Picrorhiza scrophulariiflora improves accelerated atherosclerosis through inhibition of redox-sensitive inflammation.

Background: Accumulation of advanced glycation end products (AGEs) or advanced oxidation protein products (AOPPs) has been identified as a risk factor for accelerated atherosclerosis seen in diabetes and chronic kidney disease. However, little is known about the intervention for atherogenesis associated with these oxidized proteins. The rhizome of Picrorhiza scrophulariiflora (PS) has long been used to treat inflammatory diseases as a traditional medication.

Advanced oxidation protein products accelerate renal fibrosis in a remnant kidney model.

Accumulation of plasma advanced oxidation protein products (AOPP) has been found in patients with chronic kidney disease. However, the biologic consequences of AOPP consumption on progression of renal disease still are unclear. For testing of the hypothesis that AOPP accelerate progression of chronic kidney disease, Sprague-Dawley rats were subjected to five-sixths nephrectomy (5/6 Nx) or to sham operation.

[Effect of advanced oxidation protein products on nitric oxide production in mouse peritoneal macrophages].

Objective: To investigate the effect of advanced oxidation protein products (AOPP) on nitric oxide (NO) production in mouse peritoneal macrophages (MPMs).

Methods: MPMs were incubated in the absence or presence of lipopolysaccharide (LPS) with AOPP-modified bovine serum albumin (BSA) prepared by exposure of BSA to hypoclorous acid or pre-treated with AOPP-BSA and subsequent stimulation with LPS. NO production in the supernatants of the culture media was determined spectrophotometrically using Griess method.

Advanced oxidation protein products accelerate atherosclerosis through promoting oxidative stress and inflammation.

Objective: Increased level of plasma advanced oxidation protein products (AOPPs) has been found in patients with uremia and nonuremic subjects with coronary artery disease. This study was conducted to test the hypothesis that AOPPs play a causal role in atherosclerosis.

Methods And Results: Hypercholesterolemic (0.

[Advanced oxidation protein products-induced tumor necrosis factor alpha secretion in monocytes via reactive oxygen species generation].

Objective: To investigate the effect of advanced oxidation protein products (AOPP) on the secretion of tumor necrosis factor alpha eTNFalphae in monocytes and its possible mechanism.

Method: Human monocyte cell line THP-1 and peripheral blood monocytes were incubated with AOPP-bovine serum albumin(BSA) prepared by incubation of BSA with hypochlorous acid. TNFalpha in the supernatant of the culture medium of THP-1 cells was measured by enzyme-linked immunosorbent assay and the production of reactive oxygen species (ROS) evaluated by measuring the fluorescent product from the oxidation of an oxidant-sensitive 2,7-dichlorefluorescin using Wallac 1420 multilabel counter.

[Advanced oxidation protein products induce reactive oxygen species production in endothelial cells].

Objective: To investigate the effect of advanced oxidation protein products (AOPP) on production of reactive oxygen species (ROS) in endothelial cells.

Methods: Human umbilical vein endothelial cell line ECV304 were stimulated with AOPP-modified bovine serum albumin (AOPP-BSA) prepared by oxidation of BSA with HOCl in vitro. ROS production in the cells was evaluated by kinetic measurement of dichlorofluoroscein (DCF) fluorescence produced by oxidation of an oxidant-sensitive dye 2,7-dichlorefluorescin (DCFH) using VICTOR 1420 multilabel counter.

[Advanced glycation end products accelerate atherosclerosis via enhancement of oxidative stress].

Objective: To investigate the effect of advanced glycation end products (AGE) on atheromatous plaque formation and its possible mechanisms.

Methods: Fifty rabbits were randomly divided into five groups of 10 rabbits: group A, fed with hypercholesterolemic diet and injected intravenously with AGE modified rabbit serum albumin (AGE-RSA); group B, fed with hypercholesterolemic diet and injected with unmodified RSA; group C, fed with hypercholesterolemic diet; group D, fed with normal diet alone: and group E, fed with normal diet and injected with AGE-RSA. Ten weeks after the rabbits were killed.

[Proteins modified with glycation or oxidation products accelerate atherosclerosis in experimental hypercholesterolemic rabbits].

