Objective： To observe the effect of Safflor Yellow （SY） Injection on acute lung injury （ALl） 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 （PaCO2） and decreased arterial oxygen partial pressure （PaO2）, arterial oxygen saturation （SO2）, HCOs concentration and pH, and increased LWCI, MPO activity, interleukin （IL）-I β, IL-6 and tumor necrosis factor （TNF）-ot mRNA 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 PaCO2 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- K B p65 staining and in TNF-α, IL-1 β 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）. Conclusion： SY I
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- κ B） p65 subunit nuclear binding activity in EC; Western blot technology was used to monitor mitogen activated protein kinase （MAPKs） and NF- κ 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- κ B p65 subunit DNA binding （P〈0.01） and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor α （I κ B α） 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.
