myeloperoxidase activity
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Fucoxanthin is a natural carotenoid obtained from seaweed which exhibits antioxidant properties. This research aimed to assess whether fucoxanthin, immobilized on aluminum-silicon carrier particles, has a toxic effect on immune cells. The viability, proliferation, nitric oxide production and myeloperoxidase activity of thymocytes and splenocytes of mice in vitro were studied. It was shown that fucoxanthin, immobilized on aluminum-silicon carrier particles, increased the survival rate and proliferation of mature immunocytes (splenocytes) after 24 hours exposure and increased the survival rate of naïve immunocytes (thymocytes) when exposed for 120 hours. In terms of myeloperoxidase, the activity of the immune cells was not affected by fucoxanthin immobilized on the carrier particles. The obtained results indicated that fucoxanthin, immobilized on particles of an aluminum-silicon carrier, did not have a toxic effect on mouse immunocytes. Keywords: Cylindrotheca closterium, fucoxanthin, γ-aluminum oxide, polydimethylsiloxane, thymocytes, splenocytes, viability, proliferation, nitric oxide, myeloperoxidase activity

Sexual hormones are determinant players in cardiovascular diseases. The aim of this study was to investigate the effects of testosterone deficiency, induced by castration, on oxidative status and the histopathology of the aor-tic media tunica. The experiments were undertaken on a batch of 30 Wistar males’ rats randomised into 3 groups, 10 control (Con), 10 castrated (Cas) and 10 castrated then supplemented with testosterone (Cas-T). Our results showed that testosterone deficiency induced a significant decrease in myeloperoxidase activity (19,95 ± 1, 79 vs 34,86 ± 1,13, p˂0,0001) this was maintained even after testosterone replacement. Furthermore, testosterone deficiency decreased the antioxidant capacity by reducing GSH in plasma (0,118 ± 0,003 vs 0,15 ± 0,011, p˂0,05). Our results also indicate that testos-terone supplementation leads to a significant increase in ceruloplasmin lev-els (62,37 ± 15,89 vs 148,12 ± 27,77, p ˂0.05). The histomorphometric exami-nation of the aortic tunica media in castrated rats showed a significant de-crease of media thickness (274,7 ± 2,96 vs 317,6 ± 5,19, p ˂0.0001) and VSMC count (108,1 ± 6,47 vs 130 ± 6,147, p ˂ 0.05) associated with damaged and broken elastic lamina. Testosterone supplementation restores the media thickness and the count of VSMC. Our findings demonstrate that testos-terone deficiency leads to a decrease in the count of VSMC and a rupture of elastic lamina. Testosterone altered the plasma oxidative status through ac-tions on GSH, MPO and ceruloplasmin.

Abstract Colitis-associated colorectal cancer serves as a prototype of inflammation-associated cancers which is linked with repeated cycles of inflammation and DNA repair deficits. Several preclinical and clinical data reported that aspirin has chemo preventive effect in colorectal cancer and is associated with dose dependent side effects. Further, it has been reported that zinc supplementation improves the quality of life in patients undergoing chemotherapy by alteration of colonic cancer cell gene expression. However, explication of the detailed molecular mechanisms involved in combined administration of aspirin and zinc mediated protection against the colitis associated colorectal cancer deserves further investigation. For the induction of colitis associated colorectal cancer, male BALB/c mice were administered 1, 2-dimethylhydrazine dihydrochloride (DMH) 20 mg/kg/bw thrice, before the initiation of every DSS cycle (3%w/v in drinking water). One week after the initiation of DSS treatment, aspirin (40 mg/kg; p.o.) and zinc in the form of zinc sulphate (3 mg/kg; p.o.) was administered for 8 weeks. Combination of aspirin and zinc as intervention significantly ameliorated DAI score, myeloperoxidase activity, histological score, apoptotic cells and protein expression of various inflammatory markers including nuclear factor kappa light chain enhancer of activated B cells (NFκBp65), cycloxygenase -2 (COX-2), interleukin-6 (IL-6); proliferation markers such as proliferating cell nuclear antigen (PCNA), signal transducer and activator of transcription 3 (STAT3) expression significantly decreased and antioxidant enzymes nuclear factor erythroid 2–related factor 2 (Nrf-2), metallothionein, catalase and superoxide dismutase (SOD) significantly increased as evaluated by immunohistochemistry and western blot analysis.

