A new notable compression source of left renal vein entrapment: right renal artery.

PURPOSE: To estimate the incidences of left renal vein (LRV) entrapment by right renal artery (RRA), a phenomenon primarily reported as case reports. METHODS: The cross-sectional study consecutively screened renal vessel CT data of 38 (Renal) patients with nephropathy and 305 (Non-renal) patients with peripheral arterial diseases in a teaching hospital in northeast China between November 2018 and March 2023. The LRV compression by adjacent anatomical structures, including but not limited to RRA and multiple compression-related parameters, were investigated through multiplanar analysis of the CT data. RESULTS: The overall LRV entrapment rates by adjacent structures were 41.93% (12/31) and 24.00% (6/25), the rates of RRA-sourced LRV compression 22.58% (7/31) and 20.00% (5/25), and the rates of compression by superior mesenteric artery (SMA) 16.13% (5/31) and 4.00% (1/25) in the Renal and Non-renal groups, respectively, with no significance. The venous segments distal to the RRA-compressed site had a significantly larger transectional lumen area than those of the non-compressed veins in both groups (3.09 ± 1.29 vs. 1.82 ± 0.23, p < 0.001 and 4.30 ± 2.65 vs. 2.12 ± 0.55, p = 0.006; maximum-to-minimum area ratios in Renal and Non-renal groups, respectively). Nearly 80% of RRAs were found arising anteriorly rightwards instead of passing straight to the right. CONCLUSION: RRA-sourced LRV compression was not rare, and its incidence was higher than that of the compression by SMA in both patient cohorts. RRA could be a more common compression source than SMA concerning LRV entrapment. Further investigations involving different populations, including healthy individuals, are needed.

Fabrication of Ag/ZnO@N-Carbon Core@Shell Photocatalyst for Efficient Photocatalytic Degradation of Rhodamine B.

Photocatalytic degradation method has been recognized as an effective way to eliminate the contamination of environment. However, developing photocatalysts with excellent photocatalytic properties are still a big challenge. In this paper, Ag doped ZnO coating with a layer of N doped porous carbon (Ag/ZnO@N-carbon) was successfully synthesized by using polyvinyl pyrrolidone (PVP) modified ZIF-8 as precursor via adsorption, hydrothermal treatment, in situ growth and carbonization processes. The physical and chemical properties of all samples were characterized by X-ray powder diffraction (XRD), scanning electron microscope (SEM), electron transmission microscopy (TEM) and so on. The results show that Ag doping does not change the crystallinity of ZnO, but broaden its photo-response property. The coating of N doped carbon can improve the specific surface area of photocatalyst. The photocatalytic activity of all samples was evaluated by degradation of rhodamine B (RhB) solution under UV light irradiation for 25 min. Ag/ZnO@N-carbon exhibits the highest photocatalytic activity for degradation of RhB with a degradation of 98.65%. Furthermore, Ag/ZnO@N-carbon also has high stability. Based on the characterization, possible mechanism for degradation of RhB by Ag/ZnO@N-carbon under UV light irradiation was proposed.

Aloin suppresses lipopolysaccharide-induced acute lung injury by inhibiting NLRP3/NF-κB via activation of SIRT1 in mice.

OBJECTIVE: The purpose of this study was to explore the protective effects and potential mechanisms of aloin on lipopolysaccharide (LPS)-induced acute lung injury (ALI). METHODS: Mice were pretreatment with aloin 1 h before LPS administration. The number of inflammatory cells and the levels of TNF-α and IL-1ß was detected. The lung histopathological changes, wet/dry ratio, MPO activity, GSH, MDA, SOD, and the expression of NF-κB and NLRP3 inflammasome were measured. RESULTS: The results showed that aloin significantly inhibited the number of total cells, neutrophils, and macrophages, as well as the levels of TNF-α and IL-1ß in BALF induced by LPS. In addition, pretreatment with aloin also inhibited LPS-induced lung histopathological injuries, lung wet/dry ratio, MPO activity, and MDA content. The levels of GSH and SOD were decreased by LPS and treatment of aloin could increase the levels of GSH and SOD. To study the protective mechanisms of alion on LPS-induced ALI, the expression of SIRT1, NF-κB and NLRP3 inflammasome were tested. We found that aloin significantly inhibited the activation of NF-κB and NLRP3 inflammasome in ALI induced by LPS. Meanwhile, aloin was found to increase the expression of SIRT1 and inhibition of SIRT1 by EX-527 reversed the protective effects of aloin. CONCLUSIONS: These results suggest that aloin exerts its protective effects on LPS-induced ALI by activation SIRT1, which subsequently results in the suppression of NF-κB and NLRP3 inflammasome.

