Global trends in research on endothelial cells and sepsis between 2002 and 2022: A systematic bibliometric analysis

The dataset uploaded here is the primary search data, and these data can be imported into VOSviewer or Citespace software for further analysis. The Web of Science Core Collection (WoSCC) database was initially searched on September 27, 2022, with an updated search performed on March 18, 2023. The search query was: TS= (endothelium* OR endothelial cell* OR ECs OR endothelia) AND TS= (sepsis OR septic shock OR endotoxemia OR severe sepsis OR SIRS OR systemic inflammatory response syndrome). The time frame for retrieval spanned from January 1, 2002, to December 31, 2022. The document type was restricted to "articles," and the search was confined to publications in English. Comprehensive data from the included publications, encompassing the year of publication, author, title, source, number of citations, abstract, address, affiliation, document type, keywords, and cited reference count, were systematically gathered from the WoSCC.</p

Serum Levels of IL-1β, IL-6, TGF-β, and MMP-9 in Patients Undergoing Carotid Artery Stenting and Regulation of MMP-9 in a New In Vitro Model of THP-1 Cells Activated by Stenting

Inflammation plays an important role in the pathophysiological process after carotid artery stenting (CAS). Monocyte is a significant source of inflammatory cytokines in vascular remodeling. Telmisartan could reduce inflammation. In our study, we first found that, after CAS, the serum IL-1β, IL-6, TGF-β, and MMP-9 levels were significantly increased, but only MMP-9 level was elevated no less than 3 months. Second, we established a new in vitro model, where THP-1 monocytes were treated with the supernatants of human umbilical vein endothelial cells (HUVECs) that were scratched by pipette tips, which mimics monocytes activated by mechanical injury of stenting. The treatment enhanced THP-1 cell adhesion, migration and invasion ability, and the phosphorylation of ERK1/2 and Elk-1 and MMP-9 expression were significantly increased. THP-1 cells pretreated with PD98095 (ERK1/2 inhibitor) attenuated the phosphorylation of ERK1/2 and Elk-1 and upregulation of MMP-9, while pretreatment with telmisartan merely decreased the phosphorylation of Elk-1 and MMP-9 expression. These results suggested that IL-1β, IL-6, TGF-β, and MMP-9 participate in the pathophysiological process after CAS. Our new in vitro model mimics monocytes activated by stenting. MMP-9 expression could be regulated through ERK1/2/Elk-1 pathway, and the protective effects of telmisartan after stenting are partly attributed to its MMP-9 inhibition effects via suppression of Elk-1

Treatment with ML385 mitigated the protective effects of β-PAE on cognitive function and neuroinflammation.

ML385 reversed β-PAE mediated neuroprotective effects as shown in the behavioral test. ML385(1mg/kg in 3μL) was i.c.v injected 2 hours post-CLP. The inhibitory avoidance test and open field test were performed at 24h post-surgery (n = 6–8 in each group). (B) ML385 partially mitigated the anti-inflammatory effects of β-PAE in the brain. TNF-α, IL-1β and IL-6 were measured in brain homogenate by ELISA (n = 6–8 in each group). (C) The protein expression of Sirt1, Nrf2, HO-1 and cleaved-caspase 3 was determined by western-blotting. Samples of hippocampus were collected and prepared in homogenate at 24h after procedure. Summary data are obtained from three independent experiments (n = 4 in each group). *P<0.05 vs.CLP control; #P<0.05 vs. CLP+β-PAE group.</p

β-PAE improved the cognitive function in SAE mice.

Mice were i.c.v injected with a low dose(0.2mg/kg) of β-PAE, high dose(1mg/kg) of β-PAE or saline, respectively. Reagents were all prepared in equal volume of 3μL. Step down inhibitory avoidance test and open field test were performed at 24h, 48h and 7days post-surgery. All presented data are a composite of three independent experiments (n = 6–10 in each group). *P<0.05 vs. Sham control; #P<0.05 vs. CLP control; β-PAE(L), low dose of β-PAE group; β-PAE(H), high dose of β-PAE group.</p

PD-L1 Blockade Attenuated Sepsis-Induced Liver Injury in a Mouse Cecal Ligation and Puncture Model

Liver plays a major role in hypermetabolism and produces acute phase proteins during systemic inflammatory response syndrome and it is of vital importance in host defense and bacteria clearance. Our previous studies indicated that programmed death-1 (PD-1) and its ligand programmed death ligand-1 (PD-L1) are crucial modulators of host immune responses during sepsis. Our current study was designed to investigate the role of PD-L1 in sepsis-induced liver injury by a mouse cecal ligation and puncture (CLP) model. Our results indicated that there was a significant increase of PD-L1 expression in liver after CLP challenge compared to sham-operated controls, in terms of levels of mRNA transcription and immunohistochemistry. Anti-PD-L1 antibody significantly alleviated the morphology of liver injury in CLP mice. Anti-PD-L1 antibody administration decreased ALT and AST release in CLP mice, decreased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 mRNA in liver after sepsis challenge. Thus, anti-PD-L1 antibody might have a therapeutic potential in attenuating liver injury in sepsis

Plasma TRAIL levels in septic patients and healthy controls.

<p>*compared with healthy controls, P<0.01; # compared with the sepsis group, P<0.05. H: healthy control; S: sepsis; SS: severe sepsis; SH: septic shock.</p

Fe₃O₄ Nanoparticles Embedded in Pectin–Doxorubicin Composites as pH-Responsive Nanoplatforms for Tumor Diagnosis and Therapy by <i>T</i>₁‑Weighted Magnetic Imaging

Multifunctional nanomaterials with diagnostic and therapeutic capabilities offer promising customized nanomedicines for cancers. However, achieving good execution of these functions in vivo employing a single nanoframework remains challenging, and only a few of these magnetic nanocarriers have been validated for clinical use. In this study, based on biocompatibility and remarkable multifunctionalities, we describe a novel approach to synthesize small Fe3O4 nanoparticles conjugated with natural polysaccharide pectin and assembled into a pH-responsive T1-weighted magnetic resonance imaging contrast agent, Fe3O4@PD, for better chemotherapeutic efficacy. In vitro studies revealed that the conjugated doxorubicin (DOX) was quickly released in the tumor microenvironment by cleavage of the acid-sensitive acylhydrazone bond at a release rate of 89.72% and exerted a considerable inhibitory effect on breast cancer cells. In vivoT1-weighted images of mice showed that Fe3O4@PD displayed darkening to brightening contrast enhancement at tumor sites, and the relative signal-to-noise ratio of the tumor site reached its maximum (increased to about 2.27-fold) for distinguishing the normal and tumor tissues. Thus, this Fe3O4@PD-based system has the potential to be a multifunctional nanodrug delivery system, and as a smart theragnostic platform, it has broad application prospects in clinical and biological works, such as cell-based diagnostics and in vivo medication monitoring