the case group, and 88 pregnant women without adverse pregnancy outcomes and seeking induced abortion in the outpatient clinic of the same hospital were selected as the control group. The levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-iso-prostaglandin F2α (8-iso-PGF2α) in urine were determined by enzyme-linked immunosorbent assay, and the level of urinary nicotine was determined by gas chromatography-mass spectrometry. Conditional logistic regression was used to analyze the associations of nicotine, 8-OHdG, and 8-iso-PGF2α with the risk of URSA. Multiple linear regression was used to analyze the association of nicotine with 8-OHdG and 8-iso-PGF2α. The potential mediating effect of oxidative stress on URSA after nicotine exposure was explored by dichotomous mediating model. Results The median concentrations (creatinine corrected) of nicotine, 8-OHdG, and 8-iso-PGF2α in urine of the case group were 7.78, 4.84, and 44.10 μg·g−1, respectively, while those of the control group were 6.48, 3.34, and 29.39 μg·g−1, respectively. The concentrations of nicotine, 8-OHdG, and 8-iso-PGF2α in urine of the case group were all higher than those of the control group (P < 0.05). The results of conditional logistic regression model showed that after adjusting selected confounding factors, compared with the Q1 groups of nicotine and 8-iso-PGF2α, the OR (95%CI) values of URSA in the Q4 groups were 4.20 (1.33-13.29) and 6.25 (1.66-23.59), respectively. Compared with the Q1 group of 8-OHdG, the OR (95%CI) values of URSA in the Q1, Q2, and Q3 groups were 5.47 (1.43-20.93), 4.24 (1.28-14.07), and 6.36 (1.82-22.28), respectively. The results of multiple linear regression showed that after adjusting confounding factors, there was a positive correlation between urinary nicotine and 8-OHdG in both the case group and the control group, and the b (95%CI) values were 0.76 (0.67-0.86) and 0.81 (0.67-0.95) respectively; there was a positive correlation between urinary nicotine and 8-iso-PGF2α in both the case group and the control group, and the b (95%CI) values were 0.65 (0.55-0.75) and 0.76 (0.64-0.87), respectively. The results of dichotomous mediating analysis showed that the mediating effect of 8-iso-PGF2α and its 95%CI on the relationship between nicotine exposure and URSA was 1.518 (0.749-2.311). Conclusion Internal nicotine exposure is a risk factor for URSA and is positively correlated with oxidative stress, and it may lead to URSA through lipid peroxidation damage.
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8-iso-prostaglandin F2α is a stable end product of lipid peroxidation of cell membrane lipid arachidonic acid under oxidative stress,which is formed by non-enzymatic beta lysis and recombination.It is an ideal index for evaluating the degree of lipid peroxidation and damage.Oxidative stress can damage biological molecules,cause cell death and tissue damage,and participate in the process of Henoch-Schonlein purpura and kidney damage.This article reviews the oxidative stress state and lipid peroxidation process of the body,the production and significance of 8-iso-prostaglandin F2α,the mechanism of oxidative stress in the pathogenesis of Henoch-Schonlein purpura and renal damage,and the important clinical significance of measuring 8-iso-prostaglandin F2α for Henoch-Schonlein purpura,which will provide evidence for future targeted therapy.
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8-iso-prostaglandin F2α is a stable end product of lipid peroxidation of cell membrane lipid arachidonic acid under oxidative stress, which is formed by non-enzymatic beta lysis and recombination.It is an ideal index for evaluating the degree of lipid peroxidation and damage.Oxidative stress can damage biological molecules, cause cell death and tissue damage, and participate in the process of Henoch-Schonlein purpura and kidney damage.This article reviews the oxidative stress state and lipid peroxidation process of the body, the production and significance of 8-iso-prostaglandin F2α, the mechanism of oxidative stress in the pathogenesis of Henoch-Schonlein purpura and renal damage, and the important clinical significance of measuring 8-iso-prostaglandin F2α for Henoch-Schonlein purpura, which will provide evidence for future targeted therapy.
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ObjectiveTo observe the effects of mild hypothermia on post-resuscitation myocardial dysfunction in rabbits in order to elucidate the underlying mechanism of hypothermia.Methods After setting up rabbit model of cardiopulmonary resuscitation,20 rabbits were randomly ( random number)divided into two groups,namely normothermic resuscitation group (group A,n =10 ) and post-ROSC hypothermia group ( group B,n =10).In the group A,animals wore treated with standard CPR after cardiac arrest.In post-ROSC hypothermia group,the body temperature of animals was cooled to 32 ～ 34°C after successful ROSC.The left ventricular end-diastolic pressure (LVEDP),left ventricular pressure rise and fall rates ( ± dp/dtmax,serum concentrations of heart-type fatty acid-binding protein (H-FABP) and 8-isoprostaglandin F2a (8-iso-PGF2a) and Cyclooxygenase-2 (COX-2) were observed. Results Compared with the A group,the B group had significantly better hemodynamics,and lower serum H-FABP,8-isoPGF2a and COX-2 levels in the early stage of post-resuscitation ( both P ＜ 0.05 ).ConclusionsMild hypothermia attenuated post-resuscitation myocardial dysfunction during the early period of postresuscitation.The cryoprotective effect on myooardium is likely associated with the reduction of 8-iso-PGF2a and COX-2.
