scholarly journals Modulation of the Complement system by Zingiberacea Aframomum Melegueta in mice-induced Schizophrenia

Author(s):  
Thona Wusu

Introduction: Schizophrenia is a severe mental disorder among nationalities of the world, which has a substantial social and economic effect. Scientific therapeutic drugs have proved abortive due to adverse effects. Aim: The study investigated the repression of the complement system by aqueous extract of alligator pepper on schizophrenia. Methods: Male mice were induced with schizophrenia using ketamine and dexamethasone; the mice were treated with aqueous extract of alligator pepper (200mg/ml and 400mg/ml) respectively for ten days. After which their brain was removed, and analysed for dopamine. Blood samples was collected from the animal and plasma was used to determine the level of complement component (3 and 4), and C-reactive protein spectrophotometrically. Phytochemical content of the aqueous extract was also done spectrophotometrically, and characterization was confirmed using FTIR. Result: The alligator plant extract constituent includes flavonoids, tannins, saponin, steroids, phlabotannis, terpenoids, and cardiac glycoside. With a tannins having a concentration of 1292.6 µg/ml and 726.8µg/ml, phenol had a concentration of 221.7 µg/ml and 94.2 µg/ml and flavonoids had a concentration of 105.3 µg/ml and 100.0 µg/ml at 200mg/ml and 400mg/ml plant concentration respectively. The alligator pepper reversed the effect of ketamine and dexamethasone induced schizophrenia by decreasing the level of C-reactive protein , complement component (3 and 4) and dopamine significantly (<0.0001) in a dose dependent manner, in all the groups compared to the control. Conclusion: The high phenolic and flavonoids content in alligator pepper may be responsible for the antipsychotic property of alligator pepper. Thus, probable natural therapy for schizophrenia.

2001 ◽  
Vol 1 (S2) ◽  
Author(s):  
Niubel Diaz-Padilla ◽  
Wim KBleeker ◽  
C Erik Hack

2020 ◽  
pp. 30-34
Author(s):  
V. V. Boyko ◽  
D. O. Yevtushenko ◽  
I. V. Kryvorotko ◽  
I. A. Taraban ◽  
D. V. Minukhin ◽  
...  

Summary. The etiology of the development of adhesive disease — the most common postoperative complication — can be determined by epigenomic disorders related to various links of resistance and immunogenetic control. Purpose of the study. To study the epigenomic factors in the development of adhesive disease, the immune status of patients operated on in the abdominal cavity was studied. The comparison group included 55 patients with a complicated course of peritoneal commissural disease, the main group consisted of 59 patients operated on on the abdominal organs on the background of peritoneal commissural disease, the course of which was asymptomatic. Results and its discussion. The revealed epigenomic factors associated with the risk of developing adhesive disease: belongs to an increase in the concentration of acute phase proteins - ceruloplasmin, haptoglobin, C-reactive protein, C3 fragment of the complement system proteins, changes in the expression of adhesion molecule genes (CD31 increased by 10 %, CD54 increased to 24.1 % in comparison with the comparison group — 13.25 %). Conclusions. The results of our studies showed that patients with adhesive disease have a wide range of epigenome trigger factors. Epigenomic factors associated with the risk of developing adhesive disease include an increase in the concentration of acute phase proteins - ceruloplasmin, haptoglobin, C-reactive protein, C3 fragment of the complement system proteins, changes in the expression of adhesion molecule genes (CD31 increased by 10 %, CD54 increased to 24, 1 % compared with the comparison group - 13.25 %)


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Oliver Zimmermann ◽  
Dimitar E Manolov ◽  
Ziya Kaya ◽  
Thomas P Zwaka ◽  
Magdalena Bienek-Ziolkowski ◽  
...  

