Редактирование: MPO

Myeloperoxidase precursor (EC 1.11.2.2) (MPO) [Contains: Myeloperoxidase; 89 kDa myeloperoxidase; 84 kDa myeloperoxidase; Myeloperoxidase light chain; Myeloperoxidase heavy chain]

==Publications==

{{medline-entry
|title=Aging influences in the blood-brain barrier permeability and cerebral oxidative stress in sepsis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32827711
|abstract=Sepsis is a set of serious manifestations throughout the body produced by an infection, leading to changes that compromise cellular homeostasis and can result in dysfunction of the central nervous system. The elderly have a higher risk of developing sepsis than younger peoples. Under the influence of inflammatory mediators and oxidizing agents released in the periphery as a result of the infectious stimulus, changes occur in the blood-brain barrier (BBB) permeability, with neutrophil infiltration, the passage of toxic compounds, activation of microglia and production of reactive species that results in potentiation of neuroimmune response, with the progression of neuronal damage and neuroinflammation. The objective of this study is to compare BBB permeability and the development of oxidative stress in the hippocampus and prefrontal cortex of young and old rats submitted to polymicrobial sepsis induction. Male Wistar rats grouped into sham (60d), sham (210d), cecal ligation and perforation (CLP) (60d) and CLP (210d) with n = 16 per experimental group were evaluated using the CLP technique to induce sepsis. The brain regions were collected at 24 h after sepsis induction to determine BBB permeability, myeloperoxidase ([[MPO]]) activity as marker of neutrophil activation, nitrite/nitrate (N/N) levels as marker of reactive nitrogen species, thiobarbituric acid reactive substances as marker of lipid peroxidation, protein carbonylation as marker of protein oxidation, and activity of antioxidant enzyme catalase ([[CAT]]). There was an increase in the BBB permeability in the CLP groups, and this was enhanced with aging in both brain region. [[MPO]] activity in the brain regions increased in the CLP groups, along with a hippocampal increase in the CLP 210d group compared to the 60d group. The concentration of N/N in the brain region was increased in the CLP groups. The damage to lipids and proteins in the two structures was enhanced in the CLP groups, while only lipid peroxidation was higher in the prefrontal cortex of the CLP 210d group compared to the 60d. [[CAT]] activity in the hippocampus was decreased in both CLP groups, and this was also influenced by age, whereas in the prefrontal cortex there was only a decrease in [[CAT]] in the CLP 60d group compared to the sham 60d. These findings indicate that aging potentiated BBB permeability in sepsis, which possibly triggered an increase in neutrophil infiltration and, consequently, an increase in oxidative stress.

|keywords=* Aging
* Blood-brain barrier
* Brain
* Oxidative stress
* Sepsis
|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111063
}}
{{medline-entry
|title=Increased cardiovascular and atherosclerosis markers in blood of older patients with atopic dermatitis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31622668
|abstract=Atopic dermatitis (AD) is associated with increased systemic inflammation and cardiovascular risk. Although previous studies have found increased inflammatory proteins in the blood of patients with AD, detailed comparison among patients with AD of different ages is unavailable. To characterize the blood proteomic signature of patients with AD as a function of age. We used the OLINK high-throughput proteomic assay to measure serum inflammatory and cardiovascular risk proteins in 71 patients with moderate to severe AD from 3 age groups (18-40 years old [n = 26], 41-60 years old [n = 24], and >60 years old [n = 21]) compared with 37 age-matched controls. Total and allergen-specific serum IgEs were also measured. When we compared patients with AD from 3 different age groups with their respective controls, we identified a total of 172 differentially expressed proteins. T 2 chemokines (CCL13, CCL17) were consistently elevated in patients with AD across all ages (P < .05), whereas T 1 (CXCL10) and T 17 (KYNU, CCL20) markers incrementally increased with age in both patients with AD and healthy subjects. Elderly patients with AD (>60 years old) exhibited striking upregulation of key proinflammatory proteins, including markers of atherosclerosis (CCL4, [[CCL7]], SORT1), cardiovascular risk (GDF15, [[MPO]], ST2), cell adhesion (CDH3), and apoptosis (FAS; all P < .05) compared with younger patients with AD and age-matched controls. We also found that total and allergen-specific serum IgEs decreased significantly with age in patients with AD (P < .05). Elderly patients with AD had increased levels of systemic inflammatory markers, including those associated with cardiovascular and atherosclerosis risk, which may explain their increased incidence of cardiovascular disease. This finding suggests that older patients with AD may benefit from cardiovascular disease screening and prevention.
|mesh-terms=* Adolescent
* Adult
* Age Factors
* Aged
* Aging
* Apoptosis
* Atherosclerosis
* Biomarkers
* Cardiovascular Diseases
* Cell Adhesion
* Chemokines
* Dermatitis, Atopic
* Humans
* Immunoglobulin E
* Inflammation
* Middle Aged
* Severity of Illness Index
* Th1 Cells
* Th17 Cells
* Young Adult