IRF-1 contributes to the pathological phenotype of VSMCs during atherogenesis by increasing CCL19 transcription.

Atherosclerosis (AS) is a chronic inflammatory disease that mainly involves the large and middle arteries, but the specific mechanism is not precise. Chemokine ligand 19 (CCL19) has been reported highly expressed in peripheral blood of patients with atherosclerosis, but its role lacks explicit data. By ELISA assay and immunohistochemical (IHC) analysis, we found that the CCL19 was significantly up-regulated in AS. Therefore, we tried to clarify whether CCL19 expression was related to the progression of AS. QRT-PCR and western blot demonstrated that overexpression of CCL19 promoted the secretion of inflammatory factors and the deposition of the extracellular matrix, and facilitated the proliferation and migration of VSMCS. Besides, knockdown of CCL19 reduced the inflammation, collagen secretion, proliferation and migration of VSMCS induced by PGDF-BB. The results of database analysis, chromatin immunoprecipitation (ChIP) and luciferase assay showed that interferon regulatory factor 1 (IRF-1) activated the expression of CCL19 at the transcriptional level. Importantly, silencing IRF-1 inhibited atherosclerosis in high-fat-fed mice, inhibited the proliferation and migration of VSMCS, and down-regulated the expression of CCL19. Summing up, the results demonstrated that IRF-1 contributed to the pathological phenotype of VSMCs during atherogenesis by increasing CCL19 transcription.

Esculin prevents Lipopolysaccharide/D-Galactosamine-induced acute liver injury in mice.

Liver injury is an important cause of serious liver disease and is characterized by inflammatory and oxidative responses. Esculin, a coumarinic derivative found in Aesculus hippocastanum L., has been shown to exhibit anti-inflammatory and anti-oxidative effects. Here, we investigated the effects and molecular mechanism of esculin on Lipopolysaccharide/D-Galactosamine (LPS/D-Gal)-induced acute liver injury. A mouse model for acute liver injury was induced by intraperitoneal injection with D-Gal and LPS, and was assessed by histology, and serum transaminase analyses. The results showed that esculin significantly reduced the pathological symptoms of acute liver injury, as well as serum AST and ALT levels. LPS/D-Gal-induced liver myeloperoxidase (MPO) activity and malondialdehyde (MDA) content were also suppressed by esculin. Furthermore, LPS/D-Gal-induced liver tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) production were attenuated by esculin. Our data demonstrate that esculin can inhibit nuclear factor kappa B (NF-κB) activation as well as increase nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression. In conclusion, this paper demonstrates that esculin protects liver injury induced by LPS/D-Gal via inhibiting inflammatory and oxidative responses.

Geniposide attenuates Staphylococcus aureus-induced pneumonia in mice by inhibiting NF-κB activation.

Staphylococcus aureus (S. aureus) is a major cause of pneumonia that often affects young and immunocompetent patients. Inflammation plays an important role in the development of S. aureus-induced pneumonia. Geniposide, a major iridoid glucoside component of gardenia fruit, has been reported to have anti-inflammatory and anti-oxidative effects. The purpose of this study was to investigate the protective effects of geniposide on S. aureus-induced pneumonia in mice. Lung histopathological changes were detected by hematoxylin-eosin (H&E) staining. Lung myeloperoxidase (MPO) activity, wet-to-dry (W/D) ratio, and inflammatory cytokine levels in bronchoalveolar lavage fluid (BALF) were measured. The results showed that S. aureus-induced lung histopathological changes were attenuated by geniposide. S. aureus-induced MPO activity and lung W/D ratio were inhibited by treatment of geniposide. Furthermore, the levels of TNF-α and IL-1ß in the BALF were also suppressed by geniposide. In addition, geniposide significantly inhibited S. aureus-induced nuclear factor kappa B (NF-κB) activation. Taken together, these results showed that geniposide inhibited S. aureus-induced pneumonia in mice by inhibiting NF-κB signaling pathway. Geniposide might be used as a potential agent for the treatment of S. aureus-induced pneumonia.

Protective effects of tenuigenin on Staphylococcus aureus-induced pneumonia in mice.

Pneumonia is the leading cause of death in infants and young children. Staphylococcus aureus (S.aureus) is one of the most important bacteria that leads to pneumonia. Tenuigenin (TGN), a major active component isolated from the root of the Chinese herb Polygala tenuifolia, has been known to have anti-inflammatory effect. In this study, we aimed to investigate the protective effects of TGN on S.aureus-induced pneumonia in mice. The results showed that TGN significantly attenuated S.aureus-induced lung histopathological changes. TGN also inhibited lung wet/dry (W/D) ratio, and inflammatory cytokines TNF-α and IL-1ß production. Furthermore, S.aureus-induced NF-κB activation was significantly inhibited by the treatment of TGN. In conclusion, the results of this study showed that TGN protected against S.aureus-induced pneumonia by inhibiting NF-κB activation. TGN might be a potential agent in the treatment of pneumonia induced by S.aureus.