Background: C-reactive protein (CRP) has been suggested as a risk factor in cardiovascular disease. Recently, it has been shown that CRP binds to ligands exposed in ischaemic damaged tissue and activates the complement system. Furthermore, CRP was demonstrated to be strongly and independently associated with the occurrence of heart failure in men. In this study we have investigated the presence of CRP and the Terminal Complement Complex (C5b-9) in the myocardium of patients suffering from non-ischaemic heart failure. Methods and Results: Endomyocardial biopsies were taken from 151 patients suffering from dilated cardiomyopathy. Biopsies were immunohistochemically analysed for the presence and distribution pattern of CRP and C5b-9. In 39 patients plasma levels of hsCRP and NT-proBNP were measured and correlated with myocardial biopsy findings. In 47 patients a positive staining for CRP and in 141 patients a positive staining for C5b-9 was detected. CRP and C5b-9 significantly co-localised within the myocardium. A negative correlation was observed for plasma hsCRP levels and myocardial CRP. Conclusions: This study shows for the first time that CRP is frequently present in the myocardium of patients suffering from non-ischaemic dilated cardiomyopathy and co-localises with the Terminal Complement Complex. CRP may contribute to myocardial damage in dilated cardiomyopathy via activating the complement system.


1975 ◽  
Vol 142 (5) ◽  
pp. 1065-1077 ◽  
Author(s):  
A.P. Osmand ◽  
R.F. Mortensen ◽  
Joan Siegel ◽  
H. Gewurz

Interactions of CRP with various substrates in the presence of human serum have been shown to result in efficient activation of C components C1-C5. We now report the ability of CRP to initiate C-dependent hemolysis. For this purpose CRP was isolated by affinity chromatography using pneumococcal CPS and gel filtration; its purity was established by several criteria. Erythrocytes were coated with CPS (E-CPS) and passively sensitized with CRP. C-dependent lysis of these cells was observed upon the addition of suitably absorbed human serum, and the efficiency of hemolysis compared favorably with that initiated by rabbit IgG anti-CPS antibody. CRP also sensitized E-CPS for lysis by guinea pig C; partial lysis was seen when C4-deficient guinea pig serum was used, suggesting that CRP also shares with antibody the ability of CRP to fully activate the C system and provide further evidence for a role for CRP similar to that of antibody in the initiation and modulation of inflammatory reactions via the complete system.


Author(s):  
Barry D Kyle ◽  
Terence A Agbor ◽  
Shajib Sharif ◽  
Usha Chauhan ◽  
John Marshall ◽  
...  

Abstract Background This study aimed to compare fecal calprotectin (FC) levels with other commonly used parameters as part of patient care during evaluation for inflammatory bowel disease (IBD). Methods We recruited adult IBD patients with ulcerative colitis (UC) and Crohn’s disease (CD) and compared the results of the patient’s biopsy results (i.e., inflamed versus noninflamed) for six sites (i.e., ileum, ascending colon, transverse colon, descending colon, sigmoid colon, rectum) with concentrations of C-reactive protein (CRP), total leucocytes and fecal calprotectin (FC). Results We found that FC was significantly elevated in a concentration-dependent manner that correlated with the number of active inflammation sites reported in biopsy. Although CRP and leucocyte measurements trended upwards in line with inflammation reported from biopsy, the results were highly variable and highlighted poor reliability of these biomarkers for indicating IBD inflammation. Conclusions These results strongly suggest that FC correlates best with biopsy reports and is a superior marker than CRP and leucocytes.


2021 ◽  
Vol 23 (4) ◽  
pp. 927-932
Author(s):  
O. B.J. Po ◽  
A. A. Konoplya ◽  
I. N. Medvedeva

