## 1 Introduction  
Ox oxidative stress induced by excessive reactive oxygen species (ROS) contributes to inflammatory diseases and metabolic syndromes, including vascular and neurodegenerative diseases and various cancers [1, 2]. Specifically, aberrant ROS production causes cellular lipid oxidation and DNA damage, which affect cellular malfunction in cell division and differentiation, ion-homeostasis, regulation of apoptosis, and inflammation [3, 4]. To maintain homeostasis of ROS levels, several antioxidant systems and agents are present in our body; however, ROS production that exceeds antioxidant capacity causes physiological and pathological damage to cells [5; 6]. Among antioxidant mechanisms, nuclear factor erythroid 2-related factor 2 (Nrf2) is an extremely crucial regulator that controls the antioxidant response element (ARE), resulting in the transcriptional activation of phase II detoxification and antioxidant enzymes, including heme oxygenase-1 (HO-1). In the absence of oxidative stress, Nrf forms a complex with Kelch-like epichlorohydrin-related proteins (Keap1) in the cytoplasm and exists with low activity in a state bound to actin [7; 8]. Under physiological and pathological stress, such as excessive ROS production, modification of the cysteine residue of Keap1 releases Nrf2 through its conformational change and phosphorylation. This complex forms a complex with Maf protein to translocate into the nucleus and binds to AREs [9]. Then, Nrf initiates transcriptional activation of phase II detoxification and antioxidant enzymes, such as HO-1 and NAD(P)H:quinone oxidoreductase, resulting in the stimulation of cellular protective mechanisms against oxidative stress [10]. Therefore, pharmacological activators or agonists of Nrf2 are a promising strategy for oxidative stress-induced inflammatory diseases such as neurodegenerative, cardiovascular, and autoimmune diseases. [PERSON] et al. recently demonstrated that Nrf2 is an excellent biomarker in the maintenance of cellular redox and metabolic homeostasis, and some Nrf2 activators, including dimethyl fumarate, bardoxolone methyl, oligtraz, and sulforaphane, are clinical compounds in humans [11]. Furthermore, some Nrf2 agonists are in clinical trials to investigate the therapeutic effects in various inflammation and age-related diseases such as rheumatoid arthritis, Alzheimer's disease (AD), Parkinson's disease (PD), lupus erythematosus (LE), and liver damage [12]. In addition, Nrf2 deficiency favors the carcinogenesis of many different types of cancers [13], and phytochemicals targeting the Nrf2/HO-1 pathway reduce excessive carcinogenic metabolites and inhibit carcinogenesis [14; 15]. Therefore, the discovery of novel Nrf2 activators or agonists has the nutritional potential to inhibit inflammatory diseases. Plant-derived extracts and products are widely recognized for their potential as functional foods and traditional medicines due to their rich content of bioactive compounds with significant health benefits. These compounds have been shown to target various pathophysiological conditions, such as oxidative stress, aging, lipid oxidation, diabetes, gut inflammation, and cancer progression [16]. Additionally, plant-derived antioxidants may have an enhanced therapeutic potential due to their ability to reduce toxicity and inhibit the pathophysiological hallmarks of many human diseases by reducing oxidative stress [17; 18]. In proving the potential antioxidative activity related to the human disease models, zebrafish larvae have been a very promising technique to evaluate the overall performance of the agent which is being tested. The zebrafish model has been beneficial in human disease models or drug screening due to the shorter-timed response from larvae and the advantages of the smaller size of larvae, facilitating more accurate average data [19]. Numerous studies have demonstrated the effectiveness of natural antioxidants in treating oxidative stress-mediated inflammatory and metabolic diseases by activating the Nrf2-HO-1 signaling pathway [20].