Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Complement Inactivator Proteins”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 685 records · Page 38Linked to original sources
PubMed1998

Unexpected sarcolemmal complement membrane attack complex deposits on nonnecrotic muscle fibers in muscular dystrophies.

Antibody-dependent complement-mediated muscle fiber injury is a hypothetical immune effector response in inflammatory muscle diseases. Moreover, a sarcolemmal alteration in muscular dystrophies might trigger antibody-independent activation of the alternative complement pathway. We therefore searched for C5b9 complement membrane attack complex (MAC), immunoglobulin (Ig)G, and IgM deposits on nonnecrotic muscle fibers in muscle specimens from 81 patients with inflammatory myopathies, 45 patients with muscular dystrophies, and 19 patients with necrotizing myopathies. Sarcolemmal MAC deposits were present on nonnecrotic fibers (C+ fibers) in only two unusual types of inflammatory myopathy. By contrast, seven of 17 facioscapulohumeral dystrophy, four of nine limb-girdle dystrophy, and three of six merosin (laminin-alpha-2)-positive congenital muscular dystrophy but none of the Becker or Duchenne dystrophy specimens harbored C+ fibers. None of the C+ fibers immunostained for IgG or IgM, and none failed to immunostain for CD59 or CD46-inhibitors of the complement cascade. Our findings do not support a role for antibody-dependent complement-mediated muscle fiber injury in the major inflammatory muscle diseases. The cause and pathogenetic significance of the C+ fibers in the different types of muscular dystrophies remains to be elucidated.

Adolescent↗
PubMed1998

Anti-complement activity of tiliroside from the flower buds of Magnolia fargesii.

As part of the search for anticomplementary active components from natural products, the anticomplementary properties of methanolic extracts from the flower buds of Magnoliafargesii have been investigated. Bioassay-guided chromatographic separation of the active constituents led to the isolation of compound 1, whose structure was identified by spectroscopic methods to be kaempferol 3-O-beta-D-(6"-O-coumaroyl)glucopyranoside (tiliroside). Tiliroside showed very potent anti-complement activity (IC50=5.4 x 10(-5) M) on the classical pathway of the complement system, even higher than rosmarinic acid, which is a well-known inhibitor against the complement system. On the other hand, the hydrolysates of tiliroside, kaempferol, astragalin and p-coumaric acid showed very weak activity on this system.

Benzopyrans↗
PubMed1998

Studies on Alismatis Rhizoma. II. Anti-complementary activities of methanol extract and terpene components from Alismatis Rhizoma (dried rhizome of Alisma orientale).

A methanol extract (TMe-ext) from the dried rhizome of Alisma orientale was screened for anti-complementary activity in experimental models. In the animal models, it was found that TMe-ext inhibits zymosan-induced hind paw edema in rats and zymosan-activated rat serum (ZAS)-induced vascular permeability in mice. TMe-ext showed an inhibitory effect on complement-induced hemolysis through both the classical pathway and the alternative pathway. And TMe-ext inhibited hypotonic shock-induced hemolysis, but this effect was weak compared with the anti-complementary activities of TMe-ext. Four triterpenes (alisol A, alisol A monoacetate, alisol B and alisol B monoacetate) isolated from the rhizome also inhibited the complement-induced hemolysis through the classical pathway, but two sesquiterpenes (alismol and alismoxide) were ineffective. These results indicate that Alismatis Rhizoma shows anti-complementary activity, and its anti-complementary components are partially attributable to the terpene components mentioned above.

Animals↗
PubMed2003

Anti-complement activity of constituents from the stem-bark of Juglans mandshurica.

Four known flavonoids and two galloyl glucoses isolated from the stem-bark of Juglans mandshurica (Juglandaceae), namely taxifolin (1), afzelin (2), quercitrin (3), myricitrin (4), 1,2,6-trigalloylglucose (5), and 1,2,3,6-tetragalloylglucose (6), were evaluated for their anti-complement activity against complement system. Afzelin (2) and quercitrin (3) showed inhibitory activity against complement system with 50% inhibitory concentrations (IC(50)) values of 258 and 440 microM. 1,2,6-Trigalloylglucose (5) and 1,2,3,6-tetragalloylglucose (6) exhibited anti-complement activity with IC(50) values of 136 and 34 microM. In terms of the evaluation of the structure-activity relationship of 3,5,7-trihydroxyflavone, compounds 2, 3, and 4 were hydrolyzed with naringinase to give kaempferol (2a), quercetin (3a), and myricetin (4a) as their aglycones, and these were also tested for their anti-complement activity. Of the three aglycones, kaempferol (2a) exhibited weak anti-complement activity with an IC(50) value of 730 microM, while quercetin (3a) and myricetin (4a) were inactive in this assay system. Among the compounds tested, 1,2,3,6-tetragalloylglucose (6) showed the most potent anticomplement activity (IC(50), 34 microM).