The study aimed to compare the effectiveness of various pharmacotherapy regimens for infertility of tubo-peritoneal genesis. Under constant supervision were 96 patients referred to the hospital for diagnostic laparoscopy for infertility of tubo-peritoneal genesis, divided equally into 4 groups depending on the pharmacological treatment methods: the 1st group received basic pharmacotherapy (BPT) after endoscopic surgery (antibacterial, antifungal, vitamin therapy). Patients of groups 2-4, in addition to BPT, received Hepon, Cycloferon or Lavomax, respectively. The control group consisted of 38 gynecologically healthy women. Laboratory examination was performed within 24 hours after the operation and on the 30th day after BPT. Vaginocervical lavage and plasma were assayed for the activity of lipid peroxidation processes, the state of the antioxidant system, the level of stable nitric oxide metabolites, neopterin, C-reactive protein, cytokines (TNFα, IL-1β, IL-8, IFNγ, IL-18, G-CSF, IL-4, IL-10), immunoglobulins (IgM, IgG, IgA, sIgA), components of the complement system (C3, C4, C5, C5А), phagocytic and oxygen-dependent activity of polymorphonuclear leukocytes. It was established that the use of immunomodulatory and antiviral activity medication with BPT according to the degree of increasing efficiency in the correction of immunometabolic laboratory parameters at the systemic and local level in infertility of tuboperitoneal genesis is as the following sequence: basic pharmacotherapy < basic pharmacotherapy + Hepon < basic pharmacotherapy + Cycloferon < basic pharmacotherapy + Lavomax. 


PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0244307
Author(s):  
Nikolaos E. Efstathiou ◽  
Giannis A. Moustafa ◽  
Daniel E. Maidana ◽  
Eleni K. Konstantinou ◽  
Shoji Notomi ◽  
...  

Rationale Age-related macular degeneration (AMD) is the most prevalent form of irreversible blindness in the developed world. Aging, inflammation and complement dysregulation affecting the retinal pigment epithelium (RPE), are considered significant contributors in its pathogenesis and several evidences have linked tumor necrosis factor alpha (TNF-α) and complement component 3 (C3) with AMD. Acadesine, an analog of AMP and an AMP-activated protein kinase (AMPK) activator, has been shown to have cytoprotective effects in human clinical trials as well as having anti-inflammatory and anti-vascular exudative effects in animals. The purpose of this study was to evaluate if acadesine is able to suppress TNF-α induced C3 in RPE cells. Methods ARPE-19 and human primary RPE cells were cultured and allowed to grow to confluence. TNF-α was used for C3 induction in the presence or absence of acadesine. Small molecule inhibitors and siRNA were used to determine if acadesine exerts its effect via the extracellular or intracellular pathway and to evaluate the importance of AMPK for these effects. The expression level of C3 was determined by immunoblot analysis. Results Acadesine suppresses TNF-α induced C3 in a dose dependent manner. When we utilized the adenosine receptor inhibitor dipyridamole (DPY) along with acadesine, acadesine’s effects were abolished, indicating the necessity of acadesine to enter the cell in order to exert it’s action. However, pretreatment with 5-iodotubericidin (5-Iodo), an adenosine kinase (AK) inhibitor, didn’t prevent acadesine from decreasing TNF-α induced C3 expression suggesting that acadesine does not exert its effect through AMP conversion and subsequent activation of AMPK. Consistent with this, knockdown of AMPK α catalytic subunit did not affect the inhibitory effect of acadesine on TNF-α upregulation of C3. Conclusions Our results suggest that acadesine suppresses TNF-α induced C3, likely through an AMPK-independent pathway, and could have potential use in complement over activation diseases.


2015 ◽  
Vol 396 (11) ◽  
pp. 1181-1197 ◽  
Author(s):  
Yi Wu ◽  
Lawrence A. Potempa ◽  
Driss El Kebir ◽  
János G. Filep

