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1.
Acta Neurochir Suppl ; 127: 35-41, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31407060

RESUMO

Given the poor outcome of subarachnoid hemorrhage due to rupture of intracranial aneurysms (IAs) and high prevalence of IAs in general public, elucidation of mechanisms underlying the pathogenesis of the disease and development of effective treatment are mandatory for social health. Recent experimental findings have revealed the crucial contribution of macrophage-mediated chronic inflammation to and greatly promoted our understanding of the pathogenesis. Also a series of studies have proposed the potential of anti-inflammatory drugs as therapeutic ones. In this process, a rodent model of IAs plays an indispensable role. Basic concept of IA induction in such kind of models is that IA formation is triggered by hemodynamic stress loaded on damaged arterial walls. To be more precise, although detailed procedures are different among researchers, animals are subjected to a ligation of a unilateral carotid artery and systemic hypertension achieved by a salt overloading, and IAs are induced at the contralateral bifurcation site. Importantly, trigger of IA formation in the model mimics human one, and IA lesions induced share similarity in histology with human ones such as degenerative changes of media. For further elucidating the pathogenesis, we need to well understand variations, usefulness, and also limits of this model.


Assuntos
Modelos Animais de Doenças , Hemodinâmica , Aneurisma Intracraniano , Hemorragia Subaracnóidea , Animais , Humanos , Inflamação , Macrófagos , Ratos
2.
Acta Neurochir Suppl ; 127: 69-75, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31407066

RESUMO

BACKGROUND: Subarachnoid hemorrhage (SAH) is a severe and emergent cerebrovascular disease, the prognosis of which usually very poor. Microthrombi formation highlighted with inflammation occurs early after SAH. As the main cause of DCI, microthrombosis associated with the prognosis of SAH. The aim of this study was to show HSP90 inhibitor 17-AAG effect on microthrombosis after SAH in rats. METHODS: Ninety-five SD rats were used for the experiment. For time course study, the rats were randomly divided into five groups: sham group and SAH group with different time point (1d, 2d, 3d, 5d). Endovascular perforation method was conducted for SAH model. Neurological score, SAH grade, and mortality were measured after SAH. The samples of the left hemisphere brain were collected. The expression of HSP90 was detected by Western blot. The microthrombosis after SAH in rats' brain was detected by immunohistochemistry. For mechanism study, rats were randomly divided into three groups: sham, SAH + vehicle, and SAH +17-AAG (n = 6/group). 17-AAG was given by intraperitoneal injection (80 mg/kg) 1 h after SAH. Neurological function were measured at 24 h after SAH. The expression of RIP3, NLRP3, ASC, and IL-1ß was measured by Western blot. Microthrombosis was detected by immunohistochemistry. RESULTS: Our results showed that the HSP90 protein level increased and peaked at 2 days after SAH. Microthrombosis caused by SAH was increased in 1 day and peaked at 2 days after SAH. Administration HSP90 specific inhibitor 17-AAG reduced expression of RIP3, NLRP3, ASC, and IL-1ß, reduced microthrombosis after SAH, and improved neurobehavior when compared to vehicle group. CONCLUSIONS: 17-AAG can ameliorate microthrombosis via HSP90/RIP3/NLRP3 pathway and improve neurobehavior after SAH.


Assuntos
Inibidores Enzimáticos , Proteína 3 que Contém Domínio de Pirina da Família NLR , Hemorragia Subaracnóidea , Trombose , Animais , Córtex Cerebral , Inibidores Enzimáticos/farmacologia , Proteínas de Choque Térmico HSP90 , Inflamação , Ratos , Ratos Sprague-Dawley , Proteína Serina-Treonina Quinases de Interação com Receptores , Hemorragia Subaracnóidea/tratamento farmacológico , Hemorragia Subaracnóidea/metabolismo , Trombose/tratamento farmacológico
3.
Einstein (Sao Paulo) ; 18: eAO4784, 2020.
Artigo em Inglês, Português | MEDLINE | ID: mdl-31553356

