Tissue & cell · 2026
Rhizoma Dioscoreae Nipponicae targets SIRT1 to regulate p38 MAPK and eosinophils mitophagy in asthma.
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Hong Huihua, Li Mengyao, Xue Shengzhong, Wang Weiyi
Аннотация
AIM: This study aimed to investigate the mechanism by which Rhizoma Dioscoreae Nipponicae (RDN) targets SIRT1 to relieve the airway inflammation in asthma.
METHODS: An OVA-induced asthma mouse model was established and eosinophils (Eos) were isolated to investigate the effects of RDN on Eos and mice. RDN, the SIRT1 inhibitor nicotinamide (Nic), and the p38 MAPK inhibitor SB203580 were administered. Pathological injury, inflammatory factors, and Eos counts were evaluated by hematoxylin and eosin (HE) staining, ELISA, and blood analysis, respectively. Eos viability was measured using the CCK-8 kit, while immunofluorescence was used to quantify Eos and assess the colocalization of mitophagy markers LC3 and Tom20. Mitochondrial function and mitophagy were analyzed through transmission electron microscopy (TEM), mitochondrial membrane potential (MMP) assay, H2DCFDA fluorescent probe, and ATP detection. Western blotting analysis was performed to detect mitophagy-related proteins and p38 MAPK molecules.
RESULTS: RDN significantly reduced Eos viability, inflammatory factors, and pathological injury, whereas these effects were reversed by Nic addition, suggesting that RDN alleviates asthma by targeting SIRT1. Additionally, RDN decreased mitophagy, ROS, and ATP levels, while it increased MMP; these alterations were reversed by Nic addition, indicating that SIRT1 plays a regulatory role in mitochondrial function and mitophagy in both Eos and mice. Moreover, Nic addition reversed the RDN-induced reduction in the p-p38/p38 ratio and SB203580 addition restored the effects of RDN, indicating that SIRT1 regulates the p38 MAPK signaling pathway in both Eos and mice.
CONCLUSION: Our study confirms that RDN targets SIRT1 to inhibit airway inflammation and pathological injury in eosinophils and OVA-induced asthma mice through regulation of the p38 MAPK pathway and Eos mitophagy.
METHODS: An OVA-induced asthma mouse model was established and eosinophils (Eos) were isolated to investigate the effects of RDN on Eos and mice. RDN, the SIRT1 inhibitor nicotinamide (Nic), and the p38 MAPK inhibitor SB203580 were administered. Pathological injury, inflammatory factors, and Eos counts were evaluated by hematoxylin and eosin (HE) staining, ELISA, and blood analysis, respectively. Eos viability was measured using the CCK-8 kit, while immunofluorescence was used to quantify Eos and assess the colocalization of mitophagy markers LC3 and Tom20. Mitochondrial function and mitophagy were analyzed through transmission electron microscopy (TEM), mitochondrial membrane potential (MMP) assay, H2DCFDA fluorescent probe, and ATP detection. Western blotting analysis was performed to detect mitophagy-related proteins and p38 MAPK molecules.
RESULTS: RDN significantly reduced Eos viability, inflammatory factors, and pathological injury, whereas these effects were reversed by Nic addition, suggesting that RDN alleviates asthma by targeting SIRT1. Additionally, RDN decreased mitophagy, ROS, and ATP levels, while it increased MMP; these alterations were reversed by Nic addition, indicating that SIRT1 plays a regulatory role in mitochondrial function and mitophagy in both Eos and mice. Moreover, Nic addition reversed the RDN-induced reduction in the p-p38/p38 ratio and SB203580 addition restored the effects of RDN, indicating that SIRT1 regulates the p38 MAPK signaling pathway in both Eos and mice.
CONCLUSION: Our study confirms that RDN targets SIRT1 to inhibit airway inflammation and pathological injury in eosinophils and OVA-induced asthma mice through regulation of the p38 MAPK pathway and Eos mitophagy.