## 1 Introduction  
In 1956, [PERSON] presented the free radical theory, which suggested that the physiological damage triggered by free radicals was the prime determinant of aging [1]. The free radical theory was followed by the discovery of glutathione peroxidase (GPx) in 1957 and superoxide dismutase (SOD) in 1969, opening a new avenue for the study of antioxidants [2, 3]. [PERSON] and colleagues (1980) further expanded the free radical theory with mitochondria as the principal source and prime target of free radicals, creating a \"vicious cycle\" [4]. It was consolidated by the introduction of the concept of oxidative stress in 1985 which highlights that cellular damage is partly due to excess pro-oxidative factors over antioxidants [5]. The imbalance in metabolic sinks of pro- and anti-oxidants leads to redox alterations and cellular damage to carbohydrates, lipids, proteins, and DNA [6]. Among the free radical species, superoxide anion radical (O\({}_{2}\)\({}^{\bullet-}\)) and hydrogen peroxide (H\({}_{2}\)O\({}_{2}\)) play a vital role in oxidative damage [7]. Therefore, alleviation of oxidative stress and subsequent damage by increasing levels of endogenous antioxidants (GPx or SOD) is a rational approach. In recent years, polyphenols of plant-based diet have gained tremendous interest as dietary antioxidants [8]. Chemically, polyphenols are compounds with at least one aromatic ring and one or more hydroxyl groups [9]. Among the structural chemistry of polyphenols, catechol moiety, in particular, has the ability to occupy delocalized unpaired electrons, which is one of the antioxidant activities [10; 11]. Apart from the ability to directly scavenge free radicals, polyphenols act as signaling molecules to activate endogenous antioxidant pathways such as nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream targets [12]. By maintaining protective oxidoreductase and their nucleophilic substrates, the Nrf2 pathway boosts endogenous antioxidant enzymes [13]. During its activation, Nrf2 migrates from the cytoplasm into the nucleus, where it acts as a transcription factor and binds to the antioxidant response element (ARE) of genes involved in the antioxidant defense system, phase II drug detoxification, immunomododulation, and intracellular signaling [14]. Among its downstream effectors are SOD2 and GPx that can act as vital cytoprotective enzymes against oxidative stress. SOD2 protects cells by scavenging O\({}_{2}\)\({}^{\bullet-}\), while GPx enzymes play a well-recognized role in H\({}_{2}\)O\({}_{2}\) detoxification [15]. Therefore, the activation of these two enzymes presents a cogent strategy to tackle vital triggers of oxidative stress, i.e., O\({}_{2}\)\({}^{\bullet-}\) and H\({}_{2}\)O\({}_{2}\). Multiple polyphenols activate the Nrf2 pathway and its downstream SOD2 and GPx enzymes [7; 9]. In addition, the extracellular signal-regulated kinase (ERK) is an important upstream kinase that triggers the transcription of the Nrf2 pathway [16]. Multiple antioxidants such as erythropoietin, Puerrin, luteolin, and sulfuretin elicit their pharmacological impact via activation of the Nrf2 pathway [17; 18; 19; 20]. Among dietary antioxidants, phenolic acids, one of the major classes of polyphenols, have shown a strong ability to activate the Nrf2 pathway. Phenolic acids abundant in plant-based foods such as caffe acid (CA), gallic acid (GA), and ferulic acid (FA) have all shown the ability to activate endogenous antioxidants [21; 22; 23; 24; 25]. However, guided by their chemistry and structure-function, new analogs of phenolic acids are continuously synthesized to improve their antioxidant ability and expand their pharmacological outcome. Given the significant physiological importance of the Nrf2/ARE pathway, the identification of activators of this pathway has been a growing research interest.