RESUMO

OBJECTIVE: To evaluate the effect of three types of muscular resistance training on adiposity, inflammation levels and insulin activity in Swiss mice with fat-rich diet-induced obesity. METHODS: Lean and obese male Swiss mice were selected and allocated to one of eight groups comprising eight mice each, as follows: standard diet + no training; standard diet + muscular resistance training; standard diet + hypertrophy training; standard diet + strength training; high-fat diet + no training; high-fat diet + muscular resistance training; high-fat diet + hypertrophy training; high-fat diet + strength training. The training protocol consisted of stair climbing for a 10-week period. Blood samples were collected for lactate analysis, glucose level measurement and insulin tolerance test. After euthanasia, adipose tissues were removed and weighed for adiposity index determination. Fragments of epididymal adipose tissue were then embedded for histological analysis or homogenized for tumor necrosis factor alpha level determination using the ELISA method. RESULTS: Ausency of differences in total training volume and blood lactate levels overall emphasize the similarity between the different resistance training protocols. Body weight loss, reduced adipocyte area and lower adiposity index were observed in trained obese mice, regardless of training modality. Different training protocols also improved insulin sensitivity and reduced inflammation levels. CONCLUSION: Resistance training protocols were equally effective in reducing body fat, inflammation levels and insulin resistance in obese mice.


Assuntos
Adiposidade/fisiologia , Hipertrofia/fisiopatologia , Inflamação/fisiopatologia , Resistência à Insulina/fisiologia , Exercícios de Alongamento Muscular/métodos , Obesidade/fisiopatologia , Condicionamento Físico Animal/fisiologia , Tecido Adiposo Branco/fisiopatologia , Animais , Glicemia/análise , Peso Corporal/fisiologia , Dieta Hiperlipídica , Ensaio de Imunoadsorção Enzimática , Masculino , Camundongos , Camundongos Obesos , Reprodutibilidade dos Testes , Treinamento de Resistência/métodos , Fatores de Tempo , Fator de Necrose Tumoral alfa/análise
4.
J Environ Pathol Toxicol Oncol ; 38(3): 229-238, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31679310

RESUMO

Asthma has affected more than 300 million people worldwide and is considered one of the most debilitating global public health problems based on a recent statistical report from the Global Initiative for Asthma. Inflammation of the airways leads to the various interrelated mechanisms of innate and adaptive immunity acting mutually with the epithelium of the respiratory organ. Fucoxanthin is an orange or brown pigment which is naturally found in various seaweeds. To the best of our knowledge, there are no scientific claims or evidence of the curative effects of fucoxanthin against asthma. Hence, this present research was designed to investigate the curative activity of fucoxanthin against ovalbumin-induced asthma in a mouse model. Fucoxanthin (50 mg/kg) showed significant (P < 0.001) antiasthma activity. It effectively decreased intracellular secretion of reactive oxygen species and increased antioxidant enzyme activity. Fucoxanthin also decreased inflammatory cytokine markers in bronchoalveolar lavage fluid. Because fucoxanthin showed effective antiasthma activity against ovalbumin-induced asthma in experimental animals, further research on this natural antioxidant could lead to development of a novel drug for the treatment of asthma in humans.


Assuntos
Antiasmáticos/farmacologia , Antioxidantes/metabolismo , Asma/tratamento farmacológico , Citocinas/imunologia , Inflamação/tratamento farmacológico , Espécies Reativas de Oxigênio/metabolismo , Xantofilas/farmacologia , Animais , Biomarcadores/metabolismo , Líquido da Lavagem Broncoalveolar/química , Citocinas/efeitos dos fármacos , Inflamação/induzido quimicamente , Masculino , Camundongos , Ovalbumina/toxicidade
5.
J Environ Pathol Toxicol Oncol ; 38(3): 239-251, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31679311

