Amyotrophic Lateral Sclerosis and Oxidative Stress: A Double-Blind Therapeutic Trial After Curcumin Supplementation

2018 ◽  
Vol 17 (10) ◽  
pp. 767-779 ◽  
Author(s):  
Lucia Chico ◽  
Elena Caldarazzo Ienco ◽  
Costanza Bisordi ◽  
Annalisa Lo Gerfo ◽  
Lucia Petrozzi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amyotrophic Lateral Sclerosis ◽  
Control Group ◽  
Therapeutic Trial ◽  
Entire Study ◽  
Reducing Ability ◽  
Group A ◽  
Group B ◽  
And Oxidative Stress ◽  
Lateral Sclerosis

Objective: To investigate the efficacy of curcumin oral supplementation (600 mg/day, Brainoil), a natural antioxidant compound, in Amyotrophic Lateral Sclerosis (ALS). Methods: Patients were randomized into two groups: Group A received placebo for 3 months, then Brainoil for the following 3 months, Group B took Brainoil for 6 months. The evaluations were conducted at basal (T0), after 3 months of double blinded Brainoil or placebo treatment (T1), and after the 3 month open-label phase (T2). Clinical evaluations and oxidative stress biomarkers, including oxidative protein products (AOPPs), ferric reducing ability (FRAP), total thiols (T-SH) and lactate, were evaluated, compared to a control group, during an incremental forearm exercise test. Results: Over the entire study Group B showed a stable score of the ALS-FRS-r which decreased in Group A (p<0.01), in parallel with a reduction of AOPPs (p<0.01) which was not detected into Group A. Also FRAP exercise values remained stable in Group B, while in Group A they were reduced without treatment at T1 (0.05<p<0.01), for then increase at T2 with introduction of therapy (p<0.05). In Group B T1>T0 exercise lactate was lower compared to Group A (p<0.01). Compared to controls, the whole ALS population showed a greater oxidative stress (p<0.001), those treated with curcumin (Group B) exhibiting decreased exercise AOPPs at T2 with values approaching those of controls. Conclusion: Although further studies are needed to confirm these data, treatment with curcumin shows encouraging results indicating a slight slowdown in disease progression, improving aerobic metabolism and oxidative damage, this also contributing to deepen knowledge into the pathogenic mechanisms of ALS.

Glycine and L-Arginine supplementation ameliorates gastro-duodenal toxicity in a rat model of NSAID (Diclofenac)-gastroenteropathy via inhibition of oxidative stress

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Akinleye Stephen Akinrinde ◽  
Halimot Olawalarami Hameed
Keyword(s):  
Oxidative Stress ◽  
Total Protein ◽  
Therapeutic Index ◽  
Control Treatment ◽  
Control Group ◽  
Protective Effects ◽  
Serum Total Protein ◽  
Significant Amelioration ◽  
Group A ◽  
Group B

Abstract Objectives This study examined the possible protective roles of exogenous glycine (Gly) and L-Arginine (l-Arg) against Diclofenac (DIC)-induced gastro-duodenal damage in rats. Methods Rats were divided into Group A (control), Group B (DIC group) and Groups C–F which were pre-treated for five days with Gly1 (250 mg/kg), Gly2 (500 mg/kg), l-Arg1 (200 mg/kg) and l-Arg2 (400 mg/kg), respectively, before co-treatment with DIC for another three days. Hematological, biochemical and histopathological analyses were then carried out. Results DIC produced significant (p<0.05) reduction in PCV (13.82%), Hb (46.58%), RBC (30.53%), serum total protein (32.72%), albumin (28.44%) and globulin (38.01%) along with significant (p<0.05) elevation of serum MPO activity (83.30%), when compared with control. In addition, DIC increased gastric H2O2 and MDA levels by 33.93 and 48.59%, respectively, while the duodenal levels of the same parameters increased by 19.43 and 85.56%, respectively. Moreover, SOD, GPx and GST activities in the DIC group were significantly (p<0.05) reduced in the stomach (21.12, 24.35 and 51.28%, respectively) and duodenum (30.59, 16.35 and 37.90%, respectively), compared to control. Treatment with Gly and l-Arg resulted in significant amelioration of the DIC-induced alterations although l-Arg produced better amelioration of RBC (29.78%), total protein (10.12%), albumin (9.93%) and MPO (65.01%), compared to the DIC group. The protective effects of both amino acids against oxidative stress parameters and histological lesions were largely similar. Conclusions The data from this study suggest that Gly or l-Arg prevented DIC-induced gastro-duodenal toxicity and might, therefore be useful in improving the therapeutic index of DIC.

