Nigella sativa (NS) has been used for centuries in various inflammatory conditions because of its anti-inflammatory and antioxidant activities. The study aimed to evaluate the anti-inflammatory, antinociceptive and antioxidant activity of Nigella sativa oil (NSO) in two models of acute (carrageenan-induced) and sub-acute inflammation (complete Freund’s adjuvant induced) in rats. Materials and Methods: NSO was administered orally 1, 2 and 4 mL/kg in the acute phase. For subacute phase, NSO was administered 4 mL/kg, 7 days before or after inflammation induction, or in association with diclofenac 5 mg/kg. Results: The gas chromatography coupled with mass spectroscopy (GC-MS) analysis showed that NSO is an important source of bioactive compounds, especially p-cymene and thymoquinone. In the acute phase, 1.5 h after administration, NSO (2 and 4 mL/kg) determined an anti-inflammatory effect comparable with that of diclofenac. In the sub-acute administration, NSO had no anti-inflammatory effect. The analgesic effect of NSO was observed only in the sub-acute inflammation in the analgesy-meter test. NSO as treatment proved its antioxidant effect through the reduction of malondialdehyde (MDA) and oxidized glutathione (GSSG), and increases in hydrogen donor capacity (DH) compared to the control group, but the effect was not as intense as that of diclofenac. Conclusion: The present study has proven inconstant anti-inflammatory, analgesic and antioxidative properties of NSO.
The study’s aim was to characterize the composition of Nigella sativa seed (NSO) and grape seed (GSO) oils, and to evaluate their cardioprotective and anti-inflammatory effect on isoproterenol (ISO)-induced ischemia in rats. Materials and Methods: NSO and GSO supplements were physicochemically characterized. Liquid chromatography–mass spectrometry (HPLC-MS), Fourier-transform infrared spectroscopy (FTIR), and gas chromatography–mass spectrometry (GC-MS) analyses were used to determine the phytochemical composition in the oils. Total polyphenol content (TPC) and in vitro antioxidant activity were also determined. Pretreatment with 4 mL/kg/day NSO or GSO was administered to rats for 14 days. The experimental ischemia was induced by a single administration of ISO 45 mg/kg after 14 days. An electrocardiogram (ECG) was performed initially and 24 h after ISO. Biological evaluation was done at the end of experiment. Results: The HPLC-MS, GC-MS, and FTIR analyses showed that both NSO and GSO are important sources of bioactive compounds, especially catechin and phenolic acids in GSO, while NSO was enriched in flavonoids and thymol derivatives. Pretreatment with GSO and NSO significantly reduced ventricular conduction, prevented the cardiotoxic effect of ISO in ventricular myocardium, and reduced the level of proinflammatory cytokines and CK-Mb. Conclusion: Both NSO and GSO were shown to have an anti-inflammatory and cardioprotective effect in ISO-induced ischemia.
Background and objectives: Ragweed pollen is a major source of allergen, which has rarely been observed in Romania until now. In this study, we evaluated the symptoms and associated factors in patients with allergic rhinitis to ragweed pollen in two distinct regions of Romania. Materials and Methods: We evaluated the records of patients newly diagnosed with allergic rhinitis induced by ragweed pollen in two allergological centers from North-West (NW) and Central parts of Romania between 2013 and 2015. The patients were clinically evaluated regarding disease length, presence, and severity of the allergic rhinitis symptoms and the association with other allergic manifestations (asthma and conjunctivitis). Results: The sensitization to ragweed was significantly higher in the NW part compared to the Central part (18.27% vs 4.1%, p < 0.001). More patients with monosensitization to ragweed pollen were observed in the NE center (27%) compared to the Central one (20.7%). Patients with monosensitization to ragweed pollen presented more severe forms of rhinitis (70% vs 31.5%, p = 0.02) in the NW part compared to polysensitized patients. The total symptoms score was significantly higher in patients from the Central part compared to the NW part (9.21 ± 2.01 vs 5.76 ±1.96, p < 0.001). Bronchial asthma was associated at a similar frequency to allergic rhinitis in both centers, but it was more frequently observed in monosensitized patients in the NW center. Allergic conjunctivitis was more frequently reported by patients from the Central part (75.86 vs 41.9, p = 0.02), while in the NW region it was noticed more commonly in monosensitized patients (65% vs 33.33, p = 0.02). Conclusions: Allergic rhinitis to ragweed pollen has been more frequently reported in the NW part of Romania. Patients with severe forms of rhinitis were observed in the central part, while in the NW the severe forms of disease were reported by patients with monosensitization. Ragweed pollen is intensely allergogenic and determines association of ocular and asthma symptoms. Co-sensitization increases the risk of asthma association.