RESUMO

Fucoxanthin, a potent carotenoid present in various natural sources especially from seaweeds; it exhibits several biological effects like anti-neoplastic, anti-mutagenic, anti-diabetic, anti-obesity and anti-inflammatory actions. Fucoxanthin role in chemoprevention of lung cancer in mouse model induced using benzo(a)pyrene [B(a)P] has been presented here. Oral administration of fucoxanthin with and without B(a)P were studied, the results from our study shows that fucoxanthin significantly decreased tumor progression in mice exposed to B(a)P, the obtained data were correlated with increased antioxidant, apoptosis and decreased tumour marker and anti-apoptotic molecules. With respect to apoptosis, fucoxanthin treated animals shows increased apoptosis compared to tumor induced mice by increased expression of caspase 9 and 3 and decreased expression of anti-apoptotic Bcl2 protein. Finally, histopathological and immuno histochemical analysis also revealed that fucoxanthin shows potent anticancer agent by bringing back the damaged tissue treated with B(a)P and also decreases the expression of PCNA in cancer induced mice. The anticancer effect of fucoxanthin may be attributed by several independent mechanisms which play a important roles in the prevention of cancer development, there is also substantial evidences to show that fucoxanthin acts indirectly by increasing the antioxidant capacity of affected tissue and prepared to cope up with oxidative stress which is proved in our study. Thus from our study it is clearly established that fucoxanthin act as a persuasive anticancer drug against lung cancer.


Assuntos
Anti-Inflamatórios/farmacologia , Apoptose/imunologia , Inflamação/tratamento farmacológico , Neoplasias Pulmonares/tratamento farmacológico , Transdução de Sinais/imunologia , Xantofilas/farmacologia , Animais , Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Benzo(a)pireno/toxicidade , Inflamação/induzido quimicamente , Masculino , Camundongos , Transdução de Sinais/efeitos dos fármacos
6.
J Environ Pathol Toxicol Oncol ; 38(3): 285-295, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31679314

RESUMO

Psoriasis is an autoregulated immune and inflammation-based skin disease affecting approximately 3-4% of the worldwide population. Pinitol, conservatively used in ayurvedic medicine, has been shown to disclose an antiinflammatory effect, hold back the T-helper cells, and postpone cardiovascular diseases. In the present study we aimed to reveal the effect of D-pinitol on imiquimod (IMQ)-induced psoriasis-like skin inflammation in a mouse model via the nuclear factor-κB (NF-κB) pathway genes. In the current study, we found that D-pinitol ameliorated the skin abrasion and abridged epithelial thickness, inflammation numbers, and collagen-occupied regions in IMQ-induced psoriasis-like mice. The same results (epithelial thickness, inflammation numbers, and collagen-occupied regions) we achieved in dorsal skin regions. In addition, D-pinitol modified the lipid profile and antioxidant enzyme levels, which means that the IMQ-induced group showed elevated malondialdehyde when compared to D-pinitol. Downregulated expression of glutathione, superoxide dismutase, and catalase in the IMQ-induced group was incomparable with D-pinitol, control, and standard group. Additionally, inflammatory and NF-kB pathway gene levels in the psoriatic mouse skin, which includes tumor necrosis factor-α, interleukin [IL]-6, IL-17A, IL-23,TRAF3, NIK, IKKα, and RelB, were dramatically increased or decreased by treatment with D-pinitol. Histological and morphometric studies disclose the efficiency of D-pinitol. Finally, we found that D-pinitol reserved the TRAF3, NIK, IKKα, and RelB in the psoriatic skin, signifying that it restrains the commencement of NF-κB signaling pathways. The present results suggest that D-pinitol could prove to have tremendous preventive potential against the treatment and prevention of inflammatory disease.


Assuntos
Anti-Inflamatórios/farmacologia , Imiquimode/imunologia , Inflamação/tratamento farmacológico , Inositol/análogos & derivados , Psoríase/tratamento farmacológico , Animais , Inflamação/induzido quimicamente , Inflamação/imunologia , Inositol/farmacologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , NF-kappa B/imunologia , Psoríase/imunologia
7.
Prague Med Rep ; 120(2-3): 103-106, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31586509

RESUMO

Myristic acid was identified as a metabolite with the highest diagnostic sensitivity and specificity in the metabolome of patients with bacteraemia. Subsequently, its significant decrease was observed in patients in septic shock not responding to treatment. In our study we have captured myristic acid serum level kinetics in 96 hours following accidental intravenous self-administration of eubiotic Hylak forte causing infection-like systemic inflammatory response syndrome (SIRS). To our knowledge, this is the first time the kinetics of myristic acid levels is presented in a septic patient. Myristic acid was evaluated in comparison with other inflammatory biomarkers and with its level in a control group of healthy subjects. Myristic acid levels during septic response were significantly elevated in comparison with the control group. The peak level was recorded almost immediately after the insult with a gradual decrease within 96 hours. Myristic acid appears to be a promising biomarker in sepsis diagnostics, further research by our group into this topic is ongoing.


