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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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OBJECTIVE: To observe the effect of acupoint catgut embedding on levels of prostaglandin F2α(PGF2α), cyclooxygenase-2(COX-2) and nuclear factor kappa B(NF-κB) in the uteruses of rats with primary dysmenorrhea (PD), so as to explore its mechanisms underlying improvement of PD. METHODS: Forty female SD rats were randomly divided into normal, model, acupoint catgut embedment and medication groups, with 10 rats in each group. The PD model was established by subcutaneous injection of estradiol benzoate (0.5 mg on the 1st day, and 0.2 mg thereafter) once daily for 10 days, followed by i．p. of oxytocin 2 U(0.5 mg•5 U－1•mL－1) on the 11th day. Catgut embedment was applied to "Guanyuan"(CV4) and "Sanyinjiao"(SP6) on day 1 and 5 while modeling, and rats of the medication group received gavage of ibuprofen (1.25 mg/mL, 0.8 mL/rat) once daily for 10 d. The level of PGF2αin the uterus tissuewas assayed by ELISA, and the expression levels of uterine COX-2, phospho (p)-NF-κB p65, NF-κB p65 proteins were detected by Western blot. RESULTS: Compared with the normal group, the levels of PGF2α， COX-2, p-NF-κB p65 and NF-κB p65 in the uterine tissues were significantly increased in the model group (P<0.05). Compared with the model group, the levels of PGF2α and COX-2 in both catgut embedment and medication groups as well as p-NF-κB p65 in the catgut embedment group were significantly decreased (P<0.05). Compared with the medication group, the level of p-NF-κB 65 in the catgut embedment group was significantly decreased (P<0.05). CONCLUSION: The analgesic effect of acupoint catgut embedding may be related to its effects in down-regulating the expression of p-NF-κB and the levels of COX-2 and PGF2αin uteruses of PD rats.
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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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Objective To evaluate the anti-dysmenorrhea efficacy of habitat fresh-cut processed and traditional processed Linderae Radix based on the dysmenorrhea model. Methods By using the estrogen-induced dysmenorrhea model of ICR mice, the effect of treatment from two different processing methods on dysmenorrhea was compared by recording the writhing reaction as well as the changes of levels of prostaglandin E2 (PGE2), prostaglandin F2α (PGF2α), vasopressin (AVP), and β-endorphin (β-EP). Results Compared with the model group, Linderae Radix from two different processing methods significantly reduced the frequency of writhing (P 0.05). Conclusion The two processing methods of Linderae Radix both have good therapeutic effect on dysmenorrhea model mice, and the effect of habitat processed Linderae Radix is not inferior to that of traditional processed Linderae Radix.
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This research apply Dingkun Dan to treat patients with dysmenorrhea of cold stagnation and blood stasis syndrome. This study observed its effectiveness and safety of the treatment of the disease and its influence on the serum prostaglandin F2α, endothefin, pulsatility index and resistant index of uterine artery blood, to explore the possible mechanism of effect of Dingkun Dan in the treatment of dysmenorrhea and provide scientific basis for clinical application. The 75 patients with dysmenorrhea of cold stagnation and blood stasis who met the inclusion criteria, were divided into treatment group (n=37) and control group (n=38) by using random number remainder grouping method. In the treatment group patients were treated with Dingkun Dan, the other group were given Fuke Zaizao Jiaonang. Two groups have same time to take the medicine, three days prior to the menstruation for ten days. Medication for three menstrual cycles was seen as a course of treatment. To observe and compare the two groups of patients before and after treatment VAS score, syndrome integral, serum levels of prostaglandin F2α and endothelin, pulsation index and resistance index of uterine artery blood flow and related safety index changes. Finally makes statistical analysis. It has been identified that, Treatment group and control group can reduce pain symptom of dysmenorrhea patients and improve the syndromes scores, compare with control group, effect of the treatment group is more significant(P<0.01). VAS pain curative effect: the treatment group and control group total effective rate respectively were, 97.22%, 69.44%, markedly effective rate were 83.33%, 30.56%, comparison between two groups, treatment group is better than that of control group(P＜0.01). Syndromes curative effect: the treatment group and control group total effective rate respectively were 97.22%, 94.44%, markedly effective rate was 66.67%, 2.78%, respectively. The comparison between two groups, the total effective rate has no obvious difference, but markedly effective rate of treatment group is better than that of control group(P＜0.01). The treatment group can significantly reduce the patients' serum level of prostaglandin F2α(P<0.01), but no obvious difference was found in the control group before and after treatment. Both groups can significantly reduce the serum level of endothelin(P<0.01), comparison between two groups, the treatment group is more significant(P<0.01).Both treatment group and control group were significantly lower left and right pulsation index and resistance index of uterus artery blood flow(P<0.01). Between groups to compare the effect, the treatment group is more significant(P<0.01). Both treatment group and control group in the security check before and after treatment found no significant anomalies. Dingkun Dan in treating dysmenorrhea with cold stagnation and blood stasis syndrome seems to have remarkable clinical curative effect and safety, which may be achieved by significantly reducing the serum level of prostaglandin F2αand endothefin of the patients, and reducing the pulsation index and resistance index of uterine artery blood flow of the patients, to improve uterine artery condition of blood, and correcting local tissue ischemia to relieve pain.
