Insights into the Therapeutic and Pharmacological Properties of Resveratrol as a Nutraceutical Antioxidant Polyphenol in Health Promotion and Disease Prevention.

Resveratrol (3, 5, 4'-trihydroxystilbene) is a polyphenolic derivative with herbal origin. It has attracted considerable attention in recent decades. Many studies have revealed the benefits of Resveratrol over several human disease models, including heart and neurological diseases, nephroprotective, immune regulation, antidiabetic, anti-obesity, age-related diseases, antiviral, and anticancer in experimental and clinical conditions. Recently, the antioxidant and anti-inflammatory activities of Resveratrol have been observed, and it has been shown that Resveratrol reduces inflammatory biomarkers, such as tissue degradation factor, cyclooxygenase 2, nitric oxide synthase, and interleukins. All of these activities appear to be dependent on its structural properties, such as the number and position of the hydroxyl group, which regulates oxidative stress, cell death, and inflammation. Resveratrol is well tolerated and safe even at higher pharmacological doses and desirably affects cardiovascular, neurological, and diabetic diseases. Consequently, it is plausible that Resveratrol can be regarded as a beneficial nutritional additive and a complementary drug, particularly for therapeutic applications. The present review provides an overview of currently available investigations on preventive and therapeutic characteristics and the main molecular mechanisms of Resveratrol and its potent derivatives in various diseases. Thus, this review would enhance knowledge and information about Resveratrol and encourage researchers worldwide to consider it as a pharmaceutical drug to struggle with future health crises against different human disorders.

Multiple sclerosis: new insights into molecular pathogenesis and novel platforms for disease treatment.

BACKGROUND: Multiple sclerosis (MS), a chronic inflammatory disorder, affects the central nervous system via myelin degradation. The cause of MS is not fully known, but during recent years, our knowledge has deepened significantly regarding the different aspects of MS, including etiology, molecular pathophysiology, diagnosis and therapeutic options. Myelin basic protein (MBP) is the main myelin protein that accounts for maintaining the stability of the myelin sheath. Recent evidence has revealed that MBP citrullination or deamination, which is catalyzed by Ca2+ dependent peptidyl arginine deiminase (PAD) enzyme leads to the reduction of positive charge, and subsequently proteolytic cleavage of MBP. The overexpression of PAD2 in the brains of MS patients plays an essential role in new epitope formation and progression of the autoimmune disorder. Some drugs have recently entered phase III clinical trials with promising efficacy and will probably obtain approval in the near future. As different therapeutic platforms develop, finding an optimal treatment for each individual patient will be more challenging. AIM: This review provides a comprehensive insight into MS with a focus on its pathogenesis and recent advances in diagnostic methods and its present and upcoming treatment modalities. CONCLUSION: MS therapy alters quickly as research findings and therapeutic options surrounding MS expand. McDonald's guidelines have created different criteria for MS diagnosis. In recent years, ever-growing interest in the development of PAD inhibitors has led to the generation of many reversible and irreversible PAD inhibitors against the disease with satisfactory therapeutic outcomes.

Berberine Recovered Oxidative Stress Induced by Sodium Nitrite in Rat Erythrocytes.

OBJECTIVE: Berberine, a plant derived alkaloid, present in Berberis species is well known as one of the most important antioxidants. The current research aimed to study the heamatoprotective characteristics of berberine and clarify its plausible mechanisms against sodium nitrite. METHODS: Forty numbers of male Sprague Dawley rats were categorized into five equal groups, including group 1: control (normal saline); group 2: berberine (100 mg/kg); group 3: sodium nitrite (80 mg/kg); group 4: sodium nitrite (80 mg/kg) plus berberine (50 mg/kg) and group 5: sodium nitrite (80 mg/kg) plus berberine (100 mg/kg) groups. All animals were orally administrated for two months once daily. At the end of the 60th day, blood samples were withdrawn by cardiac puncture and collected in test vials when the animals had been anesthetized with ketamine (70 mg/kg). Then, hemolysate was prepared and the oxidative stress biomarkers, lipid peroxidation, and antioxidant capacity of erythrocytes were evaluated. RESULTS: Feeding of rats with sodium nitrite remarkably enhanced malondialdehyde (MDA) (p=0.001) levels and considerably reduced the levels of glutathione (GSH) (p=0.001), and also reduced the enzymatic activities of glutathione peroxidase (GPx) (p=0.02), superoxide dismutase (SOD) (p=0.001), glutathione reductase (GR) (p=0.02), and catalase (CAT) (p=0.01). However, the co-administration of these animals with 100 mg/kg of berberine remarkably reverted the values to reach nearly a normal level. While 50 mg/kg berberine failed to restore significantly all of these antioxidant biomarkers at a normal level. CONCLUSION: Our results clearly demonstrated that berberine in a dose-dependent manner led to protection against sodium nitrite-induced oxidative injury in rat erythrocytes, which possibly reflects the antioxidant ability of this alkaloid.

Efficacy of melatonin in restoring the antioxidant status in the lens of diabetic rats induced by streptozotocin.

BACKGROUND: Melatonin is a well-known free radical scavenger. The present study aimed to investigate the effects of melatonin treatment on the antioxidant status in the lenticular tissue of streptozotocin (STZ)-induced diabetic rats. METHODS: Thirty-four male rats were randomly divided into four groups as follows: healthy control rats (group 1, n = 10); diabetic control rats (group 2, n = 10); melatonin-treated (5 mg/kg·day) diabetic rats (group 3, n = 10) and melatonin-treated (5 mg/kg·day) healthy rats (group 4, n = 4). Diabetes was induced by injection of streptozotocin (50 mg/kg, ip). Following 8-weeks of melatonin treatment, all rats were killed and the blood plasma and their lenses were stored at -70 °C for antioxidant enzyme activities assay and biochemical determination. RESULTS: The plasma glucose and lens malondialdehyde (MDA) increased significantly in the rats of group 2 as compared to the group 1. Also, a significant decrease in the levels of catalase (CAT) and glutathione reductase (GR) activities in the lenses and plasma reduced glutathione (GSH) was found. However, the levels of lenticular MDA (not significant) and the plasma glucose significantly decreased in the rats of group 3 compared to the group 2. Besides, the levels of CAT, GR in the rats lens and plasma GSH increased significantly. CONCLUSION: Diabetes mellitus induced hyperglycemia and oxidative stress, whereas melatonin decreased the blood glucose levels and lipid peroxidation and increased the activities of antioxidant enzymes in diabetic rat lenses.