Objective: To investigate whether advanced glycation end products (AGE) or advanced oxidative protein products (AOPP) contributes to atherogenesis in experimental hypercholesterolemic rabbits.

Methods: Hypercholesterolemic (0.5% wt/wt diet) rabbits received repeated intravenous injections of either AGE modified rabbit serum albumin (AGE-RSA) or AOPP modified RSA (AOPP-RSA) for 10 weeks.

The plasma membrane is the site of selective phosphatidylserine oxidation during apoptosis: role of cytochrome C.

Phosphatidylserine (PS) externalization, a functional end point of apoptosis that triggers phagocytic recognition of dying cells, may be modulated by oxidative stress in biological membranes. We previously observed selective oxidation of PS during apoptosis, but the intracellular location and molecular mechanisms responsible for PS oxidation remain to be described. Peroxidation in individual classes of cellular phospholipids was monitored in whole cells and various subcellular fractions obtained from HL-60 cells undergoing apoptosis in response to tert-butyl hydroperoxide (t-BuOOH) after metabolic acylation of phospholipids with the oxidation-sensitive fluorescent fatty acid, cis-parinaric acid.

[Detection of nuclear factor kappa B by immunochemical staining and image analysis].

Objective: To find a relatively simple and safe method for quantitative assay of nuclear factor (NF)-kappa B activity.

Methods: Immunochemical staining of NF-kappa B/p65 subunit with its antibody was performed in human umbilical vein endothelial cells stimulated with advanced glycation end products-modified human serum albumin (AGE-HSA). The ratio of p65 subunit staining in the nuclei and cytoplasm was determined by means of imaging analysis, and the results were compared with those of electrophoretic mobility shift assay (EMSA).

Macrophage recognition of externalized phosphatidylserine and phagocytosis of apoptotic Jurkat cells--existence of a threshold.

Phosphatidylserine (PS) is predominantly confined to the inner leaflet of plasma membrane in cells, but it is externalized on the cell surface during apoptosis. This externalized PS is required for effective phagocytosis of apoptotic cells by macrophages. Because PS trans-bilayer asymmetry is not absolute in different types of nonapoptotic cells, we hypothesized that the amounts of externalized PS may be critical for macrophage discrimination between apoptotic and nonapoptotic cells.

Increased S-nitrosothiols and S-nitrosoalbumin in cerebrospinal fluid after severe traumatic brain injury in infants and children: indirect association with intracranial pressure.

Nitric oxide (NO) is implicated in both secondary damage and recovery after traumatic brain injury (TBI). Transfer of NO groups to cysteine sulfhydryls on proteins produces S-nitrosothiols (RSNO). S-nitrosothiols may be neuroprotective after TBI by nitrosylation of N-methyl-D-aspartate receptor and caspases.

Redox sensor function of metallothioneins.

In summary, the redox conversions of MT cysteines are likely to be the principal mechanisms for regulation of metal binding and release by this protein. Oxidative and/or nitrosative challenges can serve to promote metal ion release from MT to render their delivery to specific target proteins. It is tempting to consider the potential roles of MTs as redox sensors because of their high sensitivity to cysteine modification, as well as their potential to amplify signals by releasing multiple metal ions.

A role for oxidative stress in apoptosis: oxidation and externalization of phosphatidylserine is required for macrophage clearance of cells undergoing Fas-mediated apoptosis.

Exposure of phosphatidylserine (PS) on the surface of apoptotic cells has been suggested to serve as an important recognition signal for macrophages. In this work we show that triggering of the death receptor Fas on Jurkat cells results in the generation of reactive oxygen species with oxidation and externalization of PS but not of the other major aminophospholipid, phosphatidylethanolamine. These cells were readily ingested by several classes of macrophages, whereas Raji cells, which are defective for Fas-induced PS exposure, remained unengulfed.

The Role of Different Components of Oxidized LDL in the Inhibition of Nitric Oxide Production in Macrophages.

The role of different components of oxidized LDL (Ox-LDL) in the inhibition of LPS-induced nitric oxide (NO) production in macrophages was studied by measuring nitrite in the media. The results showed that Ox-LDL was effective, but the native and the acetylated LDL were not. The removal of the lipid hydroperoxides in Ox-LDL by glutathione peroxidase mimic-ebselen had no effect on the inhibition.