A new xanthone glycoside, 1,3,5,6-tetrahydroxyxanthone-C-4-β-d-glucopyranoside was isolated from the methanol extract of Mangifera indica leaves (Anacardiaceae) growing in Egypt. The structure was clarified by 1D and 2D-NMR spectroscopic data. The physicochemical properties of the compound such as lipophilicity, solubility, and formulation considerations were predicted via in silico ADMET technique using the SwissADME server. This technique provided Lipinski’s rule of five, such as GIT absorption, distribution, metabolism, and skin permeation. The in vitro inhibitory activities against aging-mediated enzymes such as collagenase, elastase, hyaluronidase, and tyrosinase were assessed. The compound exhibited remarkable anti-collagenase, anti-elastase, anti-hyaluronidase, and anti-tyrosinase effects with IC₅₀ values of 1.06, 419.10, 1.65, and 0.48 µg/mL, respectively, compared to the positive control. The compound showed promising predicted aqueous solubility and reasonable skin penetration suggesting the suitability of the compound for topical formulation as an anti-aging agent for cosmetic preparations.

This study sought to examine whether supplementation of Black Seed Oil (BSO) can improve pulmonary function tests (PFTs), inflammation, and oxidant-antioxidant markers in COPD patients. The study involved 100 patients of mild to moderate COPD divided randomly into 2 groups who were appointed to receive standard medication only (control group) or with additional Black Seed Oil (BSO group). They were assessed initially and after 3 months, 44 patients responded in control group and 47 patients in BSO group. BSO group evidenced a significant decreasing in oxidant and inflammatory markers; thiobarbituric acid reactive-substances (TBARS), protein carbonyl (PC) content, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), a significant increase in antioxidants; superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), glutathione peroxidase (GPx), vitamin C, and E, and a significant improvement in PFTs versus control group and baseline levels. Supplementation of Black Seed Oil may be an effective adjunct therapy to improve pulmonary functions, inflammation, and oxidant-antioxidant imbalance in COPD patients.

Summary: Background: The aim was to evaluate the association of plasma 25-hydroxyvitamin D (25-OHD) and vitamin D binding protein (VDBP or Gc-globin) gene polymorphism with oxidant-antioxidant profiles in patients with chronic obstructive pulmonary disease (COPD), and their role as biomarker risk factors in susceptibility and severity of COPD. Methods: Eighty patients diagnosed with COPD (mild, moderate and severe according to lung function tests; FEV 1%) and 80 healthy controls were included in the study. Serum nitric oxide (NO) and lipid peroxide (LP), plasma reduced glutathione (RGSH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) activity, 25-OHD and VDBP polymorphism were analyzed in all subjects. Results: COPD patients had significantly decreased serum NO, plasma SOD, RGSH, GSH-Px, CAT and 25-OHD versus controls, but had significantly increased serum LP. In COPD patients, 25-OHD levels were significantly lower (41.49± 13.65 ng/mL) versus controls, but more lower in severe COPD patients (30.54±9.09 ng/mL; sensitivity 79.2%; spe - cificity 73.2%, p<0.001) versus mild and moderate COPD. VDBP genotypes frequencies were Gc1S-1S=23.8%, Gc1F-1S=28.8%, Gc1F-1F=15%, Gc1S-2=20%, Gc1F-2=11.3% and Gc2-2=1.3%. Also, VDBP variants frequencies were Gc1S=48.1%, Gc1F=35% and Gc2=16.6%. How ever, Gc1F-1S genotypes and Gc1F variants were significantly higher than in controls (10%, 12.5%; p=0.009, p=0.001, respectively). Moreover, in severe COPD patients, Gc1F-1S genotype was significantly higher than in mild COPD (41.7% vs 31.3%, p=0.04). Conclusion: COPD patients had significantly lower plasma 25-OHD and were associated with significantly higher VDBP Gc1F-1S genotypes and Gc1F variants frequencies than controls. Low vitamin D levels and VDBP polymorphism may be important as diagnostic risk factors in the susceptibility to and severity of COPD.