Abstract Aim: The study evaluated the effects of supplementation with three different probiotic strains B. lactis (LACT GBTM), L. rhamnosus (RHAM GBTM) and L. reuteri (REUT GBTM) on brain-intestinal immunomodulation in an animal model of LPS-induced inflammation. Methods: 50 mice Balb/C were distributed into five groups: Control; lipopolysaccharide (LPS); LPS + B. lactis (LACT GBTM); LPS + L. rhamnosus (RHAM GBTM); LPS + L. reuteri (REUT GBTM). The animals were supplemented with their respective probiotic microorganisms daily, for 30 days, at a concentration of 1x109 CFU/animal/day. After 30 days of supplementation, animals received the inflammatory insult by LPS (15mg/kg). Behavioral tests, oxidative stress and inflammation were performed, as well as gut and brain histology. Results: In the behavioral test, LPS+ B. lactis group was less anxious than the other groups. Serum interleukin IL-1β and IL-6 levels increased in all groups that received the LPS insult and there was a reduction in inflammation in the supplemented groups when compared to the LPS group in brain and gut. A reduction in myeloperoxidase activity and oxidative stress in groups supplemented with probiotics. Intestine histological analysis, damage to tissue integrity in the LPS group and preservation of integrity in the supplemented animals. In the brain, infiltrates of perivascular inflammatory cells can be seen in the LPS group. Conclusion: The three probiotic studies showed efficient immunomodulating activity and ensured integrity of the intestinal barrier function, even after the severe insult by LPS. These results show the important role of probiotics in the gut-brain axis.

Abstract BackgroundThe pathological characteristics of acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) are pulmonary edema resulting from pulmonary permeability increasing. The main cause is uncontrolled inflammatory response leading to the damage of pulmonary vascular endothelial and alveolar epithelial barriers. However, there has not been effective drugs against ALI. In this study, we investigated the function of Isopropyl 3-(3, 4-dihydroxypheny l)-2-hydroxypropanoate (IDHP), a novel metabolite of Danshen dripping pill having anti-inflammatory effect, in lipopolysaccharide (LPS) induced ALI in mice, and its underlying mechanisms.MethodsPretreatment of IDHP in LPS-induced acute lung injury in mice were observed on survival rate, pulmonary morphologic changes, total protein content in bronchoalveolar lavage fluid (BALF), and inflammatory cytokines in lung tissue and BALF. To further explore its mechanism on ALI, THP-1 macrophages was studied to analyse pyroptosis related proteins and co-culture with epithelial or endothelial cells to assess protection function of IDHP in vitro.ResultsAs revealed by survival study, pretreatment with high dose of IDHP reduced the mortality of mice from ALI. IDHP pretreatment significantly improved LPS-induced lung pathological changes, reduced protein leakage and lung myeloperoxidase activity. IDHP also inhibited the release of inflammatory mediators TNFα, IL-1β, IL-6 and IL-18 in BALF and lung tissue. Meanwhile, IDHP decreased the expression of active-caspase1 (in canonical pyroptosis pathway), caspase4/5 (non-canonical pyroptosis pathway), Nrlp3, mature IL-1β, mature IL-18, Asc speck formation, and cleaved Gsdmd, all these are required for pyroptosis, in LPS stimulated THP-1 macrophages. Moreover, IDHP also decreased ROS production in LPS-stimulated THP-1 macrophages, inhibited the expression of tight junction proteins (Occludin, Zo-1) in endothelial cells, and decreased lactate dehydrogenase activity in supernatants of epithelial or endothelial cells, co-cultured with LPS-stimulated THP-1 macrophages. ConclusionsPretreatment of IDHP improves survival rate and ameliorates LPS-induced ALI in mice possibly via inhibiting canonical and non-canonical pyroptosis pathways.