Abstract The prototypic acute-phase reactant C-reactive protein (CRP) has long been recognized as a useful marker and gauge of inflammation. CRP also plays an important role in host defense against invading pathogens as well as in inflammation. CRP consists of five identical subunits arranged as a cyclic pentamer. CRP exists in at least two conformationally distinct forms, i.e. native pentameric CRP (pCRP) and modified/monomeric CRP (mCRP). These isoforms bind to distinct receptors and lipid rafts, and exhibit distinct functional properties. Dissociation of pCRP into its subunits occurs within the inflammatory microenvironment and newly formed mCRP may then contribute to localizing the inflammatory response. Accumulating evidence indicates that pCRP possesses both pro- and anti-inflammatory actions in a context-dependent manner, whereas mCRP exerts potent pro-inflammatory actions on endothelial cells, endothelial progenitor cells, leukocytes and platelets, and thus may amplify inflammation. Here, we review recent advances that may explain how conformational changes in CRP contribute to shaping the inflammatory response and discuss CRP isomers as potential therapeutic targets to dampen inflammation.


2002 ◽  
Vol 11 (8) ◽  
pp. 787-797 ◽  
Author(s):  
Ryo Suzuki ◽  
Yasuo Yoshioka ◽  
Etsuko Kitano ◽  
Tatsunobu Yoshioka ◽  
Hiroaki Oka ◽  
...  

Cell therapy is expected to relieve the shortage of donors needed for organ transplantation. When patients are treated with allogeneic or xenogeneic cells, it is necessary to develop a means by which to isolate administered cells from an immune attack by the host. We have developed “cytomedicine, ” which consists of functional cells entrapped in semipermeable polymer, and previously reported that alginate-poly-l-lysine-alginate microcapsules and agarose microbeads could protect the entrapped cells from injury by cellular immunity. However, their ability to isolate from humoral immunity was insufficient. It is well known that the complement system plays an essential role in rejection of transplanted cells by host humoral immunity. Therefore, the goal of the present study was to develop a novel cytomedical device containing a polymer capable of inactivating complement. In the screening of various polymers, polyvinyl sulfate (PVS) exhibited high anticomplement activity and low cytotoxicity. Murine pancreatic β-cell line (MIN6 cell) entrapped in agarose microbeads containing PVS maintained viability and physiological insulin secretion, replying in response to glucose concentration, and resisted rabbit antisera in vitro. PVS inhibited hemolysis of sensitized sheep erythrocytes (EAs) and rabbit erythrocytes by the complement system. This result suggests that PVS inhibits both the classical and alternative complement pathways of the complement system. Next, the manner in which PVS exerts its effects on complement components was examined. PVS was found to inhibit generation of C4a and Ba generation in activation of the classical and alternative pathways, respectively. Moreover, when the EAC1 cells, which were carrying C1 on the EAs, treated with PVS were exposed to C1-deficient serum, hemolysis decreased in a PVS dose-dependent manner. These results suggest that PVS inhibits C1 in the classical pathway and C3 convertase formation in the alternative pathway. Therefore, PVS may be a useful polymer for developing an anticomplement device for cytomedical therapy.


1995 ◽  
Vol 269 (4) ◽  
pp. L492-L497 ◽  
Author(s):  
T. M. McEachren ◽  
K. M. Keough

The influence of the acute inflammatory phase protein human C-reactive protein (CRP) on the adsorption of porcine pulmonary surfactant from a subphase into an air-water interface has been investigated. CRP was shown to detract from the ability of surfactant to rapidly adsorb to the air-water interface at a molar ratio of 0.03:1 (protein:phospholipid) (weight ratio, 0.5:1). On a weight basis, CRP was found to be more effective than fibrinogen at reducing the adsorption rate of surfactant. The effect of CRP required the presence of calcium and was reversed by the addition of phosphocholine in a concentration-dependent manner. The inhibition of surfactant adsorption by CRP was effectively eliminated by the addition of phosphocholine at a molar ratio of 300:1 (phosphocholine:CRP), but it was not diminished by the addition of identical molar ratios of o-phosphoethanolamine or DL-alpha-glycerophosphate at the same molar ratios. These data suggest that the potent inhibition of surfactant adsorption by CRP is primarily a result of a specific interaction between CRP and the phosphocholine headgroup of surfactant lipids in the subphase and that it can be reversed by the water-soluble CRP ligand, phosphocholine.


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