Gold nanoparticles alleviates the lipopolysaccharide-induced intestinal epithelial barrier dysfunction

Abstract

Nanotechnology is used in the immune response manipulation to treat various human diseases. In the present study, we explored the effects of Au nanoparticles (AuNPs) on the lipopolysaccharide (LPS)-induced epithelial barrier dysfunction and inflammatory response of colonic epithelial NCM460 cells. According to the results of cell counting kit-8 and flow cytometry analysis, the viability of NCM460 cells was inhibited, and the apoptosis was increased after LPS treatment, and AuNPs reversed these changes in a dose-dependent way. The permeability was evaluated by detecting the flux of fluorescein isothiocyanate-dextran and transepithelial electrical resistance. LPS enhanced the permeability and promoted barrier dysfunction of NCM460 cells. Enzyme-linked immunosorbent sorbent assay results revealed that the concentrations of pro-inflammatory factors and nitric oxide were elevated by LPS treatment and decreased by the AuNPs. LPS aggravated the inflammatory response, which was rescued by the AuNPs. Moreover, LPS promoted the activation of the nuclear factor kappa-B and extracellular signal-regulated kinase/c-Jun NH-terminal kinase signaling pathways, which were inhibited by AuNPs.

Nano-Hybrid Au@LCCs Systems Displaying Anti-Inflammatory Activity

“…However, little is known about the possible application of Au NPs in the treatment of intestinal inflammation. Au NPs were shown able to inactivate the NF- B and ERK/JNK pathways protecting against LPS-induced damage in colonic epithelial NCM460 cells [ 72 ]. Furthermore, Au NPs reversed the effect of LPS treatment on TJ proteins including ZO-1 and occludin, and proinflammatory cytokines, including IL-6, TNF- , inducible nitric oxide synthase, and cyclooxygenase 2.…”

Sitagliptin protects renal glomerular endothelial cells against high glucose-induced dysfunction and injury

“…In diabetic conditions, hyperglycemia or glucose by-products cause renal endothelial toxicity, as evidenced by changes in growth factors synthesis and ROS production, induction of oxidative stress and inflammation, and regulation of apoptosis in rGECs [ 14 ]. Increased intracellular glucose leads to the generation of ROS, which triggers oxidative stress, inflammatory injury, and activation of various signaling pathways, thereby mediating the apoptosis of endothelial cells [ 15 ].…”

“…Increased intracellular glucose leads to the generation of ROS, which triggers oxidative stress, inflammatory injury, and activation of various signaling pathways, thereby mediating the apoptosis of endothelial cells [ 15 ]. Besides, glucose-related endotheliotoxins notably increase the permeability of rGECs, alter endothelial glycocalyx, and induce cell apoptosis [ 14 ]. These events cause modifications to the glomerular filtration barrier and finally result in albuminuria.…”

“…Fluorescein isothiocyanate dextran (FITC-dextran) was used to assess the permeability of HrGECs as described previously [ 14 ]. HrGECs were plated in a porous upper chamber of 24-well Transwell plates (Corning, NY, USA).…”

Dexmedetomidine alleviates intestinal barrier dysfunction and inflammatory response in mice via suppressing TLR4/MyD88/NF-κB signaling in an experimental model of ulcerative colitis

“…Consequently, the integrity of the intestinal epithelium is critical to the prevention of intestinal infection, which is associated with immune perception [9]. The defect or integrity of the epithelial barrier is an important pathogenic marker for inflammatory intestinal diseases [10]. Intestinal barrier dysfunction results in the enhancement of epithelial permeability and inflammation [11].…”