Assuntos
Ácido Mirístico/metabolismo , Sepse/metabolismo , Biomarcadores/análise , Biomarcadores/metabolismo , Humanos , Inflamação/metabolismo , Cinética , Choque Séptico/metabolismo , Síndrome
8.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 31(9): 1170-1173, 2019 Sep.
Artigo em Chinês | MEDLINE | ID: mdl-31657348

RESUMO

OBJECTIVE: Sepsis is a life-threatening organ dysfunction caused by the host's imbalance in response to infection, which is still the leading cause of death in critically ill patients. In recent years, studies have found that vitamin D deficiency or insufficiency is common in critically ill patients, especially sepsis. The relationship between vitamin D and sepsis has attracted more and more attention. The mechanism of vitamin D in sepsis is described from the aspects of immune regulation, inflammation regulation, endothelial cell protection, carbon monoxide regulation, and receptor gene polymorphism, by analyzing the related literatures of vitamin D and sepsis in recent years in order to provide new ideas for clinical diagnosis and treatment of sepsis.


Assuntos
Sepse/metabolismo , Deficiência de Vitamina D , Vitamina D/metabolismo , Estado Terminal , Humanos , Inflamação
9.
Sheng Li Xue Bao ; 71(5): 732-740, 2019 Oct 25.
Artigo em Chinês | MEDLINE | ID: mdl-31646327

RESUMO

Parkinson's disease (PD) is the second most common neurodegenerative disease, characterized by loss of dopaminergic (DA) neurons in the dense part of the substantia nigra (SNpc). Postmortem analysis of PD patients and experimental animal studies found that microglial cell activation and increased levels of pro-inflammatory factors were common features of PD brain tissue. At the same time, the invasion and accumulation of peripheric immune cells were detected in the brain of PD patients. In this paper, peripheral inflammation across the blood-brain barrier (BBB), the misfolded α-synuclein (α-syn)-induced microglial cell activation and intracerebral inflammation in PD are summarized, providing potential therapeutic measures for delaying the onset of PD.


Assuntos
Inflamação/patologia , Doença de Parkinson/patologia , Substância Negra/patologia , Animais , Barreira Hematoencefálica , Neurônios Dopaminérgicos/patologia , Humanos , Microglia , alfa-Sinucleína
10.
Mol Biol (Mosk) ; 53(5): 790-798, 2019.
Artigo em Russo | MEDLINE | ID: mdl-31661478

RESUMO

Recently, much attention has been drawn to unraveling the mechanisms of neurodegenerative and neuroinflammatory disease pathogenesis. A special role in the development of neuropathologies is assigned to the interaction of the nervous and the immune systems. Microglia are the cells of the immune system that function as resident macrophages of the central nervous system (CNS) and are involved in the development of CNS, as well as in homeostatic interactions. Impaired microglia can contribute to neuroinflammation and neurodegeneration. With the help of genome editing technologies, the main paradigms in the development and functions of microglia have been addressed. At the same time, an understanding of the mechanisms of regulation of microglia in normal and pathological conditions is necessary to create an effective therapy aimed at treating various neurological diseases. This review focuses on recent findings on the origin of microglia, its regulatory role in the central nervous system, as well as its contribution to the development of neuroinflammation.


Assuntos
Sistema Nervoso Central/citologia , Sistema Nervoso Central/fisiologia , Homeostase , Inflamação/patologia , Microglia/fisiologia , Doenças Neurodegenerativas/patologia , Sistema Nervoso Central/patologia , Sistema Nervoso Central/fisiopatologia , Humanos , Inflamação/fisiopatologia , Microglia/citologia , Microglia/patologia , Doenças Neurodegenerativas/fisiopatologia
11.
Mol Biol (Mosk) ; 53(5): 799-814, 2019.
Artigo em Russo | MEDLINE | ID: mdl-31661479

RESUMO

An extensive network of regulation of systemic inflammation makes development of a reproducible experimental model of sepsis a complex task. There is no single mouse model that can capture all clinical aspects of this complicated pathology. However, a combination of existing approaches can go a long way towards analysis of specific mechanisms of sepsis development and to the design of novel therapeutic approaches. This review describes the popular mouse models of sepsis and septic shock, as well as their limitations and development strategies.