scholarly journals Oxidative Stress, Neuroinflammation and Mitochondria in the Pathophysiology of Amyotrophic Lateral Sclerosis

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 901 ◽  
Author(s):  
Elena Obrador ◽  
Rosario Salvador ◽  
Rafael López-Blanch ◽  
Ali Jihad-Jebbar ◽  
Soraya L. Vallés ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amyotrophic Lateral Sclerosis ◽  
Cell Types ◽  
T Cell Subsets ◽  
Cellular Interactions ◽  
Underlying Mechanisms ◽  
Different Cell Types ◽  
And Oxidative Stress ◽  
Different Levels ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron (MN) disease. Its primary cause remains elusive, although a combination of different causal factors cannot be ruled out. There is no cure, and prognosis is poor. Most patients with ALS die due to disease-related complications, such as respiratory failure, within three years of diagnosis. While the underlying mechanisms are unclear, different cell types (microglia, astrocytes, macrophages and T cell subsets) appear to play key roles in the pathophysiology of the disease. Neuroinflammation and oxidative stress pave the way leading to neurodegeneration and MN death. ALS-associated mitochondrial dysfunction occurs at different levels, and these organelles are involved in the mechanism of MN death. Molecular and cellular interactions are presented here as a sequential cascade of events. Based on our present knowledge, the discussion leads to the idea that feasible therapeutic strategies should focus in interfering with the pathophysiology of the disease at different steps.

scholarly journals Lack of Association between Nuclear Factor Erythroid-Derived 2-Like 2 Promoter Gene Polymorphisms and Oxidative Stress Biomarkers in Amyotrophic Lateral Sclerosis Patients

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Annalisa LoGerfo ◽  
Lucia Chico ◽  
Loredana Borgia ◽  
Lucia Petrozzi ◽  
Anna Rocchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amyotrophic Lateral Sclerosis ◽  
Gene Promoter ◽  
Redox Balance ◽  
Nuclear Factor ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Reducing Ability ◽  
Als Patients ◽  
Lateral Sclerosis

Oxidative stress involvement has been strongly hypothesized among the possible pathogenic mechanisms of motor neuron degeneration in amyotrophic lateral sclerosis (ALS). The intracellular redox balance is finely modulated by numerous complex mechanisms critical for cellular functions, among which the nuclear factor erythroid-derived 2-like 2 (NFE2L2/Nrf2) pathways. We genotyped, in a cohort of ALS patients(n=145)and healthy controls(n=168), three SNPs inNrf2gene promoter: −653 A/G, −651 G/A, and −617 C/A and evaluated, in a subset(n=73)of patients, advanced oxidation protein products (AOPP), iron-reducing ability of plasma (FRAP), and plasma thiols (-SH) as oxidative damage peripheral biomarkers.Nrf2polymorphisms were not different among patients and controls. Increased levels of AOPP(P<0.05)and decreased levels of FRAP(P<0.001)have been observed in ALS patients compared with controls, but no difference in -SH values was found. Furthermore, no association was found between biochemical markers of redox balance andNrf2polymorphisms. These data confirm an altered redox balance in ALS and indicate that, while being abnormally modified compared to controls, the oxidative stress biomarkers assessed in this study are independent from the −653 A/G, −651 G/A, and −617 C/ANrf2SNPs in ALS patients.

scholarly journals Oxidative stress profile following the co-administration of cisplatin and resveratrol in female rats: a preliminary study

2021 ◽  
Vol 25 (2) ◽  
pp. 134-145
Author(s):  
Izuchukwu Azuka Okafor ◽  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Normal Control ◽  
Intraperitoneal Injection ◽  
Female Rats ◽  
Control Group ◽  
Stress Profile ◽  
Body Tissues ◽  
Group A ◽  
Group B