Abstract Background: The pathological characteristics of acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) are pulmonary edema resulting from pulmonary permeability increasing. The main cause is uncontrolled inflammatory response leading to the damage of pulmonary vascular endothelial and alveolar epithelial barriers. However, there has not been effective drugs against ALI. In this study, we investigated the function of Isopropyl 3-(3, 4-dihydroxypheny l)-2-hydroxypropanoate (IDHP), a novel metabolite of Danshen dripping pill having anti-inflammatory effect, in lipopolysaccharide (LPS) induced ALI in mice, and its underlying mechanisms.Methods: Pretreatment of IDHP in LPS-induced acute lung injury in mice were observed on survival rate, pulmonary morphologic changes, total protein content in bronchoalveolar lavage fluid (BALF), and inflammatory cytokines in lung tissue and BALF. To further explore its mechanism on ALI, THP-1 macrophages was studied to analyse propotosis related proteins and co-culture with epithelial or endothelial cells to assess protection function of IDHP in vitro.Results: As revealed by survival study, pretreatment with high dose of IDHP reduced the mortality of mice from ALI. IDHP pretreatment significantly improved LPS-induced lung pathological changes, reduced protein leakage and lung myeloperoxidase activity. IDHP also inhibited the release of inflammatory mediators TNFα, IL-1β, IL-6 and IL-18 in BALF and lung tissue. Meanwhile, IDHP decreased the expression of active-caspase1 (in canonical pyroptosis pathway), caspase4/5 (non-canonical pyroptosis pathway), Nrlp3, mature IL-1β, mature IL-18, Asc speck formation, and cleaved Gsdmd, all these are required for pyroptosis, in LPS stimulated THP-1 macrophages. Moreover, IDHP also decreased ROS production in LPS-stimulated THP-1 macrophages, inhibited the expression of tight junction proteins (Occludin, Zo-1) in endothelial cells, and decreased lactate dehydrogenase activity in supernatants of epithelial or endothelial cells, co-cultured with LPS-stimulated THP-1 macrophages. Conclusions: Pretreatment of IDHP improves survival rate and ameliorates LPS-induced ALI in mice possibly via inhibiting canonical and non-canonical pyroptosis pathways.

Host immune response in the tumor microenvironment plays key roles in tumorigenesis. We hypothesized that D-mannose, a simple sugar with anti-inflammatory properties, could decrease oxidative stress and slow glioma progression. Using a glioma stem cell model in immunocompetent mice, we induced gliomas in the brain and tracked MPO activity in vivo with and without D-mannose treatment. As expected, we found that D-mannose treatment decreased the number of MPO+ cells and slowed glioma progression compared to PBS-treated control animals with gliomas. Unexpectedly, instead of decreasing MPO activity, D-mannose increased MPO activity in vivo, revealing that D-mannose boosted the MPO activity per MPO+ cell. On the other hand, D-glucose had no effect on MPO activity. To better understand this effect, we examined the effect of D-mannose on bone marrow-derived myeloid cells. We found that D-mannose modulated MPO activity via two mechanisms: directly via N-glycosylation of MPO, which boosted the MPO activity of each molecule, and indirectly by increasing H2O2 production, the main substrate for MPO. This increased host immune response acted to reduce tumor size, suggesting that increasing MPO activity such as through D-mannose administration may be a potential new therapeutic direction for glioma treatment.