Assuntos
Modelos Animais de Doenças , Sepse , Choque Séptico , Animais , Inflamação , Camundongos , Sepse/terapia , Choque Séptico/terapia
12.
Mol Biol (Mosk) ; 53(5): 860-870, 2019.
Artigo em Russo | MEDLINE | ID: mdl-31661484

RESUMO

It is time to celebrate the 125th anniversary of the first successful attempt to develop and use a specific high-titer antitoxic serum for treating diphtheria, a deadly infectious disease. This was followed by major advances in passive immunotherapy 75 years ago (production of pooled human IgG for subcutaneous injection) and 50 years ago (widespread technology for producing immunoglobulin preparations for intravenous administration). More than 200 tons of pooled human IgG are produced per year worldwide. The preparation is used primarily for IgG substitution in patients with primary and secondary immunodeficiencies, as well as for an immunomodulating treatment of a growing number of autoimmune and inflammatory diseases. These preparations contain the pooled IgG antibody repertoire of a large population of healthy plasma donors. This repertoire includes antibodies that neutralize pathogens and their factors of virulence, anti-idiotypic antibodies, and antibodies to other foreign and own proteins, as well as to carbohydrate antigens. Naturally polyspecific antibodies that are present in all healthy individuals play an important role as a first-line defense against bacteria and viruses. After exposure to protein-modifying agents, some IgG molecules can acquire the ability to bind novel structurally unrelated antigens. This phenomenon is referred to as induced polyspecificity. The list of these protein-modifying molecules was shown to include low-pH buffers, free heme, pro-oxidative ferrous ions, reactive oxygen species, etc. Such modified antibody preparations may have a therapeutic potential, since their administration to animals with experimental sepsis or aseptic systemic response syndromes significantly improved survival rates, while the same dose of the native preparation had no effect. We also hypothesize that the aggressive protein-modifying molecules released in sites of inflammation and tissue damage could also modify the antigen-binding behavior of surface immunoglobulin B cell receptors and the structurally related T cell receptors. This "specificity editing" of both types of receptors may play a major role in the body's defense mechanisms.


Assuntos
Imunoglobulina G/imunologia , Imunoglobulina G/uso terapêutico , Preparações Farmacêuticas/administração & dosagem , Animais , História do Século XIX , Humanos , Imunoglobulina G/administração & dosagem , Imunoglobulina G/história , Inflamação/tratamento farmacológico , Inflamação/imunologia , Preparações Farmacêuticas/história , Sepse/tratamento farmacológico , Sepse/imunologia
13.
Vestn Oftalmol ; 135(4): 19-26, 2019.
Artigo em Russo | MEDLINE | ID: mdl-31573553

RESUMO

INTRODUCTION: Fibrosis is the most important pathologic condition involved in undesirable outcomes of dacryocystorhinostomy. A number of biochemical factors are currently known to have an effect on wound healing by promoting excessive scarring. Isoforms of transforming growth factor ß (TGF-ß1) are considered the 'main' pro-fibrotic factor, but wound healing is also affected by other cytokines such as connective tissue growth factor (CTGF), which stimulates fibrosis, and fibroblast growth factor (FGF-2), which acts as antagonist to it. PURPOSE: To investigate correlations between endoscopic endonasal dacryocystorhinostomy outcomes and certain mediators of fibrosis. MATERIAL AND METHODS: The study included 45 cases of endoscopic endonasal dacryocystorhinostomy. The patients were grouped according to surgery outcome: patients with unsuccessful surgical treatment were assigned to group 1 (n=10); patients with successful surgical treatment - to group 2 (n=34). One patient was excluded from the study. Full-layer biopsy specimen were taken from patients' nasal mucosa before the surgery. TGF-ß1, TGF-ß2, TGF-ß3, CTGF, FGF-2 concentrations were evaluated using ELISA and normalized by total protein concentration. RESULTS: Surgical failure was observed in 10 cases (22.72%). CTGF concentration was significantly correlated with negative outcome (p<0.05) and was elevated in most specimen obtained from group 1. No significant correlation was noted between the concentrations of other evaluated cytokines in nasal mucosa specimens and the surgical outcome. CONCLUSION: The study found a correlation between CTGF concentration in nasal mucosa and dacryocystorhinostomy outcome, which supports the hypothesis suggested by several authors linking dacryocystorhinostomy failure with chronic inflammation in nasal mucosa.


