Resolvin D1 attenuates imiquimod-induced mice psoriasiform dermatitis through MAPKs and NF-κB pathways

Background

Resolvin D1 (RvD1), a pro-resolution lipid mediator derived from docosahexaenoic acid (DHA), has been described to promote several kinds of inflammatory resolution. However, the effects and anti-inflammatory mechanisms of RvD1 on psoriasis have not been previously reported.

消退素D1对大鼠肝缺血再灌注损伤的保护作用

目的 探讨消退素D1(resolvin D1, RvD1)对大鼠肝缺血再灌注损伤(ischemia reperfusion injury, IRI)的作用。方法 实验动物随机分为假手术组(Sham组)、 IR组、RvD1组和ZnPP组。自动生化仪检测氨基转移酶水平;苏木精-伊红染色观察肝组织学变化;髓过氧化物酶(myeloperoxidase,MPO)试剂盒测定MPO水平;实时荧光定量聚合酶链反应(quantitative real-time PCR, qRT-PCR)检测细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)水平。结果 与IR组相比,RvD1组大鼠ALT(P<0.05)、AST(P<0.01)明显降低,肝组织IRI减轻,肝内MPO活性降低(P<0.05),ICAM-1 mRNA表达下降(P<0.05)。而ZnPP组则与RvD1组表现相反。结论 RvD1通过降低MPO活性及ICAM-1 mRNA表达发挥对大鼠肝IRI的保护作用,且可以被ZnPP所逆转。     

消退素在牙髓、根尖周及牙周组织炎症环境中的活髓保存及再生作用

背景:细菌感染是牙髓及根尖周组织感染的主要病因,保存活髓和再生牙髓逐渐成为临床治疗牙髓及根尖周疾病的重要研究方向。消退素(resolvin)是ω-3多不饱和脂肪酸衍生而来的脂质介质,具有促进组织炎症消退、炎症状态恢复的作用。目的:回顾消退素在炎症调控中的研究进展及其在牙髓、根尖周及牙周组织炎症中的应用,以期为临床牙髓组织炎症状态的恢复及再生提供研究基础。方法:应用计算机在PubMed数据库、维普数据库、万方数据库及中国知网(CNKI)中国期刊全文数据库检索2014年1月至2020年6月相关文献,以“消退素,作用,信号通路”为中文检索词,以“resolvin,effect,signaling pathway”为英文检索词,最终纳入35篇文献归纳总结消退素的作用;以“消退素,牙髓炎,根尖周炎,牙周炎,口腔”为中文检索词,以“resolvin,pulptitis,periapical,periodontitis,dental”为英文检索词,最终纳入31篇文献归纳总结消退素在口腔不同组织和疾病中的应用,其余3篇解释说明文章内容。结果与结论:文章系统回顾了消退素的种类及作用,详细回顾了消退素在牙髓、根尖周及牙周组织炎症性疾病中的作用及机制,为其临床应用于牙髓组织炎症后的活髓保存及再生提供研究依据。     

人趋化因子受体1及其与某些疾病的关系

人趋化因子受体1(CMKLR1/ChemR23)是趋化脂肪因子chemerin及ω-3脂肪酸衍生分子resolvin E1的共享性受体.CMKLR1与其特异性配体结合后能刺激细胞内Ca2+释放,激活ERK1和NF-κB等信号级联反应,与炎性反应、免疫性疾病、糖尿病、代谢性疾病、心血管系统疾病、骨病、肿瘤、生殖系统疾病、精神疾病和肝脏等疾病发病相关.     

Effects of resolvin D1 on inflammatory responses and oxidative stress of lipopolysaccharide-induced acute lung injury in mice

Background A variety of inflammatory mediators and effector cells participate together in acute lung injury,and lead to secondary injury that is due to an inflammatory cascade and secondary diffuse lung parenchyma injury.Inflammation is associated with an oxidative stress reaction,which is produced in the development of airway inflammation,and which has positive feedback on inflammation itself.Resolvin D1 can reduce the infiltration of neutrophils,regulate cytokine levels and reduce the inflammation reaction,and thereby promote the resolution of inflammation.The purpose of this study is to investigate the effects of resolvin D1 on an inflammatory response and oxidative stress during lipopolysaccharide （LPS）-induced acute lung injury.Methods LPS （3 mg/kg） was used to induce the acute lung injury model.Pretreatment resolvin D1 （100 ng/mouse） was given to mice 30 minutes before inducing acute lung injury.Mice were observed at 6 hours,12 hours,1 day,2 days,3 days,4 days and 7 days after LPS was administrated,then they were humanely sacrificed.We collected bronchoalveolar lavage fluid （BALF） and the lung tissues for further analysis.Paraffin section and HE staining of the lung tissues were made for histopathology observations.Parts of the lung tissues were evaluated for wet-to-dry （W/D） weight ratio.tumor necrosis factor （TNF）-α,inter leukin （IL）-1β,IL-10 and myeloperoxidase （MPO） were detected by enzyme-linked immunosorbent assay （ELISA）.A lipid peroxidation malondialdehyde （MDA） assay kit was used to detect MDA.A total superoxide dismutase assay kit with WST-1 was used to analyze superoxide dismutase （SOD）.We determined the apoptosis of neutrophils by Flow Cytometry.A real-time quantitative PCR Detecting System detected the expression of mRNA for heme oxygenase （HO）-1.Results Pretreatment with resolvin D1 reduced the pathological damage in the lung,decreased the recruitment of neutrophils and stimulated their apoptosis.It markedly decreased the expressions of TNF-α,IL-1β and increased the expressions of IL-10,and decreased the production of MDA and increased the expressions of SOD.The mRNA expression of HO-1 was also significantly increased.Conclusions Resolvin D1 displays potent anti-inflammatory actions by regulating cytokines,inhibiting aberrant neutrophil recruitment and stimulating apoptosis of neutrophils.Resolvin D1 can also relieve the injury due to oxidative stress.The mechanisms might be related to increase HO-1 expression.     

Aspirin-triggered resolvin D1 down-regulates inflammatory responses and protects against endotoxin-induced acute kidney injury

The presence of endotoxin in blood can lead to acute kidney injury (AKI) and septic shock. Resolvins, the endogenous lipid mediators derived from docosahexaenoic acid, have been reported to exhibit potent anti-inflammatory action. Using a mouse model of lipopolysaccharide (LPS)-induced AKI, we investigated the effects of aspirin-triggered resolvin D1 (AT-RvD1) on inflammatory kidney injury. Administration of AT-RvD1 1 h after LPS challenge protected the mice from kidney injury as indicated by the measurements of blood urea nitrogen, serum creatinine, and morphological alterations associated with tubular damage. The protective effects were evidenced by decreased neutrophil infiltration in the kidney indicating reduction in inflammation. AT-RvD1 treatment restored kidney cell junction protein claudin-4 expression, which was otherwise reduced after LPS challenge. AT-RvD1 treatment inhibited endotoxin-induced NF-κB activation and suppressed LPS-induced ICAM-1 and VCAM-1 expression in the kidney. Moreover, AT-RvD1 treatment markedly decreased LPS-induced IL-6 level in the kidney and blocked IL-6-mediated signaling including STAT3 and ERK phosphorylation. Our findings demonstrate that AT-RvD1 is a potent anti-inflammatory mediator in LPS-induced kidney injury, and AT-RvD1 has therapeutic potential against AKI during endotoxemia.