Sun N, Zhang R X, Wang Y, Huang Z J, Han J, Bao Y S, Duan W Y, Dong C R, Deng G S, Zhuang Guoshun
Department of Otorhinolaryngology, Huadong Hospital, Fudan University, Shanghai 200040, China.
Department of Environmental, Shanghai 200232, China.
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2022 Jul 7;57(7):860-867. doi: 10.3760/cma.j.cn115330-20210701-00412.
To investigate the effects of ursolic acid (UA) on oxidative stress and inflammatory factors in a rat model of AR after PM2.5 exposure. Sixty healthy female SD rats were randomly divided into five groups: normal control group (NC group), PM2.5 unexposed AR group (AR group), PM2.5 exposed AR group (ARE group), UA intervention AR group (AR+UA group), and UA intervention PM2.5 exposed AR group (ARE+UA group), with 12 rats in each group. AR model was performed by a basal sensitization with intraperitoneal injection of ovalbumin (OVA) and followed by nasal instillation. PM2.5 exposure was carried out by inhalation exposure system at a concentration of 200 μg/m for 3 h/d for 30 days. UA intervention group was given UA intragastric administration at 20 mg/(kg·d). AR symptoms including sneezing, nasal scratching and nasal secretion of rats in each group were observed. The activities of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in nasal mucosa were tested. The pathological changes of nasal mucosa were observed by HE staining. The levels of OVA-sIgE, IL-6 and IL-17 in serum were measured by enzyme-linked immunosorbent assay (ELISA). Protein microarray was used to measure the expression of multiple inflammation cell factors in nasal mucosa. Statistical analysis was performed with SPSS 20.0. After UA intervention, the frequency of nasal sneezing, scratching and nasal secretion in ARE+UA group were lower than those of ARE group (<0.05). Pathological examination of nasal mucosa showed that ARE+UA group had less inflammatory granulocyte infiltration and less pathological damage to the epithelial layer than ARE group. The activities of SOD in nasal mucosa of ARE+UA group were higher than those of ARE group ((50.10±3.09) U/mg (20.13±1.30) U/mg, value was 597.54, <0.01). The contents of MDA in nasal mucosa of ARE+UA group were lower than those of ARE group ((57.78±12.36) nmol/g (124.12±9.40) nmol/g, value was 115.51, <0.01). The expression levels of OVA-sIgE, IL-6 and IL-17 proteins were lower in the ARE+UA group than those in ARE group ((11.61±0.27) ng/ml (20.30±0.67) ng/ml, (47.59±15.49) pg/ml (98.83±10.98) pg/ml, (623.30±8.75) pg/ml (913.32±9.06) pg/ml, value was 283.42, 80.45, 683.73, respectively, all <0.01). After UA intervention, protein microarray analysis showed that the expression of IL-4, IL-6, IL-13, chemokine CXCL7, IL-1α, IL-1β, MMP-8 and MCP-1 in ARE+UA group was decreased compared with ARE group while IFN-γ and IL-10 increased (all <0.01). UA can reduce the aggravated AR symptoms and pathological damage of nasal mucosa, inhibit oxidative stress and release of inflammatory factors after PM2.5 exposure, and thus plays a protective role in the pathological damage of AR induced by PM2.5 exposure.
探讨熊果酸（UA）对PM2.5暴露后变应性鼻炎（AR）大鼠模型氧化应激及炎症因子的影响。将60只健康雌性SD大鼠随机分为5组：正常对照组（NC组）、未暴露于PM2.5的AR组（AR组）、暴露于PM2.5的AR组（ARE组）、UA干预AR组（AR + UA组）和UA干预暴露于PM2.5的AR组（ARE + UA组），每组12只。通过腹腔注射卵清蛋白（OVA）进行基础致敏，随后滴鼻建立AR模型。通过吸入暴露系统以200 μg/m的浓度、每天3小时、持续30天进行PM2.5暴露。UA干预组给予20 mg/(kg·d)的UA灌胃给药。观察每组大鼠的AR症状，包括打喷嚏、抓鼻和鼻分泌物。检测鼻黏膜中超氧化物歧化酶（SOD）活性和丙二醛（MDA）水平。通过苏木精-伊红（HE）染色观察鼻黏膜的病理变化。采用酶联免疫吸附测定（ELISA）法检测血清中OVA-sIgE、白细胞介素-6（IL-6）和白细胞介素-17（IL-17）水平。使用蛋白质芯片检测鼻黏膜中多种炎症细胞因子的表达。采用SPSS 20.0进行统计分析。UA干预后，ARE + UA组的鼻打喷嚏、抓鼻和鼻分泌物频率低于ARE组（<0.05）。鼻黏膜病理检查显示，ARE + UA组的炎症粒细胞浸润少于ARE组，上皮层病理损伤也少于ARE组。ARE + UA组鼻黏膜中SOD活性高于ARE组（（50.10±3.09）U/mg对（20.13±1.30）U/mg，t值为597.54，<0.01）。ARE + UA组鼻黏膜中MDA含量低于ARE组（（57.78±12.
