Objective To study the protective effects and mechanism of aqueous extract of arctium lappa root on vas?cular endothelial cell injury in hypertensive rats. Methods The hypertensive rat model was induced by N-nitro-L-argi?nine. Rats were randomly divided into normal control group, model control group, positive control group (aptopril 15 mg/kg), low concentration of aqueous extract of arctium lappa root (0.5 g/kg), medium concentration of (1 g/kg) and high concentra?tion of (2 g/kg) groups. After six weeks of continuous intragastric administration, the systolic blood pressure levels at tail ar?tery were measured at 1, 4, 7, 10, 13, 16, 19, 22, 29, 36 and 42 d after treatment. And other indicators related to inflammato?ry factors were detected including C-reactive protein (CRP) and interleukin (IL)-6. The intercellular adhesion molecule-1 (ICAM-1) level was detected by taking samples of thoracic aorta. Results (1) The systolic blood pressure level at tail ar?tery was significantly lower in aqueous extract of arctium lappa root group than that of model control group ( P<0.05). (2) The aqueous extract of arctium lappa root can significantly improve the vascular endothelial cell injury, suppress vascular endo?thelial cell loss and blood cell adhesion, and cell proliferation with collagen fibers in muscle membrane. ( 3) The serum levels of IL-6, CRP and vascular endothelial ICAM-1 were significantly reduced in aqueous extract of arctium lappa root group than that of model control group (P<0.05). Conclusion Aqueous extract of arctium lappa root can significantly improve vascular endothelial cell injury in hypertensive rats. The mechanism may be related to the inhibition of inflammatory cyto?kines like IL-6, CRP and the expression of ICAM-1, and the improvement of chronic inflammatory response in vascular en?dothelium of hypertensive rats.

Objective To explore the role of Toll-like receptor 4 in the transformation of the bone marrow-derived macrophage polarity through observation on the effects of CLI-095 on phenotype of macrophages.Methods Our research subjects were the cultured mouse marrow-derived macrophages, and were randomly divided into three groups:the control group ( marrow-derived macrophages cul-tured for 48 h without any drug treatment), the model group (marrow-derived macrophages cultured routine for 24 h, then, addition of 100 U/mlγinterferon and 5 ng/ml lipopolysaccharide into the culture medium and cultured for another 24 h) and the treatment group( first in-cubated in 1 μg/ml CLI-095 for 24 h, then, after change of the fluid, addition of 100 U/mlγinterferon and 5 ng/ml lipopolysaccharide into the culture medium and cultured for another 24 h) .Real-time quantitative PCR was used to detect the mRNA expression of TLR4. The expression of membrane molecules CD16/32, CD206 was detected by using fluorescence activated cell sorting (FACS), and enzyme linked immunosorbent assay (ELISA) was used to detect the secretion of interleukin-10 (IL-10) and IL-12.Results As compared with those of the control group, the expression levels of CD16/32 and IL-12 in the model group were increased significantly, and the level of CD206 was decreased markedly, which was in conformity with the features of macrophages.When compared with those of the model group, the level of TLR4 mRNA was decreased.This indicated that the expression level of TLR4 was inhibited, the levels of CD16/32 and IL-12 were decreased and the levels of CD206 and IL-10 were increased with statistical significance and they were also in conformity with the features of macrophages.Conclusion TLR4 seemed to play an important role in the modulation of macrophage polarity.The inhibited expression level of TLR4 could promote inflammatory macrophages towards an anti-inflammatory M2 phenotype.

Objective To explore the anti-inflammatory mechanisms of high density lipoprotein (HDL) by observing the effects of apoprotein (apo) A Ⅰ,a major protein component of HDL,on the inflammatory macrophage cell polarity.Methods Cultured mice marrow-derived macrophages were stimulated with lipopolysaccharide and interferon after 10 μg/ml of apoA Ⅰ were added to the macrophages for 24 hours.The expression of membrane molecules CD16/32,CD206 were detected by fluorescence activated cell sorting (FACS).ELISA was used to detect the secretion of IL-10 and IL-12.Real-time quantitative PCR was used to detect the mRNA expression of TLR4,MyD88 and IRF5.Results Compared to macrophages stimulated by interferon and lipopolysaccharide but without pretreatment with apoA Ⅰ,pre-incubation with apoA Ⅰ significantly downregulated the expression of CD16/32 (91.17％ ± 1.99％ vs.50.47％ ± 1.02％,P ＜0.05),IL-12 [(747.27 ±3.74) pg/ml vs.(73.80 ±4.56) pg/ml,P ＜0.05],upregulated the expression of CD206 (0.33％ ± 0.12％ vs.3.00％ ± 0.36％,P ＜ 0.05),IL-10 expression [(23.56 ±4.30) pg/ml vs.(32.91 ± 2.47) pg/ml,P ＜ 0.05],and reduced the mRNA expression of TLR4(1.000±0.025 vs.0.708 ±0.003,P＜0.05),MyD88(1.591 ±0.005 vs.1.341 ±0.005,P＜ 0.05),IRF5 (0.954 ± 0.005 vs.0.463 ± 0.003,P ＜ 0.05).Conclusion ApoA Ⅰ enhances the switch of inflammatory macrophages to anti-inflammatory macrophages possibly through inhibiting TLR4-MyD88-IRF5 pathway.