Table 2.
List of important nutraceuticals and their mode of action at molecular and cellular level in asthma
| Nutraceuticals | Mode of action | Reference |
|---|---|---|
| Phycocyanobilin | Inhibits NADPH oxidase complexes | (McCarty 2007) |
| Lipoic acid | Inhibits airway inflammation and hyperresponsiveness | (Cho et al. 2004) |
| Glycine | NF-κB and NLRP3 inhibition of inflammasome signaling pathway | (Fogarty et al. 2004) |
| Selenium | Ability to inhibit the path of free radicals and reduces the degree of inflammation | (Norton and Hoffmann 2012) |
| Zinc | Immunomodulator and oxidative stress severity control | (Rerksuppaphol and Rerksuppaphol 2016) |
| Mg | Ability to improve calcium influx to activate myosin light chain kinase (MLCK) | (Ohki et al. 1997) |
| Citrulline | L-citrulline can improve asthma control by increasing S-nitrosoglutathione (GSNO), the major source of NO bioactivité in the lung. It reduces NOS2 decouplement and reduces nitrosating stress asthma controller | (Holguin et al. 2019) |
| Folate | Suppresses allergic reactions and reduces allergy and asthma severity | (Blatter et al. 2013) |
| Biotin | Promotes human natural killer (NK) lymphocytes, for the generation of cytotoxic T lymphocytes (CTLs) | (Agrawal et al. 2016) |
| n-acetylcystine (NAC) | Supports H2S biosynthesis | (Lee et al. 2020) |
| Glycine | Dilates bronchioles | (Comhair et al. 2015) |
| Vitamin A | Regulation and production of pro-inflammatory cytokines such as TNF-α at cellular level and its control | (Bansal et al. 2014) |
| Vitamin C | Mitigates bronchoconstriction caused by exercise in asthma and stimulates the immune system | (Bansal et al. 2014; Harada et al. 2015) |
| Vitamin E | Inhibits airway eosinophilia and mucus cell hyperplasia AHR and inhibits iNOS, prostaglandin E2, pro-inflammatory cytokines, cyclo-oxygenase-2, and NF-κB expression | (Harada et al. 2015) |
| Omega-3-(n-3) fatty acids: α-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). | Protective effects against exercise-induced bronchoconstriction, and an inhibited release of pro-inflammatory cytokines | (Hodge et al. 1996) |
| Omega-6-(n-6) fatty acids: linoleic acid (LA), γ-linolenic acid (GLA), and arachidonic acid (ARA) | Mechanism remains to be elucidated | (Hodge et al. 1996) |
| Glutathione | GSH balances Th1/Th2 responses, modifies the metabolism of nitric oxide, and impedes ROS | (Ferrini et al. 2013) |
| Superoxide dismutase (SOD) | SOD protects from harmful ROS and inflammation of the airways | (Kim et al. 2015) |
| Glutathione peroxidases | Glutathione peroxidases prevent inflammation and destruction of the airways | (Shaheen et al. 2015) |
| Apocynin | Inhibits NADPH oxidase in airway inflammation | (Kim et al. 2012) |
| Naringenin | Inhibits airway inflammation by downregulating gene expression of IL-6, IL-8, IL-1β, TNF-α | (Chin et al. 2020; Wadhwa et al. 2021) |
LCNs, liquid crystalline nanoparticles; BEAS-2B, human bronchoepithelial cell line; ROS, reactive oxygen species; NADPH, Nicotinamide adenine dinucleotide phosphate; Nox, NAPDH oxidase; Nqo1, NADPH dehydrogenase quinone 1; GCLC, glutamate-cysteine ligase catalytic subunit; NO, nitric oxide; iNOS, inducible nitric oxide synthase; EPO, eosinophil peroxidase; HFD, high fat diet; PLCg1: phospholipase C gamma 1; PKCb2, protein kinase C beta 2; MAPK, mitogen activated protein kinase; ERK, extracellular regulated terminal kinase; JNK, c-Jun N-terminal kinase; SOD, superoxide dismutase