Oroxylin A attenuates cigarette smoke-induced lung inflammation by activating Nrf2.

Oroxylin A, a natural flavonoid isolated from the medicinal herb Scutellaria baicalensis Georgi, has been reported to have anti-inflammatory and antioxidant properties. However, the effect of oroxylin A on cigarette smoke (CS)-induced lung inflammation remains unclear. In this study, the ability of oroxylin A to protect against CS-induced lung inflammation was detected in vivo and in vitro. Oroxylin A was administered intraperitoneally to mice 2h prior CS exposure every day for five consecutive days. BEAS-2B bronchial epithelial cells and RAW264.7 cells were used to investigate the molecular mechanism of oroxylin A in vitro. In vivo, the results showed that oroxylin A dose-dependently attenuated CS-induced lung histopathologic changes, expression of cytokines TNF-α, IL-1ß, and MCP-1, and levels of oxidative biomarkers 3-nitrotyrosine and 8-isoprostane. Meanwhile, oroxylin A up-regulated GSH level and glutathione reductase (GR) activity in lung tissues. In vitro, oroxylin A significantly up-regulated Nrf2 expression and total cellular glutathione level in cigarette smoke extract (CSE)-stimulated cells. In addition, oroxylin A promoted Nrf2 binding to antioxidant response element (ARE) and up-regulated ARE-regulated gene such as heme oxygenase-1 (HO-1), GPx, and GR in CSE-stimulated cells. Oroxylin A could protect both epithelial cells and macrophages from damage by cigarette smoke in vitro. Taken together, these data indicated that oroxylin A attenuated oxidative stress and lung inflammation induced by CS via activating Nrf2 signaling pathway. Oroxylin A may be a protective agent against CS-induced lung inflammation and chronic obstructive pulmonary disease.

Citral inhibits lipopolysaccharide-induced acute lung injury by activating PPAR-γ.

Citral, a component of lemongrass oil, has been reported to have many pharmacological activities such as anti-bacterial and anti-inflammatory effects. However, the effects of citral on acute lung injury (ALI) and the molecular mechanisms have not been reported. The aim of this study was to detect the effects of citral on lipopolysaccharide (LPS)-induced acute lung injury and investigate the molecular mechanisms. LPS-induced acute lung injury model was used to detect the anti-inflammatory effect of citral in vivo. The alveolar macrophages were used to investigate the molecular mechanism of citral in vitro. The results showed that pretreatment with citral remarkably attenuated pulmonary edema, histological severities, TNF-α, IL-6 and IL-1ß production in LPS-induced ALI in vivo. In vitro, citral inhibited LPS-induced TNF-α, IL-6 and IL-1ß production in alveolar macrophages. LPS-induced NF-κB activation was also inhibited by citral. Furthermore, we found that citral activated PPAR-γ and the anti-inflammatory effects of citral can be reversed by PPAR-γ antagonist GW9662. In conclusion, this is the first to demonstrate that citral protects LPS-induced ALI in mice. The anti-inflammatory mechanism of citral is associated with activating PPAR-γ, thereby inhibiting LPS-induced inflammatory response.

Shikonin exerts anti-inflammatory effects in a murine model of lipopolysaccharide-induced acute lung injury by inhibiting the nuclear factor-kappaB signaling pathway.

Shikonin, an analog of naphthoquinone pigments isolated from the root of Lithospermum erythrorhyzon, was recently reported to exert beneficial anti-inflammatory effects both in vivo and in vitro. The present study aimed to investigate the potential therapeutic effect of shikonin in a murine model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). Dexamethasone was used as a positive control to evaluate the anti-inflammatory effect of shikonin in the study. Pretreatment with shikonin (intraperitoneal injection) significantly inhibited LPS-induced increases in the macrophage and neutrophil infiltration of lung tissues and markedly attenuated myeloperoxidase activity. Furthermore, shikonin significantly reduced the concentrations of TNF-α, IL-6 and IL-1ß in bronchoalveolar lavage fluid induced by LPS. Compared with the LPS group, lung histopathologic changes were less pronounced in the shikonin-pretreated mice. Additionally, Western blotting results showed that shikonin efficiently decreased nuclear factor-kappaB (NF-κB) activation by inhibiting the degradation and phosphorylation of IκBα. These results suggest that shikonin exerts anti-inflammatory properties in LPS-mediated ALI, possibly through inhibition of the NF-κB signaling pathway, which mediates the expression of pro-inflammatory cytokines. Shikonin may be a potential agent for the prophylaxis of ALI.