Anju Singh

Research into drugs that can enhance cardiovascular health has been sparked by the rising prevalence of cardiovascular illnesses (CVDs). In addition to its anti-inflammatory and antioxidant qualities, Resveratrol (RES) is well known for its capacity to increase endothelial NO synthase (eNOS) activity. This page summarises RES's wide effects on energy metabolism, resilience to stress, exercise mimicking, circadian rhythm, lifespan control, and microbiome composition. This article addresses the poor and contradictory results shown in preclinical and clinical trials provides an update on the cardiovascular preventive properties of RES. The activation of AMP-activated protein kinase (AMPK), silent information regulator 1 (SIRT1), and natural antioxidant enzymes is associated with some of the positive effects of RES on the cardiovascular system. A microarray data summary indicates a strong correlation between the heart's reaction to calorie restriction and the transcriptional responses to RES. RES has been demonstrated to reduce contractile dysfunction, cardiac remodelling, and hypertrophy in several animal models of heart failure. Its preventive properties are believed to be due to several molecular pathways, including the suppression of prohypertrophic signalling molecules, enhancement of cardiac Ca2+ handling, control of autophagy, and decreases in inflammation. RES thus has the potential to be used in several novel therapeutic approaches for treating diseases such as atherosclerosis, ischemia/reperfusion damage, metabolic syndrome, heart failure, and inflammatory changes associated with ageing.

Arsenic-induced neurotoxicity is increasingly recognized as a major global health issue, leading to both developmental and degenerative neurological impairments, therefore, arsenic is becoming one of the potent environmental neurotoxins that can lead to significant health risks, particularly through long-term exposure via water, food, and air. Arsenic exposure can initiate a range of pathological events such as-disruption of mitochondrial function, oxidative stress, apoptosis, and inflammatory processes, which result in neuronal damage and cognitive dysfunction. Conversely, neurotrophins growth factors that regulate neuronal survival, growth, and function, are emerging as promising neuroprotective agents against such neurotoxic effects. This article explores the neuroprotective roles of BDNF (Brain-derived neurotrophic factor) and NGF (Nerve growth factor) in counteracting arsenic-induced neurodegeneration, through the analysis of epidemiology and mechanism-based preclinical studies of last decade. Arsenic disrupts neurotrophin signaling by inhibiting Trk (Tropomyosin receptor kinase) receptor phosphorylation and downstream survival pathways PI3K-AKT (Phosphoinositide 3-kinase–Protein kinase B), ERK-CREB (Extracellular signal-regulated kinase-cAMP response element-binding protein), thus contributing to neurodegeneration. In animal models, BDNF supplementation exhibited reduction in oxidative stress by 45–60%, neuronal apoptosis declined by about 55%, and improvement in cognitive function up to 40%. Additionally, NGF supplementation shows a 40-55% reduction in apoptosis. By integrating toxicological mechanisms with therapeutic perspectives, this narrative review underscores the potential of neurotrophin-based strategies to mitigate arsenic-related neurodegeneration and highlights future research directions for translational applications.