Assuntos
Dacriocistorinostomia , Citocinas , Fibrose , Humanos , Inflamação , Fator de Crescimento Transformador beta
14.
Medicine (Baltimore) ; 98(39): e17285, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31574846

RESUMO

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha), among cytokines that mediate the inflammatory process, plays an important role in diseases involving the loss of intestinal barrier integrity. Several molecules with anti-TNF-alpha activity have been studied aiming to develop new therapies. The purpose of this paper is to describe the systematic review protocol of experimental studies that determine mechanisms of action of molecules with anti-TNF-alpha activity on intestinal barrier inflammation. METHODS: This protocol is guided by the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes Protocols (PRISMA-P). The databases to be searched are PubMed, EMBASE, Scopus, ScienceDirect, and Web of Science. Experimental studies in rats or mice that assessed the activity of anti-TNF-alpha molecules in models of intestinal barrier inflammation will be included in the systematic review. Studies characteristics, experimental model, and main results will be described and the bias risk assessment will be performed. Two independent reviewers will perform study selection, data extraction, and methodological quality assessment. A narrative synthesis will be made for the included studies. Also, if sufficient data is available, a meta-analysis will be conducted. I statistics will be used to assess heterogeneity. RESULTS: The present protocol will assist in producing a systematic review that identifies the mechanisms underlying the reduction of TNF-alpha in intestinal barrier inflammation models. CONCLUSION: The systematic review may contribute to the theoretical basis of research on new molecules with anti-TNF-alpha potential and, consequently, in the development of new therapies employed in humans. PROSPERO REGISTRATION NUMBER: CRD42019131862.


Assuntos
Fármacos Gastrointestinais/farmacologia , Mucosa Intestinal/efeitos dos fármacos , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Animais , Humanos , Inflamação , Projetos de Pesquisa , Revisão Sistemática como Assunto , Fator de Necrose Tumoral alfa/antagonistas & inibidores
15.
Expert Opin Investig Drugs ; 28(10): 871-889, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31566013

RESUMO

Introduction: Functional dyspepsia (FD), defined as the presence of chronic functional symptoms originating from the gastroduodenal, is one of the most common functional gastrointestinal disorders. FD is subdivided into postprandial distress syndrome (PDS), with meal-related symptoms such as postprandial fullness and early satiation, and epigastric pain syndrome (EPS), with meal-unrelated symptoms such as epigastric pain or burning. Therapeutic options for FD are very limited, probably reflecting the complex pathophysiology which comprises disorders of gastric sensorimotor function as well as low-grade duodenal inflammation.Areas covered: This review summarizes recent and ongoing drug development for FD as identifiedExpert opinion: Proton pump inhibitors (PPIs) are the traditional first-line therapy while potassiumcompetitive acid blockers are being studied. Ongoing drug development focuses on gastric motility with prokinetics (dopamine-2 antagonists and 5-HT4 agonists) and fundus relaxant therapies (acotiamide, azapirones), and on sensitivity with peripherally (guanylate cyclase and cannabinoid agonists) and centrally acting neuromodulators. Drugs under development for gastroparesis may be efficacious in PDS. There are emerging data with pro-and antibiotics and with phytotherapeutic agents. Duodenal low-grade inflammation is a newly emerging target which may respond also to PPIs, histamine and leukotriene receptor blockers.