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Objective To explore the changes of blood 8-iso-Prostaglandin F_(2a)(8-iso-PGF_(2a))content in different time after building-model and study its significance,and study the intervention effect of N-acetylcysteine(NAC) on it.Methods Seven-day-old Sprague-Dawley (SD) rats were randomly divided into 3 groups:intervention,operation and false operation groups.rats in intervention group were administered with NAC 0.1 mg/(g?d),Rats in operation group were given an equal volume of normal saline,and rats in false group operation had no administration.The blood was obtained to determine serum of 8-iso-PGF_(2a) content in 30 minutes,on the first,third,seventh and twenty first day after the building-model,respectively.EIA assay method was used to determine serum 8-(iso-PGF)_(2a) content.Results Serum 8-iso-PGF_(2a) concentration in rats from operation group,intervention and false operation groups were(168.7?(24.2)),(120.9?23.4) and (50.0?8.8) ng/L within 30 minutes after the building-model, respectively.There were a remarkable difference between serum 8-iso-PGF_(2a) concentration in three groups(P0.05).Conclusions The concentration of serum 8-iso-PGF_(2a) of rats rises remarkably early after building-model, and the peak concentration appears at 30 minutes after the building-model. NAC can effectively decrease serum 8-iso-PGF_(2a) content, which suggest that there is large value of clinical administration.
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Objective To explore the correlation of the apoptosis of peripheral blood mononuclear cell (PBMC) with plasma 8-iso-prostaglandin F2? (8-iso-PGF2?) level in order to confirm the peroxidation damage of hyperbilirubinemia in neonates with jaundice.Me-thods One hundred and twenty-nine neonates who were 2 to 7 days old were divided into 4 groups:slight jaundice (43 cases),moderate jaundice (38 cases),serious jaundice (18 cases),and healthy control(30 cases)groups.Plasma 8-iso-PGF2? levels were assayed by enzyme immunoassay(EIA),and the apoptosis rates of PBMC were determined by flow cytometry.Results 1.There was no significant difference in the apoptosis rate of PBMC between normal and slight jaundice neonates (P=0.108);apoptosis rate of PBMC was increasing with the aggravation of jaundice.2.Plasma 8-iso-PGF2? level in normal neonates was 14.74?6.71 ng/L,there was no difference between normal neonates and neonates with slight jaundice(P=0.502).Plasma 8-iso-PGF2? levels in neonates with moderate and serious jaundice were much higher(Pa=0).3.Positive correlation existed between plasma 8-iso-PGF2? level and PBMC apoptosis rate (r=0.602 P=0).Conclusions Hyperbilirubinemia can induce peroxidation damage,resulting in increase of PBMC apoptosis.Plasma 8-iso-PGF2? level can accurately eva-luate the peroxidation damage in neonates with jaundice.
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Objective To investigate the effect of vitamin E administration on the urinary level of 8-iso prostaglandin F_(2?)(8-iso- PGF_(2?))in the patients with cerebral infarction.Methods 28 patiems with acute cerebral infarction were involved in this study according to the selection criteria.They were divided into two groups:patients in test group(n=14)were treated with vitamin E,and those in control group(n=14)were not treated with vitamin E.No significant differences existed in age,gender ratio,blood pressure,lipids level and lo- cation and level of the cerebral infarct focus between two groups.The contents of urinary 8-iso-PGF_(2?) were measured in each urinary speci- men,meanwhile the levels of vitamin E and low density lipoprotein(LDL)were determined in each plasma specimen within 24 hours after onset of cerebral infarct and two weeks later.Results The concentration of urinary 8-iso-PGF_(2?) collected at two weeks after onset from pa- tients of test group was significantly lower than that of the control group(85.20?9.17 vs 91.36?4.24ng/mmol creatinine,P0.05).Conclusions The content of urinary 8-iso-PGF_(2?) and the level of oxidative stress in vivo could be decreased in the patients with acute cerebral infarction after being treated with vitamin E.
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Objective To explore the changes of myocardial enzymes,hepatic function,renal function and 8-iso-prostaglandin F2?(8-iso-PGF2?)in newborn infants with hyperbilirubinemia and their relationships.Methods One hundred and twenty-six neonates who were 2 to 7 days old were selected.Seventy-six cases were hyperbilirubinemia,and according total bilirubin(TB),they were divided into hyper bi-lirubinemia A group(HBE-A)(51 cases,TB 205-341 ?mol/L)and hyperbilirubinemia B group(HBE-B)(25 cases,TB≥342 ?mol/L).Fifty newborn infants with physiologic jaundice were control group(TB