Low-dose Aspirin Supplementation Research Articles

Low-dose aspirin improves endometrial receptivity in the midluteal phase in unexplained recurrent pregnancy loss.

To evaluate differences in Doppler parameters and pregnancy outcomes, if any, and to determine the predictive accuracy of such indices, as well as the effects of low-dose aspirin (LDA) in unexplained recurrent pregnancy loss (URPL). An observational study was conducted at Ren Ji Hospital, Shanghai, China, from May 2015 to December 2016. The endometrial thickness, and the pulsatility index (PI), resistive index (RI), and systolic-to-diastolic ratio (S/D) values of endometrial and uterine artery blood flow were collected. Receiver operating characteristic (ROC) curve analysis was used to analyze data from URPL patients (three or more first-trimester spontaneous abortions with unknown etiology) and patients with normal fertility. A second ultrasonography examination was performed in URPL patients who had received daily LDA for 2months. There were 190 URPL patients and 35 control patients. Endometrial thickness was significantly thinner in URPL patients than control patients (P=0.005). The PI, RI, and S/D values for endometrial blood flow and the mean PI, RI, and S/D values for uterine arteries were significantly higher in URPL patients (P<0.001). The predictive accuracy of the indices mentioned above were 0.660, 0.802, 0.852, 0.837, 0.784, 0.929, and 0.929, respectively. Following LDA supplementation, URPL patients showed a significant reduction in resistance to endometrial and uterine artery blood flow (P<0.001). URPL patients had impaired uterine perfusion. Doppler parameters are valuable in predicting women at high risk of URPL. LDA could be effective in improving endometrial receptivity.

The Impact of Aspirin Intake on Lactate Dehydrogenase, Arterial Stiffness, and Oxidative Stress During High-Intensity Exercise: A Pilot Study.

Aspirin is a common nonsteroidal anti-inflammatory drug used to reduce fever, pain, and inflammation. However, aspirin’s anti-inflammatory properties may also prevent increased levels of blood lactate dehydrogenase, vascular arterial stiffness and oxidative stress induced by high-intensity exercise. The purpose of this study was to investigate the effects of 4 weeks of aspirin supplementation on lactate dehydrogenase activity, lactate, arterial stiffness, and antioxidant capacity during high-intensity exercise in Taekwondo athletes. Participants were randomly divided into two groups: aspirin supplementation (n = 10) and placebo-control (n = 10). Blood levels of lactate dehydrogenase (LDH) enzyme activity and lactate were assessed to examine muscle damage and carotid-to-radial pulse wave velocity and the augmentation index were measured to examine arterial stiffness. Blood levels of superoxide dismutase, malondialdehyde, and glutathione peroxidase were assessed to determine antioxidant capacity and levels of oxidative stress. There were significant group × time interactions for enzyme activity of LDH (Δ-60 ± 24.36 U/L) and carotid-to-radial pulse wave velocity (Δ-1.33 ± 0.54 m/s), which significantly decreased (p < 0.05) following aspirin supplementation compared to placebo-control. Superoxide dismutase (Δ359 ± 110 U/gHb) and glutathione peroxidase (Δ28.2 ± 10.1 U/gHb) significantly decreased while malondialdehyde (0Δ3.0 ± 0.1 mmol/mL) significantly increased (p < 0.05) in the placebo-control group compared to the supplementation group. However, there were no changes in lactate concentration levels or augmentation index. These results reveal that low-dose aspirin supplementation would be a useful supplementation therapy to prevent high-intensity exercise training-induced increases in oxidative damage, inflammation, skeletal muscle fatigue, and arterial stiffness in elite Taekwondo athletes.

Effect of Low-Dose Aspirin on Midluteal Phase Uterine Artery Blood Flow in Patients With Recurrent Pregnancy Loss.

The purpose of this study was to evaluate differences in uterine artery blood flow parameters and pregnancy outcomes, if any. An investigation was conducted to determine the effects of low-dose aspirin on uterine artery blood flow indices in patients with recurrent pregnancy loss. This observational study included 353 Chinese women with a history of recurrent pregnancy loss and 85 women without a history of recurrent pregnancy loss (control group) from Ren Ji Hospital. All patients were scanned transvaginally with transvaginal Doppler sonography 6 to 8 days after ovulation to measure the pulsatility index (PI), resistive index (RI), and systolic-to-diastolic ratio (S/D) of the left and right main uterine arteries. Low-dose aspirin at a dose of 50 mg/d was administered orally in patients with recurrent pregnancy loss for 2 months, and the blood flow indices were measured subsequently. The Student t test was used for analysis of the results, P < .05 was considered significant. The mean PI and S/D of the uterine arteries in the recurrent pregnancy loss group were significantly higher than in the control group. Although not statistically significant, the RI was higher in the recurrent pregnancy loss group than the control group. Moreover, the PI and S/D increased as the number of pregnancy losses increased. Significant enhancements of the PI and S/D were observed in patients with 4 or more consecutive abortions. After low-dose aspirin supplementation, patients with recurrent pregnancy loss showed a highly significant reduction in the PI and S/D. Uterine blood flow decreased during the luteal phase in patients with recurrent pregnancy loss. Low-dose aspirin induced a reversible increase in uterine blood flow and may be of therapeutic value.