Assuntos
Dispepsia/tratamento farmacológico , Fármacos Gastrointestinais/farmacologia , Gastroenteropatias/tratamento farmacológico , Dor Abdominal/etiologia , Desenvolvimento de Medicamentos/métodos , Dispepsia/fisiopatologia , Fármacos Gastrointestinais/administração & dosagem , Gastroenteropatias/fisiopatologia , Gastroparesia/tratamento farmacológico , Gastroparesia/fisiopatologia , Humanos , Inflamação/tratamento farmacológico , Inflamação/fisiopatologia , Inibidores da Bomba de Prótons/administração & dosagem , Inibidores da Bomba de Prótons/farmacologia
16.
Isr Med Assoc J ; 21(10): 658-661, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31599506

RESUMO

BACKGROUND: The incidence of Clostridium difficile-associated diarrhea (CDAD) is increasing and is associated with significant morbidity and mortality. Therefore, there is a need to find new tools to determine the severity of the disease. OBJECTIVES: To investigate the prognostic values of inflammatory markers such as mean platelet volume (MPV), neutrophil-lymphocyte ratio (NLR), and C-reactive protein (CRP) in patients with CDAD. METHODS: The study comprised of 100 patients diagnosed with CDAD. The study included an additional control group of 69 patients with diarrhea who were negative for C. difficile toxin. The control group was age- and sex-matched and hospitalized at the same time period. NLR and MPV were obtained from complete blood count results. Serum CRP levels were measured by the latex particle enhanced immunoturbidimetric assay. Blood samples for all inflammatory markers were collected at time of diagnosis and prior to initiating the antibiotic therapy. Demographic, clinical, laboratory, and prognostic data were collected from medical records for a period of 90 days from the initial diagnosis of CDAD. RESULTS: The mean age of the CDAD group was 68.6 ± 21.5 years compared to 65.6 ± 24.5 in the control group (P = 0.29). Our findings show that patients with CDAD had significantly higher NLR, MPV and serum CRP levels compared to the control group (P < 0.001)). Moreover, significantly higher levels were observed when CDAD was fatal (P < 0.001). CONCLUSIONS: Elevated NLR, MPV, and serum CRP levels may serve as biomarkers for prediction of recurrence and mortality in patients with CDAD.


Assuntos
Infecções por Clostridium/sangue , Infecções por Clostridium/complicações , Clostridium difficile/patogenicidade , Diarreia/microbiologia , Inflamação/sangue , Inflamação/microbiologia , Idoso , Biomarcadores/sangue , Proteína C-Reativa/metabolismo , Infecções por Clostridium/diagnóstico , Diarreia/sangue , Feminino , Humanos , Linfócitos/metabolismo , Masculino , Volume Plaquetário Médio/estatística & dados numéricos , Neutrófilos/metabolismo , Prognóstico , Fatores de Risco , Índice de Gravidade de Doença
17.
Zhongguo Zhong Yao Za Zhi ; 44(16): 3460-3467, 2019 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-31602910

RESUMO

To investigate the pharmacodynamic effect and virulent effect of the main components of the toxic Chinese medicine Tripterygium wilfordii,such as triptolide,tripchlorolide,tripterine,demethylzeylasteral,wilfotrine and euonine,the admet SAR online assessment system was used to calculate the properties of the main components of T. wilfordii. The potential targets of the components were mined and collected through multiple databases,and the potential targets were enriched by the bioinformatics database DAVID.Cytoscape software was used to establish a " target-pathway" network and perform topology analysis on the network. The main chemical components of T. wilfordii were able to penetrate the blood-brain barrier and had intestinal permeability. A total of 65 targets were predicted,including pathways in cancer,hepatitis B,rheumatoid arthritis,and chagas disease( American trypanosomiasis),Toll-like receptor signaling pathway,apoptosis,colorectal cancer,NF-kappa B signaling pathway,etc. T. wilfordii mainly plays a role in the treatment of immune diseases and cancer by regulating inflammatory signaling pathways and cancer signaling pathways. Its action on apoptosis pathway and drug metabolism enzymes may be the mechanism of its toxicity.


