- Beijing ICP Preparation No. 10027328-24
- 2023(1)
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Objective: To investigate the effect of asiatica acid on the regulation of interleukin (IL)-6/signal transducer and transcription activator 3 (STAT3)/nuclear transcription factor-κB (NF-κB) pathway on the immune balance of Treg/Th17 in asthmatic mice. Methods: Ovalbumin (OVA) sensitization and excitation were used to prepare asthmatic mouse models, and were randomly divided into model group, low-dose asiatica acid group (54 mg/kg), high-dose asiatica acid group (108 mg/kg), and high-dose asiatica acid (108 mg/kg) + Colevin (IL-6/STAT3/NF-κB activator, 2 mg/kg) groups, with 10 animals in each group. In addition, 10 mice were given the same dose of normal saline as the control group during the sensitization and provocation stages, and the pathological morphology of lung tissue, the count of inflammatory cells in alveolar lavage fluid (BALF), the levels of Treg and Th17 cells in peripheral blood Treg/Th17, BALF and serum were treated as the control group, and the expression of IL-6/STAT3/NF-κB pathway-related proteins in lung tissue were detected. Results: Compared with the AND control group, the lung tissue of the mice in the model group had obvious pathological damage, and the proportion of Treg cells in peripheral blood, Treg/Th17, BALF, and serum IL-10 and IL-35 levels were decreased (P<0.05). Lung inflammation score, white blood cell count in BALF, eosinophil count, proportion of Th17 cells in peripheral blood, BALF and serum IL-17 and IL-6 levels, and IL-6 protein expression in lung tissue ANDp-STAT3/STAT3, p-NF-κB p65/NF-κB p65 were increased (P). <0.05)。 Low and high doses of asiaticoic acid can reverse the above pathological changes in asthma model mice, and high-dose asiaticoic acid has a stronger effect. Colivin can attenuate the effect of asiatica acid on the above pathological changes in asthma model mice. Conclusion: Centella asiatica acid can reduce airway inflammation and lung tissue damage and improve lung function by weakening the phosphorylation of IL-6 expression ANDSTAT3 and NF-κB, thereby inhibiting the production of inflammatory cells and inflammatory factors in asthmatic mice.
- Objective: To investigate the effect of asiatica acid on the regulation of interleukin (IL)-6/signal transducer and transcription activator 3 (STAT3)/nuclear transcription factor-κB (NF-κB) pathway on the immune balance of Treg/Th17 in asthmatic mice. Methods: Ovalbumin (OVA) sensitization and excitation were used to prepare asthmatic mouse models, and were randomly divided into model group, low-dose asiatica acid group (54 mg/kg), high-dose asiatica acid group (108 mg/kg), and high-dose asiatica acid (108 mg/kg) + Colevin (IL-6/STAT3/NF-κB activator, 2 mg/kg) groups, with 10 animals in each group. In addition, 10 mice were given the same dose of normal saline as the control group during the sensitization and provocation stages, and the pathological morphology of lung tissue, the count of inflammatory cells in alveolar lavage fluid (BALF), the levels of Treg and Th17 cells in peripheral blood Treg/Th17, BALF and serum were treated as the control group, and the expression of IL-6/STAT3/NF-κB pathway-related proteins in lung tissue were detected. Results: Compared with the AND control group, the lung tissue of the mice in the model group had obvious pathological damage, and the proportion of Treg cells in peripheral blood, Treg/Th17, BALF, and serum IL-10 and IL-35 levels were decreased (P<0.05). Lung inflammation score, white blood cell count in BALF, eosinophil count, proportion of Th17 cells in peripheral blood, BALF and serum IL-17 and IL-6 levels, and IL-6 protein expression in lung tissue ANDp-STAT3/STAT3, p-NF-κB p65/NF-κB p65 were increased (P). <0.05)。 Low and high doses of asiaticoic acid can reverse the above pathological changes in asthma model mice, and high-dose asiaticoic acid has a stronger effect. Colivin can attenuate the effect of asiatica acid on the above pathological changes in asthma model mice. Conclusion: Centella asiatica acid can reduce airway inflammation and lung tissue damage and improve lung function by weakening the phosphorylation of IL-6 expression ANDSTAT3 and NF-κB, thereby inhibiting the production of inflammatory cells and inflammatory factors in asthmatic mice.
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