Introduction: Cisplatin is one of the most widely used drugs for the treatment of various cancers but has oxidative tissue damage as one of its side effects. This study investigated the oxidative stress profile in some important body tissues following the co-administration of cisplatin (CIS) and resveratrol (RSV). Methods: Thirty-five adult female rats with an average body weight of 162g were divided into 5 groups (n=7) and used for this experimental study. Group A served as the normal control group and received distilled water only. Group B received only a single dose intraperitoneal injection of 10mg/kg CIS. Groups C, D and E were orally given 5, 10 and 20mg/kg of RSV respectively for 7 days, starting 24h after a single CIS dose intraperitoneal injection of 10mg/kg. Selected body tissues were harvested for oxidative stress profiling at the end of the experiment. Results: CIS significantly increased malondialdehyde levels and decreased glutathione, superoxide dismutase and catalase levels in all the tissues assessed (ovary, uterus, liver, kidney, pancreas, stomach and spleen) when compared to the normal control. The RSV treatment caused the reversal of these effects; malondialdehyde levels were significantly decreased, while glutathione, superoxide dismutase and catalase levels were significantly increased across all the examined tissues. Conclusion: RSV at different doses could be effective in the management of CIS-induced oxidative stress and lipid peroxidation across some body tissues. However, this effect may be dependent on the dose of CIS and RSV.

scholarly journals The Effect of MicroRNA-126 Mimic Administration on Vascular Perfusion Recovery in an Animal Model of Hind Limb Ischemia

2021 ◽  
Vol 8 ◽  
Author(s):  
Panagiotis Theofilis ◽  
Georgia Vogiatzi ◽  
Evangelos Oikonomou ◽  
Maria Gazouli ◽  
Gerasimos Siasos ◽  
...  
Keyword(s):  
Muscle Tissue ◽  
Hind Limb ◽  
Tissue Expression ◽  
Control Group ◽  
Vascular Perfusion ◽  
Entire Study ◽  
Stepwise Increase ◽  
Limb Perfusion ◽  
Group A ◽  
Group B

Background: MicroRNAs have been linked to angiogenesis and could prove to be valuable future therapeutic targets in ischemic cardiovascular diseases.Methods: Ten-week-old male C57Bl/6 mice were subjected to left femoral artery ligation and were treated with microRNA-126 mimic at a dose of 5 mg/kg (Group A, n = 10) or 5 mg/kg microRNA mimic negative control (Group B, n = 10) on days 1, 3, and 7. Laser Doppler imaging was performed to verify successful ligation on day 0 and to evaluate differences in the ischemic-to-normal (I/N) hind limb perfusion ratio on day 28. Muscle tissue expression of microRNA-126 and vascular endothelial growth factor (VEGF) was determined via PCR.Results: Following microRNA-126 mimic administration in Group A subjects, we noted a stepwise increase in I/N hind limb perfusion ratio (Day 0: 0.364 ± 0.032 vs. Day 8: 0.788 ± 0.049 vs. Day 28: 0.750 ± 0.039, p = 0.001). In Group B a stepwise increase in I/N hind limb perfusion ratio was observed (Day 0: 0.272 ± 0.057 vs. Day 8: 0.382 ± 0.020 vs. Day 28: 0.542 ± 0.028, p = 0.074). Muscle tissue expression of microRNA-126 in the ischemic hind limb of Group A was 350-fold lower compared to the ischemic hind limb of Group B (p &lt; 0.001). A higher expression (14.2-fold) of VEGF in the ischemic hind limb of microRNA-126-treated mice compared to that of control group was detected (p &lt; 0.001). A statistically significant negative correlation was noted between microRNA-126 and VEGF tissue expression levels in the ischemic limbs of the entire study population.Conclusion: MicroRNA-126 delivery in the ischemic hind limb of mice improved vascular perfusion with VEGF upregulation.