Assuntos
Medicamentos de Ervas Chinesas/farmacologia , Transdução de Sinais , Tripterygium/química , Biologia Computacional , Humanos , Inflamação
18.
J Comput Assist Tomogr ; 43(5): 755-761, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31609294

RESUMO

OBJECTIVES: This study aimed to evaluate the feasibility of intravoxel incoherent motion diffusion-weighted magnetic resonance imaging (DW-MRI) in detecting bowel inflammation in patients with Crohn disease (CD). METHODS: Sixteen patients who underwent intravoxel incoherent motion DW-MRI for CD and colonoscopy were recruited. Seventy-nine bowel segments were selected, and their mean D, D*, f, and apparent diffusion coefficient (ADC) values were measured. The receiver operating characteristic curve was performed to distinguish inflamed from normal bowel. RESULTS: The mean D, D*, f, and ADC values of inflamed bowel were significantly lower than those of normal bowel (P < 0.05). The area under the receiver operating characteristic curve for f (0.906) and ADC values (0.924) was greater than that for D (0.709) or D* values (0.686) for differentiating inflamed bowel from normal bowel (P < 0.05). CONCLUSIONS: Intravoxel incoherent motion DW-MRI is a feasible technique for detecting inflammation in CD patients. The ADC and f values have more potential than the D and D* values.


Assuntos
Doença de Crohn/diagnóstico por imagem , Imagem de Difusão por Ressonância Magnética/métodos , Adulto , Colonoscopia , Feminino , Humanos , Interpretação de Imagem Assistida por Computador , Inflamação/diagnóstico por imagem , Masculino , Estudos Prospectivos
19.
J Assoc Physicians India ; 67(10): 54-56, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31571453

RESUMO

Background: Attention has increasingly turned towards the role of factors, such as inflammation in the development of atherosclerosis and CHD. C-reactive protein (CRP) has emerged as one of the most important novel inflammatory marker. Subsequent risk modification and treatment strategies of CHD keeping on pointer towards inflammation may be the appropriate approach. Aim: The aim of this study was to determine the association of CHD with CRP, a sensitive marker of inflammation. Material and Methods: This is a case control study amongst 300 subjects (150 cases and 150 controls), conducted in the Department of Cardiology at Sri Aurobindo Medical College and P.G Institute, Indore, M.P. Subjects with definite diagnosis of CHD established by coronary angiography (CAG) was taken as cases, subjects matched with age, gender with no conventional risk factor and past history of CHD from the relatives and accompanying persons were enlisted as controls. Results: Estimation of CRP reveals ≥0.6 mg/dl in 88(58.7%) subjects out of 150, compared to 26 (17.3%) control subjects out of 150 which is statistically significant (p value<0.0001) (OR=6.7). Conclusion: CRP as a noble marker of inflammation was significantly higher in subjects of CHD and thus supported adequately the hypothesis of an activation of inflammatory cascade for coronary atheromatous plaque formation and causation of CHD.


Assuntos
Proteína C-Reativa/metabolismo , Doença das Coronárias/metabolismo , Biomarcadores/metabolismo , Estudos de Casos e Controles , Humanos , Inflamação/metabolismo , Fatores de Risco
20.
Adv Exp Med Biol ; 1175: 335-353, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31583594

RESUMO

Microglia are the most abundant immune cells in the central nervous system (CNS), where they interact with neurons and exhibit a wide array of functions in physiological and pathological conditions. Physiologically, microglia mediate synaptic pruning and remodeling crucial for neural circuits and brain connectivity. In pathological conditions such as neurodegeneration in the Parkinson's disease (PD), microglia are activated, migrated to the injury site, and prone to engulf debris, sense pathology, and secrete possible pro- and anti-inflammatory factors. Microglia mediate responses such as inflammation and phagocytosis associated with neurodegeneration and are pivotal players in exacerbating or relieving disease progression. This chapter provides an overview on microglial function in the neurodegenerative disease-Parkinson's disease (PD). An overview on the pathology of PD will first be given, followed by discussion on receptors and signaling pathways involved in microglia-mediated inflammation and phagocytosis. Mechanism of how microglia contribute to PD by inflammation, phagocytosis of α-Synuclein (α-Syn), and interaction with PD genes will also be discussed.


Assuntos
Microglia/citologia , Doença de Parkinson/fisiopatologia , Humanos , Inflamação/fisiopatologia , Fagocitose , Transdução de Sinais , alfa-Sinucleína
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