黄连素调节卵清蛋白诱导哮喘小鼠的Th细胞分化

doi:10.3969/j.issn.1006-6233.2024.05.012

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Abstract Objective: To investigate the regulation of berberine on Th cell differentiation and Notch signaling pathway in allergic asthmatic-model mice, as well as the repair of lung tissue injury. Methods: Mice were induced by OVA, and divided into control group, model group, low-dose berberine group, high-dose berberine group, and dexamethasone group after intervention with low and high doses of berberine and dexamethasone. The general conditions of the mice in each group were observed, HE staining was used to observe the inflammatory infiltration of lung tissue, flow cytometry was used to detect the proportions of Th1, Th2, and Th17 cells in lung tissue suspension, ELISA was used to detect the levels of IFN-γ, IL-4, and IL-17 in bronchoalveolar lavage fluid, and Western blot was used to detect the expression of Notch1 and Hes1 protein in lung tissue. Results: Compared with the control group, the mice in the model group had reduced food and water intake, anxiety, mucus in the nose and mouth, obvious inflammation in the lung tissue, decreased Th1 cell proportion and IFN-γ level (P<0.05), increased Th2 and Th17 cell proportions, and IL-4 and IL-17 levels (P<0.05), and increased Notch1 and Hes1 protein expression (P<0.05). Compared with the model group, the mice in the berberine and dexamethasone intervention groups had increased food and water intake, improved mental state, reduced mucus in the nose and mouth, reduced lung tissue inflammation, increased Th1 cell proportion and IFN-γ level (P<0.05), decreased Th2 and Th17 cell proportions, and IL-4 and IL-17 levels (P<0.05), and decreased Notch1 and Hes1 protein expression (P<0.05). Conclusion: Berberine intervention can alleviate lung tissue inflammatory damage in allergic asthma model by regulating Th subset differentiation and inhibiting Notch1 protein expression.

Key words： Berberine Asthma Th1/Th2 cells Th17 cells Notch1 protein

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2024.05.012 OR http://www.hbyxzzs.cn/EN/Y2024/V30/I5/768

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