Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice
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Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice
Chinese Journal of Integrative MedicineVol. 19, Issue 11, Pages: 836-843(2013)
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)
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 19(11):836-843(2013)
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/s11655-012-1151-6DOI:
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 19(11):836-843(2013) DOI: 10.1007/s11655-012-1151-6.
Effect of safflor yellow injection on inhibiting lipopolysaccharide-induced pulmonary inflammatory injury in mice
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
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.
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