BackgroundChronic obstructive pulmonary disease (COPD) is a common respiratory condition involving the airways and characterized by airflow limitation. Antioxidants are substances that may protect cells from the damage caused by unstable molecules known as free radicals. Antioxidants interact with and stabilize free radicals and may prevent some of the damage free radicals might otherwise cause. Under physiological conditions a balance exists between the amount of reactive oxygen species (ROS) produced in normal cellular metabolism and the endogenous antioxidant defense. An imbalance between the antioxidant capacity and the production of reactive oxygen species leads to oxidative stress, which is associated with the pathogenesis of several human diseases. An oxidant/antioxidant imbalance has been proposed as having a key role in the pathogenesis of COPD. The lung is directly exposed to high levels of oxygen, and therefore has to have efficient antioxidant mechanisms.Aim of the studyTo examine the role of altered levels of oxidant–antioxidants in disease severity of COPD and correlate it with the degree of airflow obstruction in the Egyptian population.Subjects and methodsEighty subjects with COPD, 20 healthy smokers, and 20 healthy nonsmokers participated in this study. The investigation included determination of the lung function and the measurements of plasma superoxide dismutase activity (SOD), glutathione content (GSH) reduced form, glutathione peroxidase activity (GSH-Px), catalase activity (CAT), lipid peroxidase (LP), and nitric oxide (NO).ResultsThe mean concentration of nitric oxide (NO) was significantly higher in the control subjects (smokers and nonsmokers) compared with the COPD group (p=0.001, 0.0001) respectively. Also the mean concentration of nitric oxide (NO) was significantly higher in control nonsmoker group compared to control smoker group (p=0.002). The mean concentration of lipid peroxidase (LP) was significantly higher in COPD patients compared with control subjects (smokers and nonsmokers), (p=0.0001, 0.0001) respectively. The mean concentration of glutathione (GSH) was significantly higher in the control subjects (smokers and nonsmokers) compared with COPD patients (p=0.001, 0.001) respectively. There is no significant difference in the concentration of glutathione-peroxidase (GSH-Px) in all study participants (COPD patients, control smokers, control nonsmokers). The mean concentration of catalase (CAT) was significantly higher in control nonsmokers, compared to COPD patients and control smokers (p=0.001, 0.018) respectively. The mean concentration of superoxide dismutase (SOD) was significantly higher in the control subjects (smokers and nonsmokers) compared with COPD patients (p=0.012, 0.001) respectively. Also the mean concentration of superoxide dismutase (SOD) was significantly higher in control nonsmoker group compared to control smoker group (p=0.001).ConclusionThese results support the hypothesis that an oxidant–antioxidant imbalance, associated with oxidative stress in COPD patients, plays an important role in the progression of disease severity, also these results revealed the presence of an oxidative presence in smokers and in subjects with COPD and that the imbalance may be important in the pathogenesis of this disease. The use of cigarette increased oxidative stress by causing plasma lipid peroxidation and imbalance in erythrocyte antioxidant. Nitric oxide (NO) metabolism was not increased in patients with chronic obstructive pulmonary disease compared to healthy subjects. It has been reported that GSH plays a major role in pulmonary antioxidant protection

PD, it is thought to arise as an outcome of environmental harm and a host’s response system, which boosts the tendency of the disease to arise. Objective To clarify the effect of smoking on the level of oxidant–antioxidant in patients with COPD. Patients and methods Thirty patients with COPD (20 smokers and 10 nonsmokers) and 40 healthy individuals (18 smokers and 22 nonsmokers) participated in this study. The investigations included measurement of malondialdehyde (MDA), superoxide dismutase (SOD) activity, catalase (CAT) activity, glutathione peroxidase (GPx), glutathione reductase (GR), vitamin C, and glutathione (GSH) content. Results SOD, CAT, GPx, GSH, GR, and vitamin C were significant lower (P<0.0001) among patients with COPD (smokers and nonsmokers) than in the control group, whereas the MDA levels were elevated (P<0.0001) in patients with COPD (smokers and nonsmokers) when compared with the control group. Moreover, the values of SOD, GSH, and GPx were significantly lower (P<0.001) in smokers with COPD as compared with nonsmokers with COPD. Finally, there was no significant difference in the level of MDA between patients with COPD (smokers and nonsmokers). Conclusion There is a significant reduction in the level of some antioxidants (SOD, GSH, and GPx) in smokers with COPD compared with nonsmokers with COPD, but other antioxidants (CAT, GR, and vitamin C) did not change significantly, whereas the oxidant levels (i.e., MDA) were relatively convergent in patients with COPD (smokers and nonsmokers). This, in turn, points to the modest role of smoking in the causation of oxidant–antioxidant imbalance in this disease....

BackgroundThe most important pathogenic mechanisms involved in the development of chronic obstructive pulmonary disease (COPD) are protease–antiprotease imbalance, inflammation, lung remodeling and oxidative stress. Interestingly, lower vitamin D levels have been related to regulation of each of these processes, that is, higher expression of proteases, modulation of inflammation, modulation of extracellular matrix turnover, and increased oxidative stress. Thus, one can speculate that lower vitamin D levels may be linked to increased risk of developing COPD. In some clinical studies, lower levels of vitamin D, measured as plasma 25-hydroxyvitamin D (25(OH)D), have been associated with lower lung function and faster lung function decline, but the results are conflicting.Aim of the studyThe aim of this study is to evaluate the evidence of the effect of vitamin D on COPD.Subjects and methodsThe present study, included 120 subjects, 80 patients diagnosed as COPD and 40 healthy volunteers (20 smokers and 20 nonsmokers). Plasma 25-OHD was measured by Enzyme Linked Immunosorbent Assay (DiaSorin, Stillwater, Minnesota, USA) in all study participants.ResultsThe mean concentration of 25-OH-D was significantly higher in the reference groups (smokers and nonsmokers) compared with severe COPD group (p=0.001, 0.001) respectively.The mean concentration of 25-OH-D was significantly higher in the reference groups (smokers and nonsmokers) compared with moderate COPD group (p=0.029, 0.049) respectively.The mean concentration of 25-OH-D was not significantly higher in the reference groups (smokers and nonsmokers) compared with the mild COPD group.ConclusionWe observed a novel association of lower plasma 25(OH)D levels with a higher risk of COPD