# Functions of Representative Terpenoids and Their Biosynthesis Mechanisms in Medicinal Plants
## 2 Function of terpenoids in Human Health  
Recent studies have demonstrated that terpenoids in medicinal plants possess pharmacological properties that promote human health [15; 16]. For example, artemisinin is a widely used anti-malarial medicine that is used to protect millions of people from malaria every year [17; 18]. Ginkgolides are natural antagonists of platelet activation, possess neuroprotective and reparative effects, and are crucial in the treatment of ischemic strokes [19]. Cannabinoids have been used for thousands of years for their anxiolytic and anesthetic effects [20]. Paclitaxel plays a significant role in anti-tumor therapy by inducing oxidative stress, and is considered one of the most successful natural anti-cancer drugs available [21]. Figure 1: Several important medicinal plants and their specific terpenoids. Furthermore, terpenoids have been found to have additional biological functions, such as anti-oxidant and anti-inflammatory effects [22; 23]. Terpenoids exert their therapeutic functions through various signaling pathways and receptors. For example, cannabinoids rely on their ability to interact with the body's endocannabinoid system--the G protein-coupled cannabinoid receptors (CB1 and CB2)--to exert their biological properties, including infection, inflammation, and hard tumors [24]. Due to the complex and diverse involvement mechanisms of terpenoids, we mainly focused on their signaling pathways in inflammatory and oxidative stress. NF-kB (Nuclear factor-kappa B) is involved in inflammatory processes, cell proliferation, and defense against apoptosis [25; 26]. Artemisinin has been shown to significantly inhibit the expression of NF-kB and mitogen-activated protein kinase (MAPK) signaling genes, making it a potential drug for inflammation treatment [27]. Tanshinone IIA has been reported to play a role in the inflammatory response through the Toll-like receptor 4 (TLR4)/transforming growth factor activated kinase-1 (TAK1)/NF-kB signaling cascade [28; 29; 30]. Cannabinoids regulate anti-inflammatory responses by inhibiting NF-kB and other pathways [31]. Ginkgolides can significantly inhibit the expression of NF-kB, reduce the phosphorylation levels of p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) proteins in the mitogen-activated protein kinase (MAPK) signaling pathway, and reduce the expression of pro-inflammatory cytokine genes, thereby exerting anti-inflammatory effects [32]. Similarly, paclitaxel can inhibit the expression of NF-kB, inhibiting tumor growth and having anti-tumor effects [33]. Oxidative stress plays a crucial role in antitumor activity, cardiovascular activity, and atherogenesis [33; 34; 35; 36]. Ginkgolide can cross the blood-brain barrier, activating the nuclear factor E2-associated factor 2 (Nrf2) signaling pathway and upregulating the expression of oxidative stress-related proteins heme oxygenase-1 (HO-1), quinone oxidoreductase 1 (NQO1), superoxide dismutase (SOD), and Nuclear factor-E2-related factor 2 (Nrf2) to reduce the cellular damage caused by oxidative stress [31]. Oxidative stress is central to the mechanism of paclitaxel's antitumor activity as it increases mitochondrial ROS production and inhibits endoplasmic reticulum utilization and antioxidant enzymes and peptides [33; 34; 35; 37; 38]. Recent studies have found that tanshinone IIA prevents oxidative stress by increasing the activities of total antioxidant capacity (T-AOC), SOD, glutathione peroxidase (GSH-Px), and catalase (CAT) to reduce atherosclerosis [35; 39]. Cannabinoids regulate antioxidants by activating antioxidant enzymes, regulating glutathione levels, and inhibiting pro-oxidases to regulate anti-inflammatory properties [40]. Although it has been discovered that terpenoids can be involved in treating diseases through multiple strategies, the specific regulatory pathways for disease treatment are not yet fully understood. Further validation is still required via utilizing more animal models or clinical trials to elucidate their regulatory mechanisms.