Objective:To observe the effect of Safflor Yellow(SY)Injection on acute lung injury(ALI)induced by lipopolysaccharide(LPS)in mice.Methods: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)-k B p65-positive cell changes were observed by HE and immunohistochemical staining.p38 mitogen-activated protein kinase(MAPK)phosphorylation was observed by Western blotting.Results:After LPS administration,all animals displayed increased arterial carbon dioxide partial pressure(PaC02)and decreased arterial oxygen partial pressure(PaO_2),arterial oxygen saturation(SO_2),HCO_3^-concentration and pH,and increased LWCI,MPO activity,interleukin(IL)-1β,IL-6 and tumor necrosis factor(TNF)-αmRNA expression,NF-k B 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_2 and the decreases in arterial PaO_2,SO_2 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-1βand 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).Conclusion:SY Injection ameliorates inflammatory ALI induced by LPS in mice.
Objective:This study observed attenuating effect of hydroxysafflor yellow A(HSYA),an effective ingredient of aqueous extract of Carthamus tinctorius L,on lipopolysaccharide(LPS)-induced endothelium inflammatory injury.Methods:Eahy926 human endothelium cell(EC) line was used;thiazolyl blue tetrazolium bromide(MTT) test was assayed to observe the viability of EC;Luciferase reporter gene assay was applied to measure nuclear factor- κB(NF- κB) p65 subunit nuclear binding activity in EC;Western blot technology was used to monitor mitogen activated protein kinase(MAPKs) and NF- k B activation.Reverse transcription polymerase chain reaction(RT-PCR) method was applied to observe intercellular cell adhesion molecule-1(ICAM-1) and E-selectin mRNA level;EC surface ICAM-1 expression was measured with flow cytometry and leukocyte adhesion to EC was assayed with Rose Bengal spectrophotometry technology.Results:HSYA protected EC viability against LPS-induced injury(P<0.05).LPS-induced NF-κB p65 subunit DNA binding(P<0.01) and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor α(I κ Bα) phosphorylation was inhibited by HSYA.HSYA attenuated LPS triggered ICAM-1 and E-selectin mRNA levels elevation and phosphorylation of p38 MAPK or c-Jun N-terminal kinase MAPK.HSYA also inhibited LPS-induced cell surface ICAM-1 protein expression(P<0.01) and leukocyte adhesion to EC(P<0.05).Conclusion:HSYA is effective to protect LPS-induced high expression of endothelium adhesive molecule and inflammatory signal transduction.
