Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice

Ming Jin; Chun-yan Sun; Chong-qiang Pei; Lin Wang; Pei-cheng Zhang

doi:10.1007/s11655-012-1151-6

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Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice

OriginalPaper | Updated：2021-08-27

- Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice
- Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice
- 中国结合医学杂志（英文版） 2013年19卷第11期页码：836-843
- Affiliations：
  
  1. Department of Pharmacology, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University,Beijing,China
  2. Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine (Ministry of Education), Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing,China
- Author bio：
- Funds：
  
  Supported by National Natural Science Foundation of China (No. 30572344), Natural Science Foundation of Beijing (No. 7102025), and Science and Technology Personnel Serve Enterprise Action (No. 2009GJA30001)
- DOI：10.1007/s11655-012-1151-6
  中图分类号：
- 纸质出版日期：2013，
  
  网络出版日期：2012-6-28，
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Jin, M., Sun, Cy., Pei, Cq. et al. Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice., Chin. J. Integr. Med. 19, 836–843 (2013). https://doi.org/10.1007/s11655-012-1151-6

Ming Jin, Chun-yan Sun, Chong-qiang Pei, et al. Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice[J]. Chinese Journal of Integrative Medicine, 2013,19(11):836-843.
Jin, M., Sun, Cy., Pei, Cq. et al. Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice., Chin. J. Integr. Med. 19, 836–843 (2013). https://doi.org/10.1007/s11655-012-1151-6 DOI：

Ming Jin, Chun-yan Sun, Chong-qiang Pei, et al. Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice[J]. Chinese Journal of Integrative Medicine, 2013,19(11):836-843. DOI： 10.1007/s11655-012-1151-6.

摘要

To observe the effect of Safflor Yellow (SY) Injection on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice. Seventy-two mice were divided into six groups: control (saline + saline); LPS (LPS + saline); SY Injection [LPS + SY (10

20 or 40 mg/kg

intravenously)] and anisodamine (AD) (LPS + AD). Thirty minutes after SY or AD administration

15 mg/kg LPS was given intraperitoneally. All animals were sacrificed 4 h after LPS injection. Arterial blood gas and lung water content index (LWCI) were measured. Lung tissue myeloperoxidase (MPO) activity was assayed. mRNA expression of inflammatory cytokines was assayed by reverse-transcription polymerase chain reaction. Lung morphological and nuclear factor (NF)-κB p65-positive cell changes were observed by HE and immunohistochemical staining. p38 mitogen-activated protein kinase (MAPK) phosphorylation was observed by Western blotting. After LPS administration

all animals displayed increased arterial carbon dioxide partial pressure (PaCO2) and decreased arterial oxygen partial pressure (PaO2)

arterial oxygen saturation (SO2)

HCO3 − concentration and pH

and increased LWCI

MPO activity

interleukin (IL)-1β

IL-6 and tumor necrosis factor (TNF)-α mRNA expression

NF-κB p65-positive staining and p38 MAPK activation compared with normal controls (all P<0.01). SY Injection significantly mitigated the LPS-induced increase in arterial PaCO and the decreases in arterial PaO2

SO2 and pH

and attenuated increases in LWCI and lung tissue MPO activity (all P<0.01). Moreover

SY Injection inhibited the increases in NF-κB p65 staining and in TNF-α

IL-1β and IL-6 mRNA expression (all P<0.01)

and promoted the expression of the antiinflammatory cytokine IL-10 (P<0.05) following LPS injection. LPS-induced pulmonary p38 MAPK phosphorylation was suppressed by pretreatment with SY Injection (P<0.01). SY Injection ameliorates inflammatory ALI induced by LPS in mice.

Abstract

20 or 40 mg/kg

intravenously)] and anisodamine (AD) (LPS + AD). Thirty minutes after SY or AD administration

all animals displayed increased arterial carbon dioxide partial pressure (PaCO2) and decreased arterial oxygen partial pressure (PaO2)

arterial oxygen saturation (SO2)

HCO3 − concentration and pH

and increased LWCI

MPO activity

interleukin (IL)-1β

IL-6 and tumor necrosis factor (TNF)-α mRNA expression

SO2 and pH

and attenuated increases in LWCI and lung tissue MPO activity (all P<0.01). Moreover

SY Injection inhibited the increases in NF-κB p65 staining and in TNF-α

IL-1β and IL-6 mRNA expression (all P<0.01)

关键词

Safflor Yellow Injectionlipopolysaccharidelunginflammation

Keywords

Safflor Yellow Injectionlipopolysaccharidelunginflammation

references

Ware LB, Matthay MA. The acute respiratory distress syndrome. N Eng J Med 2000;342:1334–1349.

Bosma K, Fanelli V, Ranieri VM. Acute respiratory distress syndrome: update on the latest developments in basic and clinical research. Curr Opin Anaesthesiol 2005;18:137–145.

Jin M, Li JR, Wu W. Study on the antioxidative effect of Safflor Yellow. Chin J Chin Mater Med (Chin) 2004;29:447–449.

Wu W, Jin M, Piao YZ, Li JR. Inhibition of safflor yellow against myocardial ischemia in jury of rats. Chin Tradit Herbal Drugs (Chin) 2007;37:1373–1375.

Zhang Q, Chen ZY, Wu LB, Wang SC, Zheng QS. Clinical non-feriority evaluation on the efficacy and safety of safflower yellow pigment lyophilized power & dripping solution in the treatment of patients with angina. Chin J Evid-Based Med (Chin) 2005;15:276–285.

Pei CQ, Sun CY, Jin M. Mitigation of Safflor Yellow Injection on acute lung injury of rats induced by oleic acid. Chin Tradit Herbal Drugs (Chin) 2010;41:596–601.

Koroush K, Jean-Pierre G, Chen MH, Chen DF, Zhang DX. Characterization of a murine model of endotoxin-induced acute lung injury. Shock 2002;17:300–303.

Chen TT, Du YJ, Liu XL, Zhu HB. Inhibitory action of hydroxysafflor yellow A on inflammatory signal transduction pathway related factors in rats with cerebral cortex ischemia. Acta Pharm Sin (Chin) 2008;43:570–575.

Sun CY, Pei CQ, Zang BX, Wang, Jin M. The ability of hydroxysafflor yellow A to attenuate lipopolysaccharideinduced pulmonary. Phytotherapy Res 2010;24:1788–1795.

Bhatia M, Moochhala S. Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome. J Pathol 2004;202:145–156.

Minamino T, Komuro I. Regeneration of the endothelium as a novel therapeutic strategy for acute lung injury. J Clin Invest 2006;116:2316–2319.

Blackwell TS, Christman JW. The role of nuclear factor kappa B in cytokine gene regulation. Am J Respir Cell Mol Biol 1997;17:3–9.

Garrean S, Gao XP, Brovkovych V, Shimizu J, Zhao YY, Vogel SM, et al. Caveolin-1 regulates NF-kappa B activation and lung inflammatory response to sepsis induced by lipopolysaccharide. J Immunol 2006;177:4853–4860.

Schnyder-Candrian S, Quesniaux VF, Di Padova F, Maillet I, Noulin N, Couillin I, et al. Dual effects of p38 MAPK on TNF-α dependent bronchoconstriction and TNF-α independent neutrophil recruitment in lipopolysaccharideinduced acute respiratory distress syndrome. J Immunol 2005;175:262–269.

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