Animals↗
PubMed2004

Anti-complementary activity of triterpenoides from fruits of Zizyphus jujuba.

In order to determine on the anti-complement activity of triterpenes, following eleven triterpenoides were isolated from the fruits of the Zizyphus jujuba MILL: ceanothane-type triterpenes: colubrinic acid (1), zizyberenalic acid (11); lupane-type triterpenes: alphitolic acid (2), 3-O-cis-p-coumaroyl alphitolic acid (3), 3-O-trans-p-coumaroyl alphitolic acid (4), betulinic acid (7), betulonic acid (9); and oleanane-type triterpenes: 3-O-cis-p-coumaroyl maslinic acid (5), 3-O-trans-p-coumaroyl maslinic acid (6), oleanolic acid (8), oleanonic acid (10). These compounds were examined for their anti-complement activity against the classical pathway of the complement system. Among them, compounds 5, 6, and 8 exhibited significant anti-complement activity with IC(50) values of 101.4, 143.9, and 163.4 microM, respectively, whereas the ceanothane-type and the lupane-type triterpenes were inactive. This suggests that the oleanane-structure plays an important role in inhibiting the hemolytic activity of human serum against erythrocytes.

Chromatography, High Pressure Liquid↗
PubMed1992

Changes in serum lipoprotein(a) and C4b-binding protein levels after acute myocardial infarction.

We investigated changes in serum lipoprotein(a) (Lp(a)) and C4b-binding protein (C4bp) levels following acute myocardial infarction (AMI). Serum lipids, apolipoproteins, C-reactive protein (CRP), sialic acid and haptoglobin (Hp) were also measured and evaluated. The study involved 16 patients (11 men, 5 women, mean age 68.2 +/- 8.4 years) with AMI admitted within 12 h after the onset of illness. CRP rose sharply and immediately after the onset of AMI, reaching its maximum level on the 3rd day of illness. This was followed by temporary increases in sialic acid and Hp, both of which peaked on the 7th day of illness. The Apo A-I level was significantly lower on the 14th day, while the Apo B level was significantly lower on the 3rd day. Serum total cholesterol (T-Ch), HDL-Ch and LDL-Ch showed temporary decreases after the onset of illness. Serial examination of the serum of patients with AMI yielded the following findings; 1) Both Lp(a) and C4bp levels rose temporarily with similar patterns of variation, and 2) they took longer time to peak (around the 14th day) and lasted longer than the increases in the other acute reactive proteins.

Aged↗
PubMed1990

Pharmacological studies on 6-amidino-2-naphthyl[4-(4,5-dihydro-1H-imidazol-2-yl)amino] benzoate dimethane sulfonate (FUT-187). I: Inhibitory activities on various kinds of enzymes in vitro and anticomplement activity in vivo.

FUT-187, a newly synthesized compound, was studied on its inhibitory activities mainly on proteolytic enzymes, in comparison with those of FUT-175 and FOY-305, known serine protease inhibitors. FUT-187, as well as FUT-175 and FOY-305, had selective inhibitory activities on serine proteases including Clr, Cls, kallikrein, trypsin, plasmin and thrombin; its activities on these enzymes except Clr and pancreatic kallikrein were relatively lower than those of FUT-175 and FOY-305. Further studies were conducted focusing on complement-mediated reactions. In spite of its lower activities against Clr and Cls, inhibitions by FUT-187 on the complement-mediated hemolysis in vitro and in vivo were only a little weaker than or equivalent to that of FUT-175. FOY-305 was ineffective in these tests. Forssman shock in guinea pigs is known to be initiated by the activation of the complement system. The protective effect of intravenous or oral FUT-187 against this shock was definitely superior to that of FUT-175. Furthermore, FUT-187 inhibited changes accompanied with Forssman shock, such as increase in lung weight, the decrease in platelet counts and CH50, and histopathological changes. These results suggested that FUT-187 should be a more potent oral therapeutic agent than FUT-175 for various inflammatory diseases attributed to the excessive activation of the complement system followed by platelet aggregation.

Amylases↗
PubMed2003

Complement components and their autoantibodies.

