榛蘑多糖对尼古丁诱导大鼠肺损伤的保护作用

目的:研究榛蘑多糖（Armillaria mellea polysaccharides）对尼古丁诱导的大鼠肺损伤的保护作用及其作用机制。方法:将SD大鼠随机分为对照组，模型组，榛蘑多糖低、高剂量组。造模时，除对照组，其余各组腹腔注射尼古丁2 mg/kg体质量，榛蘑多糖低、高剂量组分别以200、400 mg/kg体质量灌胃榛蘑多糖。苏木精-伊红染色（Hematoxylin and Eeosin staining，HE）观察肺组织形态学变化；酶联免疫吸附方法检测肿瘤坏死因子-α（Tumor necrosis factor-α，TNF-α）、白介素-6（interleukin-6，IL-6）、白细胞介素-1β（Interleukin 1β，IL-1β）水平，TBA法检测丙二醛（malonaldehyde，MDA）水平，WST-1法检测超氧化物歧化酶（superoxide dismutase，SOD）活力；蛋白免疫印迹方法观察肺组织核因子相关因子2（nuclear factor erythroid 2-relted factor，Nrf2）、血红素加氧酶（heme oxygenase 1，HO-1）蛋白表达情况以及核因子-κB（nuclear fator-kappa B，NF-κB）蛋白的磷酸化水平。结果:与对照组相比，尼古丁诱导后血浆TNF-α、IL-6、IL-1β、MDA水平升高，SOD活力降低，肺组织NF-κB蛋白磷酸化表达水平升高，Nrf2、HO-1蛋白表达水平下降；与模型组相比，榛蘑多糖干预后减轻肺组织损伤程度，明显降低血浆TNF-α、IL-6、IL-1β、MDA水平，提高SOD活力，明显下调肺组织NF-κB蛋白磷酸化表达水平，提高Nrf2、HO-1蛋白表达水平。结论:榛蘑多糖对尼古丁诱导的肺损伤有抑制作用，其作用机制可能与NF-κB、Nrf2/HO-1信号通路的调控有关。

Protective Effects of Armillaria mellea Polysaccharides on Nicotine-induced Lung Injury in Rats

Objective: To investigate the protective effects of Armillaria mellea polysaccharides on lung injury induced by nicotine in rats. Methods: SD rats were randomly divided into control group, model group and Armillaria mellea polysaccharides low and high dose groups. During modeling, except for the normal group, the other groups were intraperitoneally injected with nicotine 2 mg/kg body weight, and the low and high dose groups were gavaged with Armillaria mellea polysaccharides 200 and 400 mg/kg body weight, respectively. The morphologic changes of lung tissue were observed by HE staining. The levels of TNF-α, IL-6 and IL-1β were detected by ELISA, MDA level was detected by TBA method, SOD activity was detected by WST-1 method. The protein expression levels of Nrf2, HO-1 and p-NF-κB in lung tissues were detected by Western blot assay. Results: Compared with the control group, after intervention of nicotine, the levels of TNF-α, IL-6, IL-1β and MDA were increased, the activity of SOD was decreased in plasma, the phosphorylation expression of NF-κB protein was increased, Nrf2 and HO-1 protein expression were decreased in lung tissue. Compared with the model group, after intervention of Armillaria mellea polysaccharides, the degree of lung tissue injury was alleviated, the levels of TNF-α, IL-6, IL-1β and MDA were significantly decreased, the activity of SOD was increased in plasma, the phosphorylation expression of NF-κB protein was significantly decreased, Nrf2 and HO-1 protein expression were significantly increased in lung tissue. Conclusion: Armillaria mellea polysaccharides could inhibit the lung tissue injury by nicotine induced. The mechanism of action may be related to its regulation of NF-κB and Nrf2/HO-1 signaling pathway.