## 1 Introduction  
Oxidative stress (OS) in biological systems is characterized by a set of alterations at molecular, cellular, and tissue levels and is part of the pathogenesis of acute or chronic neurodegenerative processes [1, 2]. It arises from an imbalance between oxidants and antioxidants, caused either by elevated levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) or by dysfunction of the antioxidant system [3, 4, 5]. At physiological concentrations, ROS play an important regulatory role in different biological processes as gene expression, apoptosis, and signal transduction [6]. However, an uncontrolled increase in the levels of reactive species triggers a chain of radical reactions, disrupting cellular redox homeostasis and causing serious damage to cellular macromolecules. In one non-specific way, ROS can cause nucleic acid and lipid oxidation, protein misfolding, and aggregation, ultimately compromising cellular integrity and function and leading to apoptosis [7; 8; 9]. Hydrogen peroxide, along with superoxide anions and hydroxyl radicals, are among the most harmful ROS. Processes such as amyloid aggregation [10; 11], dopamine oxidation [12], and brain ischemia/reperfusion injury [13] are closely related to excessive hydrogen peroxide production, while an overabundance of superoxide anions is associated with N-methyl-D-aspartate (NMDA)-induced neurotoxicity [1; 2]. The brain's high oxygen consumption and lipid content make it particularly vulnerable to damage from ROS and RNS. Markers of lipid peroxidation, such as malondialdehydedehyde and 4-hydroxynonenal, have been detected in the brain of patients diagnosed with neurodegenerative disorders as a Parkinson's or Alzheimer's diseases [14]. Antioxidants are molecules that play a crucial role in managing cellular protection against oxidative stress by either preventing free radical formation or neutralizing them during their propagation phase [15]. From a scientific standpoint, natural antioxidants show great promise in aiding the prevention and treatment of neurodegenerative diseases [16]. Resveratrol (RVT, trans-3,5,4\({}^{\prime}\)-trihydroxystilbene) was isolated for the first time from Takaoka in 1940 from the root of _Veratrum grandiflora_[17]. Since then it has been discovered in more than 70 plant species, especially in highly pigmented vegetables and fruits as a grape, mulberries, bilberries, etc. [18]. As a polyphenic compound and phytoplankton, it has demonstrated several biological activities, including anti-inflammatory, vasorelasing, anticancer, antiaging, and antiallergenic properties [19; 20; 21; 22]. Resveratrol is among the most extensively studied antioxidant compounds [22; 23]. Its strong antioxidant properties have been demonstrated in numerous in vitro and in vivo studies. The cytoprotective effects of resveratrol (RVT) against H\({}_{2}\)O\({}_{2}\)-induced apoptosis in Caco-2 cells are associated with decreased malondialdehydedehyde (MDA) levels and upregulated expression of superoxide dismutase (SOD) and heme oxygenase-1 (HO-1), contributing to intracellular ROS scavenging and reduction [24]. Additionally, RVT (at concentrations of 5-25 \(\upmu\)M) has been shown to mitigate \(\Delta\beta\)-induced oxidative damage and inhibit apoptosis in various in vitro oxidative stress models, including PC12 cells, human umbilical vein endothelial cells (HUVECs), SH-SY5Y neuroblastoma cells, and hippocampal neuronal cultures [25; 26; 27; 28; 29]. In diabetic patients, RVT treatment reduces advanced glycation end product (AGE)-induced oxidative stress and apoptosis [30]. In rats with ischemic spinal cord damage, RVT reduces plasma MDA levels while enhancing the enzymatic activity of superoxide dismutase (SOD) and catalase (CAT) [31]. The limited bioavailability and poor stability of RVT significantly constrain its practical application, despite its broad spectrum of pharmacological effects [32; 33; 34].