Injection of α-13’-carboxychromanol, when administered intraperitoneally, alleviated airway hyperresponsiveness induced by OVA and reduced the infiltration of inflammatory cells around the bronchi.

α-Amplexichromanol exhibited superior efficacy compared to α-13’-carboxychromanol, as evidenced by its enhanced regulation over airway hyperresponsiveness and more pronounced reduction of subepithelial inflammation.

Both compounds conferred protective effects through the reduction of pulmonary leukotriene C4 concentrations.

The beneficial effects of α-amplexichromanol were linked to the suppression of the allergy induction process, as evidenced by reduced levels of plasma cell secreting IgE, fewer mast cells, and a weakened Th2 immune response.

α-Tocopherol plays a pivotal role in preserving mitochondrial integrity.

It reinstates the appearance of 3rd sub-unit of mitochondrial COX_ETC in cells of bronchial epithelia.

Additionally, it ameliorates ultrastructural alterations in bronchial epithelial mitochondria.

It reduces IL-4 and inhibits 12/15-LOX in vitro and its metabolites.

Furthermore, α-tocopherol diminishes fibrosis of subepithelia, and quantity of TGF-β1, thereby overall attenuating asthmatic features.

Kiliç et al. demonstrated that vitamin E caused a reduction in respiratory tract swelling and over-reactivity in their study involving a guinea pig model.

Research conducted by Li-Weber et al. demonstrated that α-tocopherol decreases IL-4 protein concentrations in human peripheral blood T cells in a manner dependent on the dose, by modulating IL-4 at the mRNA stage.

It inhibits the DNA attachment and activity of redox system-controlled transcription factors, NF-κβ, and AP-1. Studies on the molecular process reveal that vitamin E prevents those factors of transcription from adhering to two crucial IL-4 promoter regions, thereby interfering with promoter functionality during T-cell activation.

NF-κB and AP-1 activation requires PKC. The attachment of transcription factors to two vital IL-4 promoter regions for NF-κB and AP-1 is blocked by vitamin E, thereby reducing IL-4 transcription.

Boscoboinik et al. revealed that α-tocopherol impedes the movement of PKC to the cell membrane in cells activated by the esters of phorbol and suppresses phosphorylation PKC.

d-α-Tocopheryl acetate from soy (vitamin E) is a robust lipid-soluble antioxidant that intercepts and neutralizes ROS, halting their chain reactions.

Dworski et al. found that in sensitive asthmatics, airway inflammation caused by allergens severely reduces NRF2 activity of the macrophages and SOD, leaving them unresponsive to NRF2 activators. Treatment of vitamin E for extended periods mitigated this allergen-activated decrease in NRF2 activity in alveolar macrophages.

Esculetin has the potential to influence both humoral and cellular-mediated immune responses.

Additionally, upon esculetin treatment, the production of Th17, Th2, and Th1-associated cytokines was suppressed.

Esculetin reduces airway hyperresponsiveness.

Suppresses Th2 response.

Reduces lung eotaxin levels.

Decreases eosinophilia in bronchoalveolar lavage fluid, and attenuates airway inflammation.

Lowers the levels of OVA-specific IgE.

Moreover, 15-LOX activity and lipid peroxidation are declined by vitamin E, which are crucial factors contributing to mitochondrial dysfunction, thereby restoring the function of lung mitochondria.

Baicalein alleviates OVA-induced inflammation of the airways caused by allergic reactions by controlling the NF-κB pathway.

Xu et al. findings substantiate that baicalein administration mitigates asthma-related pathological alterations by deactivating the NF-κB/inducible nitric oxide synthase pathway.

Baicalein mitigates airway inflammation and remodeling by inhibiting vascular endothelial growth factor and epidermal growth factor receptor-associated mechanistic routes in an OVA-induced asthma mouse model.

Mabalirajan et al. discovered that Baicalein treatment markedly decreased levels of metabolites of 15-LOX.

Baicalein also reduced perivascular and peribronchial inflammatory cell infiltration.

Baicalein treatment restored mitochondrial functions.

Screening a plant extract library, coupled with dereplication technology, identified baicalin as a novel PDE4-selective inhibitor.

Research by Park et al. revealed that baicalin specifically inhibits the enzymatic activity of PDE4A and 4B.

Baicalin treatment revealed a reduction in inflammatory cell infiltrates and cytokines like TNF-α in bronchoalveolar lavage fluids, suggesting baicalin’s in vivo anti-inflammatory effects are partially due to its PDE4 inhibition.