The purpose of the immune system is to defend the host from constantly changing microbial pathogens. Autoimmune diseases develop as a consequence of the production of antibodies and/or cells that react with self-antigens, and may recruit other effector mechanisms that result in tissue damage. Thus, in this context, autoimmunity represents an immune response to self-antigens that is sufficient to cause disease. This article is specifically devoted to autoantibodies directed against complement components.

Algorithms↗
PubMed2002

Roles of the complement system in human neurodegenerative disorders: pro-inflammatory and tissue remodeling activities.

Complement is an important component of the innate immune response with the capacity to recognize and clear infectious challenges that invade the CNS through a damaged blood brain barrier. For instance, the membrane attack complex is involved in cytotoxic and cytolytic activities while other smaller fragments lead to cell activation (chemotaxis) and phagocytosis of the intruders. It is noteworthy that there is a growing body of evidence that uncontrolled complement biosynthesis and activation in the CNS can contribute to exacerbate the neuronal loss in several neurodegenerative disorders. We provide here an insightful review of the double-edged sword activities of the local innate complement system in the CNS and discuss further the potential therapeutic avenues of delivering complement inhibitors to control brain inflammation.

Animals↗
PubMed1992

Protein C, protein S and C4b-binding protein in neonatal severe infection and septic shock.

We have studied the behaviour of total protein S, free protein S, protein C and C4b-binding protein fifteen neonates with severe infections, eight with septic shock and in a group of ten healthy newborns. Protein C was decreased in shock and septic patients, but only the shock group showed significant differences compared to normal neonates. Total protein S was normal in both groups of patients, although free protein S had significantly lower values in shock and nonshock infants. C4b-binding protein was higher than normal in septic and shock patients compared to the control group. Decreased values of protein C and free protein S can be explained by the activation of coagulation and their subsequent consumption. On the other hand, the increased levels of C4b-binding protein can affect the distribution of protein S in plasma, producing a shift in protein S to the complexed inactive form. These findings can contribute to an increased risk of microthrombosis during neonatal sepsis.

Carrier Proteins↗
PubMed1992

Mechanisms of evasion of Schistosoma mansoni schistosomula to the lethal activity of complement.

Schistosomula of Schistosoma mansoni became resistant to antibody-dependent complement damage in vitro after pre-incubation with normal human erythrocytes (NHuE) whatever the ABO or Rh blood group. Resistant parasites were shown to acquire host decay accelerating factor (DAF), a 70 kDa glycoprotein attached to the membrane of NHuE by a GPI anchor. IgG2a mAb anti-human DAF (IA10) immunoprecipitated a 70 kDa molecule from 125I-labeled schistosomula pre-incubated with NHuE and inhibited their resistance to complement-dependent killing in vitro. Incubation of schistosomula with erythrocytes from patients with paroxysmal nocturnal hemoglobinuria (PNHE) or SRBC, which are DAF-deficient, did not protect the parasites from complement lesion. Supernatant of 100,000 x g collected from NHuE incubated for 24 h in defined medium was shown to contain a soluble form of DAF and to protect schistosomula from complement killing. Schistosomula treated with trypsin before incubation with NHuE ghosts did not become resistant to complement damage. On the other hand, pre-treatment with chymotrypsin did not interfere with the acquisition of resistance by the schistosomula. These results indicate that, in vitro, NHuE DAF can be transferred to schistosomula in a soluble form and that the binding of this molecule to the parasite surface is dependent upon trypsin-sensitive chymotrypsin-insensitive polypeptide(s) present on the surface of the worm.

Animals↗
PubMed1981

'Nephritic factor' may be an autoantibody to C3b or C4b.

We attempted to clarify the character of 'Nephritic Factor' in the alternative (NeFA) and classical pathways (NeFC) of the complement, using an agglutinating and a hemolytic activity assay. The results suggested a possibility that NeFA and NeFC were different in their ability but might appear at the same time in some cases, and that NeFA was anti-C3b autoantibody and NeFC anti-C4b autoantibody.

Autoantibodies↗
PubMed1982

Nephritic factor (NeF) of alternate pathway (NeFA) and of classical pathway (NeFc).

NeFA and NeFc were studied in various cases (115 cases). 5 cases were followed up for a long time. NeFA assay was done by the "microtest plate method". We detected the NeF activity for the first time in the cases of Sjögren syndrome (SjS) and SjS+SLE+Hashimoto's disease (Hashimoto). In some cases NeF activity disappeared after therapy, and in one case NeFA and NeFc were positive at first, but then only NeFA activity became negative following the adequate therapy. As to the antibody nature of NeF, the possibility was suggested that NeFA might be anti C3b autoantibody and NeFc might be anti C4b and/or C4b2a auto-antibody.

Complement Activation↗