Neuroprotective potential of adenyl cyclase/cAMP/CREB and mitochondrial CoQ10 activator in amyotrophic lateral sclerosis rats

2020 ◽  
Vol 16 ◽  
Author(s):  
Mohmmad Mamtaj Alam ◽  
Elijabeth Minj ◽  
Rajeshwar Kumar Yadav ◽  
Sidharth Mehan
Keyword(s):  
Oxidative Stress ◽  
Amyotrophic Lateral Sclerosis ◽  
Drug Therapy ◽  
Therapeutic Approach ◽  
Methyl Mercury ◽  
Chronic Treatment ◽  
Adenyl Cyclase ◽  
Als Patients ◽  
And Oxidative Stress ◽  
Lateral Sclerosis

Aim: To investigate neuroprotective potential of of forskolin (FSK) in combination with solanesol (SNL) along with clinically proven drugs (riluzole, baclofen, citalopram) on behavioral, molecular and neurochemical alterations in methyl mercury-induced amyotrophic lateral sclerosis (ALS) rats. Background: ALS is a motor neuron disease in which oxidative stress is the principle mechanism ofneuronal death which can be mimicked by the dominant mutations in an antioxidant enzyme SOD-1. Due to MeHg neurotoxicity, behavioral and neurochemical alterations occur in rats. During ALS mitochondrial CoQ10 dysfunctioning and downregulation of adenyl cyclase/CREB are major pathological hallmark for neurodegeneration in ALS. Clinically proven drug therapy comes with limited therapeutic involvement, and is used as approachable therapy in ALS patients. Objective: Therefore, current research explores the up-regulation of adenyl cyclase/cAMP/CREB by FSK 30, 60 mg/kg in combination with mitochondrial ETC-coenzyme-Q10 precursor SNL 15, 30 mg/kg can be a preventive therapeutic approach to overcome the ALS like symptoms. Method: MeHg (5 mg/kg) is a neurotoxic compound that leads to ALS like behavioral & neurochemical alterations. Results: Chronic treatment with the combination of FSK 30,60 mg/kg and SNL 15,30 mg/kg alone and along with standard drugs citalopram (5 mg/kg), riluzole (5 mg/kg) and baclofen (3 mg/kg) increased the adenyl cyclase and mitochondrial CoQ10 and ETC-complexes enzyme levels and shows the neuroprotective potential by significantly improving the cognitive deficitslocomotion, , grip strength, and restoration of neurochemicals alterations along with reducing the level of inflammatory mediators and oxidative stress in ALS rats. Conclusion: Thus, we concluded that FSK in combination with SNL along with standard drugs can be a possible therapeutic approach for the treatment of ALS.

scholarly journals Systemic Oxidative Stress Markers in Cirrhotic Patients with Hepatic Encephalopathy: Possible Connections with Systemic Ammoniemia

Medicina ◽  
2020 ◽  
Vol 56 (4) ◽  
pp. 196 ◽  
Author(s):  
Cătălin Sfarti ◽  
Alin Ciobica ◽  
Ioana-Miruna Balmus ◽  
Ovidiu-Dumitru Ilie ◽  
Anca Trifan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Encephalopathy ◽  
Control Group ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Systemic Oxidative Stress ◽  
Group A ◽  
Cirrhotic Patients ◽  
Group B ◽  
Control Study

Background and objectives: Oxidative stress shows evidence of dysregulation in cirrhotic patients with hepatic encephalopathy (HE), although there are still controversies regarding the connections between oxidative stress and ammonia in these patients. The aim of this study was to evaluate the oxidative stress implication in overt HE pathogenesis of cirrhotic patients. Materials and Methods: We performed a prospective case-control study, which included 40 patients divided into two groups: group A consisted of 20 cirrhotic patients with HE and increased systemic ammoniemia, and group B consisted of 20 cirrhotic patients with HE and normal systemic ammoniemia. The control group consisted of 21 healthy subjects matched by age and sex. The activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA) levels (lipid peroxidation marker), and ammoniemia were evaluated. Results: We found a significant decrease in SOD and GPx activity and also a significant increase of MDA levels in cirrhotic patients with HE as compared to the healthy age-matched control group (1.35 ± 0.08 vs. 0.90 ± 0.08 U/mL, p = 0.002; 0.093 ± 0.06 vs. 0.006 ± 0.008 U/mL, p = 0.001; and 35.94 ± 1.37 vs. 68.90 ± 5.68 nmols/mL, p = 0.0001, respectively). Additionally, we found significant correlations between the main oxidative stress markers and the levels of systemic ammonia (r = 0.452, p = 0.005). Patients from group A had a significant increase of MDA as compared with those from group B (76.93 ± 5.48 vs. 50.06 ± 5.60 nmols/mL, p = 0.019). Also, there was a compensatory increase in the activity of both antioxidant enzymes (SOD and GPx) in patients with increased systemic ammoniemia (group A), as compared to HE patients from group B. Conclusions: Our results demonstrated a significant decrease in antioxidants enzymes activities (SOD and GPx), as well as a significant increase in MDA concentrations, adding new data regarding the influence of oxidative stress in HE pathogenesis in cirrhotic patients.

