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Abstract
Kirenol, a potential natural diterpenoid molecule, is mainly found in Sigesbeckia species. Kirenol has received a lot of interest in recent years due to its wide range of pharmacological actions. In particular, it has a significant ability to interact with a wide range of molecular targets associated with inflammation. In this review, we summarise the efficacy and safety of kirenol in reducing inflammation, as well as its potential mechanisms of action and opportunities in future drug development. Based on the preclinical studies reported earlier, kirenol has a good therapeutic potential against inflammation involved in multiple sclerosis, inflammatory bowel disorders, diabetic wounds, arthritis, cardiovascular disease, bone damage, and joint disorders. We also address the physicochemical and drug-like features of kirenol, as well as the structurally modified kirenol-derived molecules. The inhibition of pro-inflammatory cytokines, reduction in the nuclear factor kappa-B (NF-κB), attenuation of antioxidant enzymes, stimulation of heme-oxygenase-1 (HO-1) expression, and nuclear factor erythroid 2-related factor 2 (Nrf2) phosphorylation are among the molecular mechanisms contributing to kirenol’s anti-inflammatory actions. Furthermore, this review also highlights the challenges and opportunities to improve the drug delivery of kirenol for treating inflammation. According to the findings of this review, kirenol is an active molecule against inflammation in numerous preclinical models, indicating a path to using it for new drug discovery and development in the treatment of a wide range of inflammations.
Highlights
Pro-inflammatory cytokines such as the tumour necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and vascular endothelial growth factor (VEGF) play important roles in inflammation [1]
Acute and chronic inflammations are the two types of inflammation that can occur where the first is marked by pain, redness, and swelling, while the latter is marked by fatigue, fever, mouth sores, rashes, abdominal pain, and chest pain
The p anism of action of kirenol in the treatment of chronic inflammation caused Freund′s adjuvant (CFA) is outlined in Figure 2 based on the overall results f findings [24]
Summary
Pro-inflammatory cytokines such as the tumour necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and vascular endothelial growth factor (VEGF) play important roles in inflammation [1]. Inflammation is an adaptive response induced by a variety of signals, including microbial invasion or tissue damage [7]. Pattern recognition receptor (PRR) activation triggers intracellular signalling pathways that include kinases and transcription factors [11]. The signalling pathways listed above can promote the development of a range of inflammatory mediators, including cytokines. The NSAIDs target the cyclooxygenases (COX-1/2), which catalyse the first step from arachidonic acid to a variety of pro- and anti-inflammatory prostaglandins, leukotrienes, and thromboxanes, together with the lipoxygenases (LOX-5/12/15) [13]. Other important pathways include TLR-induced and mitogen-activated protein (MAP) kinase cascades, as well as glucocorticoid receptors that regulate transcription factors such as nuclear factoractivated T-cells (NFAT), nuclear factor-kappa B (NF-κB), and the signal transducer and activator of transcription 3 (STAT3).
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