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Objective To investigate the effects of icariin (ICA) on partial vasoactive substances in monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) rat model.Methods Sixty male SD rats were randomly divided into five groups:normal control group,model control group,ICA low-,middle-and high-dose (20,40,80 mg · kg-1 · d-1) group,12 rats in each group.Except for normal control group,the rats were injected with MCT (50 mg · kg-1 · d-1) to establish PAH model.After 1 week MCT-injection,ICA was given by intragastric administration for 3 weeks according to different groups.Mean pulmonary artery pressure (mPAP) was recorded through catheter connected with Power Lab system.Except for normal control group,the right ventricular hypertrophy index (RVHI) was calculated using formula:right ventricle weight/the weight of left ventricle with septum× 100％.The morphology of lung artery was assessed by HE staining.Concentration of angiotensin Ⅱ (Ang Ⅱ),endothelin (ET),prostaglandine F2α(PGF2α),thromboxane A2(TXA2) and prostacyclin (PGI2) in serum was measured by ELISA kit assay.The protein levels of angiotensin converting enzyme (ACE),cyclooxygenase-2 (COX-2) and thromboxane A2 synthetase (TXAS) were analyzed by Western blotting,expression of ACE,COX-2 and TXAS mRNA was measured by real time RT-PCR.Results Compared with the normal control group,mPAP [(48.5±5.2) mmHg] and RVHI (33.3±3.8)％in model control group were significantly increased (P ＜ 0.05),the morphology revealed there was obvious artery remodeling at distal artery,the contents of Ang Ⅱ,PGFA2,TXA2 in serum were elevated,and ACE,COX-2 and TXAS gene expression was up-regulated in rats treated with MCT.ICA (40,80 mg · kg-1 · d-1) treatment significantly attenuated mPAP,RVHI and pulmonary artery remodeling (P ＜ 0.05),and decreased the contents of serum Ang Ⅱ,ET,PGF2β,TXA2,and PGI2,and inhibited the gene expression of ACE,COX-2 and TXAS.Conclusion ICA decreases the contents of AngⅡ,ET,PGI2,PGF2α and TXA2 in the serum of MCT-induced PAH rats,which may be one of the mechanisms underlying ICA inhibiting PAH.
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Objective To investigate the correlation between urinary 8-iso-prostaglandin F2α (8-iso-PGF2α) level and carotid atherosclerotic plaque stability in patients with acute ischemic stroke.Methods The patients with acute ischemic stroke were enrolled consecutively.According to the findings of carotid artery ultrasound,they were divided into either a non-plaque group or a plaque group,and then the plaque group was redivided into a stable plaque subgroup and an unstable plaque subgroup.Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of urinary 8-iso-PGF2α.Multivariate logistic regression analysis and Spearman correlation analysis were used to investigate the relationship between 8-iso-PGF2α and carotid artery plaques.Results A total of 150 patients with acute ischemic stroke were enrolled,including 104 had carotid artery plaque (30 were stable plaques and 74 were unstable plaques) and 46 had no carotid artery plaque.The urinary 8-iso-PGF2α level (86.45 ± 6.20 ng/mmol creatinine vs.45.70 ±6.19 ng/mmol creatinine; t =37.136,P=0.001) and intima-media thickness (IMT) (2.89 ± 1.03 mm vs.0.86 ±0.53 mm; t =3.518,P =0.002) in the plaque group were significantly higher than those in the nonplaque group.Multivariate logistic regression analysis showed that urinary 8-iso-PGF2α level (odds ratio [OR] 1.183,95％ confidence interval [CI] 1.087-1.276; P=0.001) and IMT (OR 28.642,95％ CI 8.276-137.231; P =0.001) were the independent risk factors for carotid artery plaque.Pearson correlation analysis showed that there was no significant correlation between urinary 8-iso-PGF2α level and carotid artery IMT (r =0.075,P =0.264).The urinary 8-iso-PGF2α level of the unstable plaque subgroup was significantly higher than that of the stable plaque subgroup (97.30 ± 7.20 ng/mmol creatinine vs.69.17 ±9.25 ng/mmol creatinine; t =16.506,P =0.001).Multivariate logistic regression analysis showed that urinary 8-iso-PGF2α level (OR 4.652,95％ CI 1.732-12.643; P =0.001) was an independent risk factor for unstable plaque.Conelusions The urinary 8-iso-PGF2α level is associated with the existence of carotid atherosclerotie plaque and instability,its increased level is an independent risk factor for carotid plaque instability in patients with ischemic stroke.
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The animal models for pharmacologic assessment of drugs against premature delivery are reviewed, which include the measure of spontaneous delivery time between the first and the second pups in term pregnancy rats, the delay in the onset of labor in rats and premature delivery artificially induced by lipopolysaccharide, interleukin-1 α and prostaglandin F2α in mice.