蒲地蓝消炎口服液对脂多糖致大鼠急性肺损伤的影响
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摘要
目的:探讨蒲地蓝消炎口服液(PDL)对脂多糖(LPS)导致的大鼠急性肺损伤的影响及作用机制。方法:72只Wistar大鼠,按体质量随机分为空白组,模型组,地塞米松组,PDL 7,3. 5,1. 75 g·kg~(-1)·d~(-1)组。模型组,地塞米松组,PDL 7,3. 5,1. 75 g·kg~(-1)·d~(-1)组雾化吸入LPS制备大鼠急性肺损伤模型。检测各组大鼠肺泡灌洗液(BALF)中白细胞总数,酶联免疫吸附测定(ELISA)检测肺组织中核转录因子-κB(NF-κB),白细胞介素-10(IL-10)的含量,苏木素-伊红(HE)染色观察肺组织形态学改变,探讨不同剂量PDL对急性肺损伤大鼠的影响。结果:与模型组比较,PDL 7,3. 5 g·kg~(-1)·d~(-1)组BALF中白细胞总数明显降低(P <0. 05); PDL 7,3. 5,1. 75 g·kg~(-1)·d~(-1)组NF-κB表达量明显降低(P <0. 05); PDL 3. 5 g·kg~(-1)·d~(-1)组IL-10表达量明显升高(P <0. 05); PDL 7 g·kg~(-1)·d~(-1)组肺组织中炎症反应减轻,水肿、瘀血等病理改变明显缓解(P <0. 05)。结论:PDL对急性肺损伤模型具有保护作用,可减轻大鼠急性肺损伤模型中肺组织的炎症反应,其机制与NF-κB,IL-10的表达相关,对肺组织的病理损伤有修复作用。
Objective: To explore the effect and mechanism of Pudilan Xiaoyan oral liquid( PDL) on the acute lung injury rat induced by lipopolysaccharide( LPS). Method: The 72 Wistar rats were randomly divided into control group,model group,dexamethasone group,PDL 7,3. 5,1. 75 g·kg~(-1)·d~(-1) group according to body weight. The acute lung injury model was made through inhalation with lipopolysaccharide in the model group,hexadecadrol group,PDL 7,3. 5,1. 75 g·kg~(-1)·d~(-1) group. To examining each rat alveolar lavage fluid( BALF) of the total number of white blood cells,enzyme-linked immunosorbent assay( ELISA) was used to detect the levels of nuclear transcription factors-kappa B( NF-κB) and interleukin~(-1)0( IL-10). Hematoxylin-eosin( HE) staining was used to observe morphological changes of lung tissue and explore different doses of PDL effect on acute lung injury in rats. Result: Compared with model group,the account of leukocyte in BALF decreased significantly in PDL 7 g·kg~(-1)·d~(-1) group and PDL 3. 5 g·kg~(-1)·d~(-1) group( P < 0. 05). The expression of NF-κB significantly decreased in PDL 7,3. 5,1. 75 g·kg~(-1)·d~(-1) group( P < 0. 05). And the expression of IL-10 significantly increased in PDL 3. 5 g·kg~(-1)·d~(-1) group( P < 0. 05). In PDL 7 g·kg~(-1)·d~(-1) group,the inflammation,edema and congestion in lung tissue reduced( P < 0. 05). Conclusion: PDL has a significant protective effect on the inflammation of acute lung injury model,and its mechanism is related to the expressions of NF-κB and IL-10. PDL could also repair the injury of lung in acute lung injury model.
Objective: To explore the effect and mechanism of Pudilan Xiaoyan oral liquid( PDL) on the acute lung injury rat induced by lipopolysaccharide( LPS). Method: The 72 Wistar rats were randomly divided into control group,model group,dexamethasone group,PDL 7,3. 5,1. 75 g·kg~(-1)·d~(-1) group according to body weight. The acute lung injury model was made through inhalation with lipopolysaccharide in the model group,hexadecadrol group,PDL 7,3. 5,1. 75 g·kg~(-1)·d~(-1) group. To examining each rat alveolar lavage fluid( BALF) of the total number of white blood cells,enzyme-linked immunosorbent assay( ELISA) was used to detect the levels of nuclear transcription factors-kappa B( NF-κB) and interleukin~(-1)0( IL-10). Hematoxylin-eosin( HE) staining was used to observe morphological changes of lung tissue and explore different doses of PDL effect on acute lung injury in rats. Result: Compared with model group,the account of leukocyte in BALF decreased significantly in PDL 7 g·kg~(-1)·d~(-1) group and PDL 3. 5 g·kg~(-1)·d~(-1) group( P < 0. 05). The expression of NF-κB significantly decreased in PDL 7,3. 5,1. 75 g·kg~(-1)·d~(-1) group( P < 0. 05). And the expression of IL-10 significantly increased in PDL 3. 5 g·kg~(-1)·d~(-1) group( P < 0. 05). In PDL 7 g·kg~(-1)·d~(-1) group,the inflammation,edema and congestion in lung tissue reduced( P < 0. 05). Conclusion: PDL has a significant protective effect on the inflammation of acute lung injury model,and its mechanism is related to the expressions of NF-κB and IL-10. PDL could also repair the injury of lung in acute lung injury model.
引文
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[13]周雅阳,张广平,宋玲,等.痰热清吸入溶液的药效学评价[J].中国实验方剂学杂志,2019,doi:10. 13422/j. cnki. syfjx. 20190954.
