Medicinal Plant Research 2024, Vol.14, No.2, 85-96 http://hortherbpublisher.com/index.php/mpr 88 Crocus sativus, Nigella sativa, and Curcuma longa have been traditionally used to enhance neural functions by increasing antioxidant levels and inhibiting acetylcholinesterase activity, thereby improving neurotransmitter balance (Khazdair et al., 2018). Additionally, compounds like Aromatic-turmerone and Apocynin have been identified as promising agents for modulating microglial polarization, which plays a role in neurotransmitter regulation (Alghamdi et al., 2022). Aromatic compounds derived from medicinal plants, such as flavonoids found in Trichilia catigua and Turnera diffusa, interact with multiple targets in the central nervous system (CNS). These interactions result in broad neuroprotection mediated by complementary processes and synergistic interactions, which can prevent and manage neurodegenerative diseases (Bernardo et al., 2021). Furthermore, Andrographolide, a compound extracted fromAndrographis paniculata, has been shown to cross the blood-brain barrier and reduce neuroinflammatory responses, thereby protecting brain function (Lu et al., 2019). 4.2 Anti-inflammatory properties Medicinal plants exhibit anti-inflammatory properties by inhibiting the production of pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α. For example, the neuroprotective effects of certain spice herbs are attributed to their ability to reduce pro-inflammatory cytokines and total nitrite generation, which are crucial in managing neuroinflammation (Khazdair et al., 2018). A study on peppermint essential oil found that it can reduce airway inflammation induced by exposure to PM10 (particulate matter) by inhibiting the JAK2/STAT3 signaling pathway (Figure 1). The research showed that peppermint essential oil effectively decreases the production of IL-6 and other pro-inflammatory cytokines, alleviating airway remodeling and collagen deposition (Kim et al., 2020). Similarly, Brazilian medicinal plants have been shown to inhibit inflammatory mediators like nuclear factor kappa B (NF-κB) and prostaglandin E2 (PGE2), further supporting their anti-inflammatory potential (Ribeiro et al., 2018). Figure 1 Schematic diagram of potential action of MEO on asthma under exposure of PM via inhibition of IL-6/JAK2/STAT3 pathway (Adopted from Kim et al., 2020) Image caption: The figure illustrates that PM10 exposure leads to the release of IL-6, which subsequently activates the JAK2/STAT3 signaling pathway, promoting the release of inflammatory factors, increasing matrix metalloproteinases, and triggering airway remodeling. MEO inhibits the expression of IL-6, blocks the phosphorylation of JAK2/STAT3, and suppresses the nuclear translocation of NF-κB, significantly reducing inflammation and airway damage. The results validate that MEO inhibits the pathogenesis of PM10-induced asthma through multiple signaling pathways, indicating its potential therapeutic effects (Adapted from Kim et al., 2020)
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