Background: Atrial fibrillation is a major health problem due to the stroke risk associated with it. To reduce stroke risk, oral anticoagulants (OAC) are prescribed using the CHA2DS2-VASc (Congestive heart failure; Hypertension; Age ≥75 years; Diabetes Mellitus; Stroke; Vascular disease; Age 65–74 years; Sex category) risk score, a clinical probability assessment that includes a combination of risk factors predicting the probability of a stroke. Not all patients with high risk are receiving this treatment. The aim of this study was to assess physician adherence to clinical guidelines concerning the OAC treatment and to identify the factors that were associated with the decision to prescribe it. Methods: Registry data from 784 patients with non-valvular atrial fibrillation were evaluated in this retrospective cross-sectional study. Demographic data, subtype of AF, comorbidities associated with higher stroke and bleeding risk, and antithrombotic treatment received were recorded. We compared stroke and bleeding risk in patients with and without OAC treatment to determine if the clinicians followed guidelines: prescribed when necessary and abstained when not needed. Results: OAC treatment was administered in 617 (78.7%) patients. Of the 167 patients who did not receive OAC, 161 (96.4%) were undertreated according to their risk score, as opposed to those who received OAC in which the percentage of overtreated was 3.2%. Most undertreated patients (60.5%, p < 0.001) were with paroxysmal atrial fibrillation subtype. Conclusions: The decision to use anticoagulants for stroke prevention was based on the type of atrial fibrillation, rather than on the risk of stroke as quantified by CHA2DS2-VASc as per the recommended guidelines.
Introduction: Atherosclerosis represents the process by which fibrous plaques are formed in the arterial wall, increasing its rigidity with a subsequent decrease in blood flow which can lead to several cardiovascular events. Seeing as vitamin K antagonists are involved in the pathogenesis of atherosclerosis, we decided to investigate whether polymorphisms in genes that influence vitamin K metabolism might have an impact in modulating the risk of plaque formation. Patients and Methods: In the current study we included adult patients admitted in the Clinical Municipal Hospital of Cluj-Napoca without any carotid or femoral plaques clinically visible at the initial investigation, and a five year follow-up was subsequently performed. We recorded the following patient characteristics: age at inclusion, gender, area of living, smoking, presence of carotid and/or femoral plaques at five years, ischemic heart disease, arterial hypertension, atrial fibrillation, heart failure, diabetes mellitus, obesity, dyslipidemia, drug (oral anticoagulants, antihypertensives, hypolipidemic, anti-diabetic) use and status for the following gene polymorphisms: VKORC1 1639 G>A, CYP4F2 1347 G>T and GGCX 12970 C>G. Results: We observed that the major predictor of both carotid and femoral plaque formation is represented by ischemic cardiac disease. VKORC1 and CYP4F2 polymorphisms did not predict plaque formation, except for VKORC1 homozygous mutants. Nonetheless, both VKORC1 and CYP4F2 interacted with ischemic cardiac disease, increasing the risk of developing a carotid plaque, while only CYP4F2, but not VKORC1, interacted with ischemic cardiac disease to increase the risk of femoral plaque formation. Conclusions: We documented that CYP4F2 and VKORC1 polymorphisms boost the proinflammatory plaque environment (observed indirectly through the presence of ischemic heart disease), increasing the risk of plaque development.
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