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[18] Ouyang W,Rutz S,Crellin N K,et al. Regulation and functions of the IL-10 family of cytokines in inflammation and disease[J]. Annu Rev Immunol,2011,doi:10. 1146/annurev-immunol-031210-101312.
[19] Hos D,Bucher F,Regenfuss B,et al. IL-10 indirectly regulates corneal lymphangiogenesis and resolution of inflammation via macrophages[J]. Am J Pathol,2016,186(1):159-171.
[20] LIU Y,FANG S,LI X,et al. Aspirin inhibits LPSinduced macrophage activation via the NF-κB pathway[J]. Sci Rep,2017,7(1):11549.
[21] Cuzzocrea S,Mazzon E,Dugo L,et al. Absence of endogenous interleukin-10 enhances the evolution of acute lung injury[J]. Eur Cytokine Netw,2002,13(3):285-297.
[22] Nakajima H,Takatsu K. Role of cytokines in allergic airway inflammation[J]. Int Arch Allergy Immunol,2007,142(4):265-273.
[2]李清梅,袁名权,陈虎,等. FK866对脂多糖诱导大鼠急性肺损伤的影响[J].现代医药卫生,2018,34(17):2635-2637,2641.
[3] LI W,QIU X,JIANG H,et al. Ulinastatin inhibits the inflammation of LPS-induced acute lung injury in mice via regulation of AMPK/NF-κB pathway[J]. Inter Immunopharmacol,2015,29(2):560-567.
[4]杜洪喆,胡思源,钟成梁,等.蒲地蓝消炎口服液不同剂量治疗小儿急性咽-扁桃体炎肺胃实热证的多中心临床研究[J].中草药,2017,48(4):753-759.
[5]吴璇,于莉,胡涛,等.蒲地蓝消炎口服液对呼吸道合胞病毒和腺病毒的体外抗病毒作用[J].实用医学杂志,2015,31(11):1838-1840.
[6]王丽,刘金星,张师前.蒲地蓝消炎口服液治疗慢性盆腔炎的临床观察[J].中华医院感染学杂志,2015,25(22):5169-5171.
[7]张勇,王志颐,江满杰,等.蒲地蓝消炎口服液治疗慢性支气管炎急性发作临床研究[J].中国药业,2015,24(3):16-18.
[8]卞丽玲,杨丰文,王媛,等.蒲地蓝消炎口服液治疗小儿化脓性扁桃体炎有效性及安全性的系统评价[J].中国中药杂志,2017,42(8):1482-1488.
[9]钱文娟,杨瑞,谢彤,等.蒲地蓝消炎口服液治疗甲型H1N1流感病毒性肺炎的GC-MS代谢组学研究[J].中草药,2018,49(10):2258-2264.
[10]汤玉华.蒲地蓝消炎口服液治疗社区获得性肺炎伴发热患者的效果观察[J].河南医学研究,2016,25(4):674-675.
[11]王建华,李清.蒲地蓝联合左氧氟沙星治疗社区获得性肺炎的研究[J].现代中西医结合杂志,2008,17(32):4966-4967.
[12]张亚平,张广平,苏萍,等.不同途径吸入脂多糖致大鼠急性肺炎模型的优选[J].中国实验方剂学杂志,2018,24(7):82-88.
[13]周雅阳,张广平,宋玲,等.痰热清吸入溶液的药效学评价[J].中国实验方剂学杂志,2019,doi:10. 13422/j. cnki. syfjx. 20190954.
[14] Mosbah A A,Abdellatif N A,Sorour E I,et al. Serum SP-D levels as a biomarker of lung injury in children suffering of bronchopneumonia[J]. J Egypt Soc Parasitol,2012,42(1):25-32.
[15] Kitamura Y,Nomura M,Shima H,et al. Acute lung injury associated with systemic inflammatory response syndrome following subarachnoid hemorrhage:a survey by the shonan neurosurgical association[J]. Neurol Med Chir(Tokyo),2010,50(6):456-460.
[16] Hobbs S,Reynoso M, Geddis A V, et al. LPSstimulated NF-κB p65 dynamic response marks the initiation of TNF expression and transition to IL-10expression in RAW 264. 7 macrophages[J]. Physiol Rep,2018,6(21):e13914.
[17] Hoesel B,Schmid J A. The complexity of NF-kappaB signaling in inflammation and cancer[J]. Mol Cancer,2013,doi:10. 1186/1476-4598-12-86.
[18] Ouyang W,Rutz S,Crellin N K,et al. Regulation and functions of the IL-10 family of cytokines in inflammation and disease[J]. Annu Rev Immunol,2011,doi:10. 1146/annurev-immunol-031210-101312.
[19] Hos D,Bucher F,Regenfuss B,et al. IL-10 indirectly regulates corneal lymphangiogenesis and resolution of inflammation via macrophages[J]. Am J Pathol,2016,186(1):159-171.
[20] LIU Y,FANG S,LI X,et al. Aspirin inhibits LPSinduced macrophage activation via the NF-κB pathway[J]. Sci Rep,2017,7(1):11549.
[21] Cuzzocrea S,Mazzon E,Dugo L,et al. Absence of endogenous interleukin-10 enhances the evolution of acute lung injury[J]. Eur Cytokine Netw,2002,13(3):285-297.
[22] Nakajima H,Takatsu K. Role of cytokines in allergic airway inflammation[J]. Int Arch Allergy Immunol,2007,142(4):265-273.