目的 探究牡荊素對(duì)變應(yīng)性鼻炎大鼠鼻黏膜損傷的保護(hù)作用及其調(diào)控機(jī)制。方法 將SD大鼠隨機(jī)分為對(duì)照組、模型組、牡荊素（3、6、12 mg/kg），及牡荊素（12 mg/kg）＋EX527（5 mg/kg）組，每組各10只。除對(duì)照組外，其余各組大鼠均采用卵清白蛋白誘導(dǎo)建立變應(yīng)性鼻炎大鼠模型，模型構(gòu)建成功后，各組大鼠ip相應(yīng)劑量藥物，對(duì)照組和模型組大鼠ip等量的生理鹽水，1次/d，連續(xù)14 d。末次給藥結(jié)束后30 min，記錄各組大鼠行為學(xué)評(píng)分，觀察鼻黏膜組織病理形態(tài)學(xué)變化；檢測(cè)鼻黏膜組織超氧化物歧化酶（SOD）、谷胱甘肽過(guò)氧化物酶（GSH）、丙二醛（MDA）、活性氧氣簇（ROS）、鐵離子（Fe²⁺）水平，鐵死亡相關(guān)蛋白溶質(zhì)載體家族7成員11（SLC7A11）、谷胱甘肽過(guò)氧化物酶4（GPX4）、酰基輔酶A合成酶長(zhǎng)鏈家族成員4（ACSL4）以及沉默信息調(diào)節(jié)因子1（Sirt1）、叉頭框蛋白O1（FoxO1）、p-FoxO1、Ac-FoxO1蛋白表達(dá)。結(jié)果 與模型組相比，牡荊素各劑量組大鼠行為學(xué)評(píng)分均顯著降低，鼻黏膜損傷顯著改善（P＜0.05）；大鼠鼻黏膜組織勻漿SOD、GSH活性顯著升高，MDA、ROS、Fe²⁺含量均顯著降低（P＜0.05）；大鼠鼻黏膜組織SLC7A11、GPX4、Sirt1、FoxO1蛋白表達(dá)顯著升高，p-FoxO1、Ac-FoxO1、ACSL4蛋白表達(dá)顯著降低（P＜0.05），且呈劑量相關(guān)性。結(jié)論 牡荊素能夠改善變應(yīng)性鼻炎大鼠鼻黏膜損傷，其機(jī)制與激活鼻黏膜組織Sirt1/FoxO1通路，抑制細(xì)胞鐵死亡有關(guān)。

Objective To investigate the protective effect and regulatory mechanism of vitexin on nasal mucosal damage with allergic rhinitis in rats. Methods SD rats were randomly divided into control group, model group, vitexin (3, 6, and 12 mg/kg) group, and vitexin (12 mg/kg) + EX527 (5 mg/kg) with 10 rats in each group. Except for the control group, all other groups of rats were induced with ovalbumin to establish a rat model of allergic rhinitis. After the successful establishment of the model, the rats in each group were ip administered with the corresponding dose of drugs, and the rats in the control group and the model group were ip administered with the same amount of normal saline once daily for 14 consecutive days. 30 Minutes after the end of the last administration, record the behavioral scores of rats in each group and observe the pathological and morphological changes of nasal mucosa tissue. Detect the levels of SOD, GSH, MDA, ROS, and Fe²⁺ in nasal mucosa tissue, as well as the expression of ferroptosis related proteins SLC7A11, GPX4, ACSL4, Sirt1, FoxO1, p-FoxO1, and Ac-FoxO1 proteins. Results Compared with model group, the behavioral scores of rats in vitexin groups were significantly decreased, and the nasal mucosa injury was significantly improved (P＜0.05). The activities of SOD and GSH in rat nasal mucosa homogenate were significantly increased, while the contents of MDA, ROS and Fe²⁺ were significantly decreased (P＜0.05). The protein expressions of SLC7A11, GPX4, Sirt1, and FoxO1 in rat nasal mucosa were significantly increased, while the protein expressions of p-FoxO1, Ac-FoxO1, and ACSL4 were significantly decreased (P＜0.05), and were dose-dependent. Conclusion Vitexin can improve nasal mucosal damage in allergic rhinitis rats, and its mechanism is related to activating the Sirt1/FoxO1 pathway and inhibiting ferroptosis in nasal mucosal tissue.

R965

河南省高等學(xué)校重點(diǎn)科研項(xiàng)目（20B320117）