阿里红多糖对用脂多糖诱导的急性肺损伤小鼠肺组织的保护作用及相关机制
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摘要
目的:研究阿里红多糖对用脂多糖(LPS)诱导的急性肺损伤(ALI)小鼠肺组织的保护作用及相关机制。方法:将60只SPF级BALB/c小鼠随机分为假手术组、模型组、地塞米松组(DEX组)、低剂量阿里红多糖组(FOA-L组)、中剂量阿里红多糖组(FOA-M组)和高剂量阿里红多糖组(FOA-H组)。在造模前,对这6组小鼠连续进行5天的灌胃。在末次给药3h后,建立小鼠ALI模型(除假手术组小鼠以外)。在造模24h后,检测各组小鼠相关的指标。结果:DEX组小鼠肺泡灌洗液中WBC的计数、蛋白的浓度、血清TNF-α及IL-1β的含量、肺组织中TLR-4、NF-κB的表达量均较灌药前降低。与模型组小鼠比较,FOA-L组、FOA-M组、FOA-H组小鼠肺泡灌洗液中WBC的计数、蛋白的浓度、血清TNF-α及IL-1β的含量、肺组织中TLR-4、NF-κB的表达量均较低,P <0.05。结论:阿里红多糖对用LPS诱导ALI小鼠的肺组织具有保护作用,且该作用具有剂量依赖性。阿里红多糖的这一作用机制可能与其可抑制NF-κB的信号通路,进而可抑制炎症因子的产生、减轻小鼠机体中的炎症反应有关。
objective: to study the protective effect of alizarin red polysaccharide on lung tissue of ALI mice induced by lipopolysaccharide(LPS) and its related mechanism. Methods: 60 spf-grade BALB/c mice were randomly divided into sham operation group, model group, dexamethasone group(DEX group), low-dose alizarin red polysaccharide group(foa-l group), medium-dose alizarin red polysaccharide group(foa-m group) and high-dose alizarin red polysaccharide group(foa-h group).Before modeling, the mice in the six groups were given oral gavage for 5 days. Mouse ALI model was established 3 h after the last administration(except the sham group).After 24 h of modeling, the relevant indexes of each group of mice were tested. Results: WBC count, protein concentration, serum tnf-alpha and il-1 beta, and expressions of tlr-4 and nf-kappab in lung tissues were all decreased in DEX group. Compared with mice in the model group, WBC count, protein concentration, serum tnf-alpha and il-1 beta, and expressions of tlr-4 and nf-kappa in lung tissues were all lower in the foa-l group, foa-m group and foa-h group(P < 0.05). Conclusion: alizarin red polysaccharide has protective effect on lung tissue induced by LPS in ALI mice, and the effect is dose-dependent. The mechanism of action of alipab may be related to its ability to inhibit the signal pathway of nf-kappab, thereby inhibiting the production of inflammatory factors and reducing the inflammatory response in mice.
objective: to study the protective effect of alizarin red polysaccharide on lung tissue of ALI mice induced by lipopolysaccharide(LPS) and its related mechanism. Methods: 60 spf-grade BALB/c mice were randomly divided into sham operation group, model group, dexamethasone group(DEX group), low-dose alizarin red polysaccharide group(foa-l group), medium-dose alizarin red polysaccharide group(foa-m group) and high-dose alizarin red polysaccharide group(foa-h group).Before modeling, the mice in the six groups were given oral gavage for 5 days. Mouse ALI model was established 3 h after the last administration(except the sham group).After 24 h of modeling, the relevant indexes of each group of mice were tested. Results: WBC count, protein concentration, serum tnf-alpha and il-1 beta, and expressions of tlr-4 and nf-kappab in lung tissues were all decreased in DEX group. Compared with mice in the model group, WBC count, protein concentration, serum tnf-alpha and il-1 beta, and expressions of tlr-4 and nf-kappa in lung tissues were all lower in the foa-l group, foa-m group and foa-h group(P < 0.05). Conclusion: alizarin red polysaccharide has protective effect on lung tissue induced by LPS in ALI mice, and the effect is dose-dependent. The mechanism of action of alipab may be related to its ability to inhibit the signal pathway of nf-kappab, thereby inhibiting the production of inflammatory factors and reducing the inflammatory response in mice.
引文
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[2]Tuinman P R,Dixon B,Levi M,et al.Nebulized anticoagulants for acute lung injury-a systematic review of preclinical and clinical investigations[J].Crit Care,2012,16(2):R70.
[3]凌亚豪,魏金锋,王爱平等.急性肺损伤和急性呼吸窘迫综合征发病机制的研究进展[J].癌变、畸变、突变,2017,29(2):151-154.
[4]Hirano,Y,Aziz,M,Yang,W L,et al.Neutralization of osteopontin attenuates neutrophil migration in sepsisinduced acute lung injury[J].Crit.Care,2015,19:53.
[5]Tianjie Qi,Haitao Li,Shuai Li.Indirubin improves antioxidant and anti-inflammatory functions in lipopolysaccharidechallenged mice[J].Oncotarget,2017,8(22):36658-36663.
[6]Xie,W,Wang,H,Liu,Q,et al.ResolvinD1 reduces apoptosis and inflammation in primary human alveolar epithelial type 2cells[J].Lab.Invest,2016,96,526-536.
[7]李旭,陈岩,白雪松.中药治疗急性肺损伤/急性呼吸窘迫综合征作用机制研究进展[J].辽宁中医药大学学报,2017,19(1):166-170.
[8]王勇.维药阿里红多糖的提取及生物活性的初步研究[D].新疆,新疆医科大学,2010,1-44.
[9]高剑,帕丽达·阿不力孜.维药阿里红多糖对卡氏肺孢子菌肺炎大鼠外周血中TNF-α、IL-8和sICAM-1水平的影响[J].中医中药与免疫调节,2016,4:437-443.
[10]周昱.阿里红多糖抗氧化和抗肿瘤及免疫调节活性的研究[D].新疆,新疆医科大学,2016,1-55.
[11]朱贲贲,马晓鹂,吴科锋,等.13-甲基嘌呤对脂多糖诱导小鼠急性肺损伤的保护作用及其机制研究[J].中国药房,2016,27(4):464-467.
[12]洪辉华,蔡宛如.急性肺损伤的发病机制及中医药治疗的实验研究进展[J].浙江中医药大学学报,2007,31(1):33-35.
[13]李成玉.地塞米松对脂多糖致大鼠急性肺损伤的治疗作用[D].遵义:遵义医学院,2010.