Pulmonary function and oxidative stress in workers exposed to styrene in plastic factory

2011 ◽  
Vol 30 (11) ◽  
pp. 1743-1750 ◽  
Author(s):  
Prakash Chandra Sati ◽  
Farah Khaliq ◽  
Neelam Vaney ◽  
Tanzeel Ahmed ◽  
Ashok K Tripathi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mean Value ◽  
Lung Damage ◽  
Control Group ◽  
Reducing Ability ◽  
Volatile Organic ◽  
Occupationally Exposed ◽  
The Mean ◽  
Group Workers ◽  
And Oxidative Stress

Styrene is a volatile organic compound used in factories for synthesis of plastic products. The pneumotoxicity of styrene in experimental animals is known. The aim of the present study was to study the effect of styrene on lung function and oxidative stress in occupationally exposed workers in plastic factory. Thirty-four male workers, between 18 and 40 years of age, exposed to styrene for atleast 8 hours a day for more than a year were studied, while 30 age- and sex-matched healthy subjects not exposed to styrene served as controls. Assessment of lung functions showed a statistically significant reduction ( p < 0.05) in most of the lung volumes, capacities (FVC, FEV1, VC, ERV, IRV, and IC) and flow rates (PEFR, MEF75%, and MVV) in the study group (workers) as compared to controls. Malondialdehyde (MDA) was observed to be significantly high ( p < 0.05) while ferric-reducing ability of plasma (FRAP) was significantly low ( p < 0.05) in styrene-exposed subjects. Reduced glutathione (GSH) level was significantly depleted in exposed subjects as compared to control group. The mean value of serum cytochrome c in styrene-exposed subjects was found to be 1.1 ng/ml (0.89–1.89) while in control its levels were under detection limit (0.05 ng/ml). It shows that styrene inhalation by workers leads to increased level of oxidative stress, which is supposed to be the cause of lung damage.

scholarly journals Decrease of Atherosclerosis Markers and Oxidative Stress After 1 Year Administration of Omega-3 Fatty Acids Supplements in Patients with Metabolic Syndrome

2014 ◽  
Vol 21 (3) ◽  
pp. 175-183
Author(s):  
Andreea Dragomir ◽  
Emila Rusu ◽  
Mihaela Posea ◽  
Gabriela Radulian
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Atherosclerosis Progression ◽  
Group A ◽  
Group B ◽  
The Impact ◽  
And Oxidative Stress

AbstractBackground and Aims: To assess the impact of 1 year administration of omega-3 fatty acids supplements on oxidative stress parameters and atherosclerosis progression. Material and Methods: A total of 284 patients with metabolic syndrome, aged 61±6.7 years, without clinical evidence of atherosclerosis were allocated to 2 groups, matched by sex and age: group A (140 patients) - diet according to ESC/EASD recommendations; group B (144 patients) - the same diet + capsules of fish oil (1g eicosapentanoic acid, 1g docosahexanoic acid, 0,1g a-tocopherol acetate). Body fat (BF) was measured by bioimpedance analysis. For oxidative stress evaluation we used the FormOx systems monitor on a blood drop and for progression of atherosclerosis the intima-media thickness (IMT) at common carotid artery. Patients were evaluated at baseline, after 6 months and 1 year. Results: IMT significantly decreased in group B vs group A at 1 year (p<0.0001) and was correlated with %BF (p<0.001), waist-to-hip ratio (WHR) (p=0.002), leptin (p< 0.001), adiponectin (p<0.05), leptin/adiponectin ratio (p< 0.001) and oxidative stress (p<0.001). Conclusions: One year administrations of omega-3 PUFA enriched diet reduces cardiovascular risk of metabolic syndrome patients, resulting in a significant decrease of oxidative stress and atherosclerosis progression.

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