|full-text-url=https://sci-hub.do/10.1016/j.anai.2019.10.013
}}
{{medline-entry
|title=Impaired sleep quality is associated with concurrent elevations in inflammatory markers: are post-menopausal women at greater risk?
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31287027
|abstract=Chronic inflammation and impaired sleep increase the risk for cardiovascular disease. Menopausal women may be particularly at risk as a result of impaired sleep. The objective of the current investigation was to assess the relationship between poor sleep and C-reactive protein ([[CRP]]), interleukin-6 (IL-6), tumor necrosis factor alpha ([[TNF]]-α), and myeloperoxidase ([[MPO]]) in healthy non- and postmenopausal women and men. A fasting blood draw was obtained from 122 healthy men and women (31 were postmenopausal). Higher scores on the Pittsburgh Sleep Quality Index (PSQI) were used to define poor sleep. Given the sample size and healthy nature of the sample, hierarchical linear regression analyses were performed on a composite inflammatory score involving [[CRP]], IL-6, and [[TNF]]-α. Sex/menopausal group and PSQI were entered as predictors, and the interaction of the group by PSQI was entered stepwise. Analyses on [[MPO]] were performed separately. Sleep quality was associated with higher inflammatory activity (β = 0.272, P = 0.003), which remained significant (P = 0.046) after controlling for age, waist circumference, exercise times per week, and depressive symptoms. While in the same direction, sleep quality was not significantly associated with [[MPO]]. Dichotomizing sleep quality led to similar results. Impaired sleep quality is independently associated with greater inflammation in healthy adult men and women. Despite an overall less favorable metabolic and inflammatory profile in postmenopausal women, impaired sleep did not emerge as differentially related to inflammatory activity in this group.
|mesh-terms=* Adult
* Aging
* Biomarkers
* C-Reactive Protein
* Female
* Humans
* Inflammation
* Interleukin-6
* Male
* Middle Aged
* Peroxidase
* Postmenopause
* Premenopause
* Sleep Wake Disorders
* Tumor Necrosis Factor-alpha
|keywords=* C-reactive protein
* IL-6
* Menopause
* Sex
* Sleep
* TNF-α
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6615113
}}
{{medline-entry
|title=Local and systemic effects of aging on acute pancreatitis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31204259
|abstract=/Objectives: Evaluation of the local and systemic effects of aging on the severity of acute pancreatitis (AP) in an experimental rat model in elderly animals. AP was induced in Wistar rats by intraductal 2.5% taurocholate injection and divided into two groups: Young (3 month old) and Aged (18 month old). Two and 24 h after AP induction blood samples were collected for determinations of amylase, AST, ALT, urea, creatinine, glucose, and of plasma I-FABP. [[TNF]]-α and IL-6 levels were determined in serum and ascitic fluid. Liver mitochondrial function and malondialdehyde (MDA) contents, pancreas histological analysis, and pulmonar myeloperoxidade ([[MPO]]) activity were performed. Bacterial translocation was evaluated by bacterial cultures of pancreas. A significant increase in serum amylase, AST, ALT, urea, creatinine, glucose, I-FABP, and IL-6 levels, and a reduction in serum and ascitic fluid [[TNF]]-α levels were observed in the aged group compared to the young group. Liver mitochondrial dysfunction, MDA contents, and pulmonary [[MPO]] activity were increased in the Aged AP group compared to the Young AP group. Positive bacterial cultures obtained from pancreas tissue in aged group were significantly increased compared to the young group. Acinar necrosis was also increased in aged AP group when compared to young AP group. Aging worsens the course of acute pancreatitis evidenced by increased local and systemic lesions and increased bacterial translocation.
|mesh-terms=* Acute Disease
* Aging
* Animals
* Cytokines
* Fatty Acid-Binding Proteins
* Infections
* Lipid Peroxidation
* Male
* Mitochondria, Liver
* Necrosis
* Oxidation-Reduction
* Pancreatitis
* Peroxidase
* Phosphorylation
* Rats
* Rats, Wistar
|keywords=* Acute pancreatitis
* Aging
* Bacterial translocation
* Cytokines
* Liver mitochondrial function
|full-text-url=https://sci-hub.do/10.1016/j.pan.2019.06.005
}}
{{medline-entry
|title=Inflammatory signatures in older persons with physical frailty and sarcopenia: The frailty "cytokinome" at its core.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31054959
|abstract=The construct of physical frailty and sarcopenia (PF