Objectives clinical and laboratory examination of patients with acute tonsillitis for early diagnosis and prognosis of peritonsillar abscess. Material and methods. The study included 101 patient with lacunar tonsillitis complicated by peritonsillar abscess and 64 donors (control group). Immunological studies were performed according to WHO recommendations, on the basis of the immunological department of the EMB Research Institute and the immunological laboratory of the SamSMU. Results. Immunological examination of patients with abscess showed an increase in: neutrophil phagocytic activity, CD4+/CD8+, the number of cells expressing HLA-DR+ markers, complement activity, IgA, IgM, IgG plasma concentration, fibronectin level, pro-inflammatory cytokines IL-8, IL-1, IL-1 and a decrease in: the level of TNF-, myeloperoxidase activity, number of cells containing CD4+, CD8+, CD16+, CD20+, CD25+ markers. High correlation was registered between total lymphocytes and CD3+ and CD4+ cells (p 0.01); between CD3+ and CD4+ markers (p 0.01); as well as high correlation of IL-1 levels with IL-8 and IL-1 (p 0.01). Cluster analysis revealed different types of immune homeostasis. The first type (cluster) had high values of leukocytes (total), lymphocytes (total), cells with CD3+, CD4+, CD8+, CD16+, CD20+, CD95+ and HLA-DR+ markers; the second type (cluster) was characterized by significantly lower levels of these immune status indicators. 41 patient had the first type of immune response, with an explicit clinical picture and rapid formation of an abscess. The second type of immune response was registered in 60 patients having a torpid course of the disease with delayed development of abscess. Further, to assess the type of immune reactions, it is necessary to substitute the values of indicators into the model and calculate the integral coefficient of the body's reaction (ICTROI and ICTROII).

Impaired cerebral hemodynamic autoregulation, vasoconstriction, and cardiovascular and metabolic dysfunctions cause cerebral hypoperfusion (CH) that triggers pro-oxidative and inflammatory events. The sequences linked to ion-channelopathies and calcium and glutamatergic excitotoxicity mechanisms resulting in widespread brain damage and neurobehavioral deficits, including memory, neurological, and sensorimotor functions. The vasodilatory, anti-inflammatory, and antioxidant activities of cucurbitacin E (CuE) can alleviate CH-induced neurobehavioral impairments. In the present study, the neuroprotective effects of CuE were explored in a rat model of CH. Wistar rats were subjected to permanent bilateral common carotid artery occlusion to induce CH on day 1 and administered CuE (0.25, 0.5 mg/kg) and/or Bay-K8644 (calcium agonist, 0.5 mg/kg) for 28 days. CH caused impairment of neurological, sensorimotor, and memory functions that were ameliorated by CuE. CuE attenuated CH-triggered lipid peroxidation, 8-hydroxy-2′-deoxyguanosine, protein carbonyls, tumor necrosis factor-α, nuclear factor-kappaB, myeloperoxidase activity, inducible nitric oxide synthase, and matrix metalloproteinase-9 levels in brain resulting in a decrease in cell death biomarkers (lactate dehydrogenase and caspase-3). CuE decreased acetylcholinesterase activity, glutamate, and increased γ-aminobutyric acid levels in the brain. An increase in brain antioxidants was observed in CuE-treated rats subjected to CH. CuE has the potential to alleviate pathogenesis of CH and protect neurological, sensorimotor, and memory functions against CH.

We investigated the protective effects of pycnogenol (PYC), a natural anti-oxidant with an anti-inflammatory effect, on the acetaminophen (APAP)-induced hepatorenal injury in rats. Wistar albino rats were divided into four experimental groups: control, PYC (10 mg/kg, ip), APAP (1000 mg/kg), and APAP+PYC groups. Rats were decapitated 24 hours after the APAP injection, and their blood was taken to determine blood urea nitrogen (BUN), creatinine, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and pro-inflammatory cytokines; TNF-α and IL-1 β. Liver and kidney tissue samples were obtained for the histological examination and the determination of malondialdehyde (MDA) and glutathione (GSH) levels as well as myeloperoxidase (MPO) and Na+/K+-ATPase activities. PYC treatment decreased the APAP-induced elevations in serum pro-inflammatory cytokines and reduced the impairment of liver and kidney functions. Furthermore, the increase in tissue lipid peroxidation and myeloperoxidase activity and the decrease in the GSH levels and Na+/K+-ATPase activity by the APAP overdose were reversed by the PYC treatment. Besides, histologic findings reinforce the protective effect of PYC in APAP-induced hepatorenal damage. PYC, which appears to have restored the GSH and depressed neutrophil infiltration and the associated release of pro-inflammatory cytokines, merits consideration as an anti-oxidant and anti-inflammatory agent in preventing APAP-induced hepatorenal damage.