Human platelets generate phospholipid-esterified prostaglandins via cyclooxygenase-1 that are inhibited by low dose aspirin supplementation

Oxidized phospholipids (oxPLs) generated nonenzymatically display pleiotropic biological actions in inflammation. Their generation by cellular cyclooxygenases (COXs) is currently unknown. To determine whether platelets generate prostaglandin (PG)-containing oxPLs, then characterize their structures and mechanisms of formation, we applied precursor scanning-tandem mass spectrometry to lipid extracts of agonist-activated human platelets. Thrombin, collagen, or ionophore activation stimulated generation of families of PGs comprising PGE2 and D2 attached to four phosphatidylethanolamine (PE) phospholipids (16:0p/, 18:1p/, 18:0p/, and 18:0a/). They formed within 2 to 5 min of activation in a calcium, phospholipase C, p38 MAP kinases, MEK1, cPLA2, and src tyrosine kinase-dependent manner (28.1 ± 2.3 pg/2 × 108 platelets). Unlike free PGs, they remained cell associated, suggesting an autocrine mode of action. Their generation was inhibited by in vivo aspirin supplementation (75 mg/day) or in vitro COX-1 blockade. Inhibitors of fatty acyl reesterification blocked generation significantly, while purified COX-1 was unable to directly oxidize PE in vitro. This indicates that they form in platelets via rapid esterification of COX-1 derived PGE2/D2 into PE. In summary, COX-1 in human platelets acutely mediates membrane phospholipid oxidation via formation of PG-esterified PLs in response to pathophysiological agonists.

Effect of short-term, low dose aspirin supplementation on the activation of pro-inflammatory NF-κB in aged rats

The basis of our recently proposed “molecular inflammation theory of aging” is that activated inflammatory transcription factors, including versatile NF-κB, occur widespread in the organism during aging. NF-κB plays a key role in pro-inflammatory gene expression, such as cyclooxygenase (COX). Aspirin is one of the most commonly used non-steroidal anti-inflammatory drugs because of its ability to inhibit COX activity. Thus, in the present study, we investigated the effect of short-term, low dose aspirin intake on the modulation of pro-inflammatory NF-κB activation in old rats. To conduct the study, 24-month-old Fischer 344 rats were supplemented with low dose aspirin (0.015%) for 10 days. Biochemical analyses showed suppressed reactive species (RS) and COX-2 activity. The data also showed that NF-κB activation and its associated gene expressions, such as COX-2, iNOS, VCAM-1 and ICAM-1, were all suppressed by the low dose aspirin supplementation through the inhibition of phosphorylation and degradation of IκBα via the NIK/IKK pathway. Our molecular exploration further revealed that aspirin's suppressive action of NF-κB was mediated by its ability to inhibit the nuclear translocation of cytosolic thioredoxin and redox factor-1. These findings showed for the first time that in aged rat short-term low dose dietary aspirin feeding modulates the molecular signal transduction involved in the inflammatory process.

Drug supplementation in pregnancy

Since antiquity, there have been references in medicine to the role of nutrition in pregnancy outcome. Reviewing articles on nutrition and drug supplementation in pregnancy, one is struck by the variety of remedies that have been tried and the variety of effects that have been attributed to them. The number of herbal remedies that have been touted is astounding, and the entire science of Geophagia evolved in the hope identifying of those population-specific customs that may have had a positive effect on birth outcome as an adaptive mechanism. Most recently, there has been renewed interest in the role of nutritional and drug supplementation in pregnancy, specifically in the areas of pregnancy-induced hypertension and teratogenesis. In this article, I briefly review the role of drug supplementation in pregnancy, ranging from established needs such as iron to prevent iron-deficiency anemia to the controversies of low-dose aspirin supplementation for the prevention of preeclampsia and preconceptional folic acid supplementation for the prevention of neural tube defects.