RESUMEN
BACKGROUND: Both enzymatic cross-linking and hydrolysis are used to treat food proteins for functionality modification. The present study aimed to reveal the impact of limited tryptic digestion on some functional properties of a cross-linked composite generated from soy protein isolate and gelatin by transglutaminase. RESULTS: The composite was digested by trypsin for 1.5 and 4 h to produce two hydrolyzed composites with degrees of hydrolysis of 1% and 2%, respectively. Electrophoretic and chemical analysis showed that only part of the composite was degraded, and the gelatin fraction in the composite was more sensitive to tryptic digestion than the soy protein fraction. The hydrolyzed composites exhibited higher protein dispersion index at pH 4.5 or 7.0 and surface hydrophobicity, better digestibility in vitro, emulsifying property and oil absorption capacity, but lower water holding capacity and rheological properties (apparent viscosity, storage and loss modulus) than the composite. Compared to soy protein isolate, the hydrolyzed composites had better rheological properties, and higher water-holding capacity and emulsion stability index. CONCLUSION: The applied tryptic digestion conferred some improved properties on the hydrolyzed composites compared with the composite or soy protein isolate, and has potential for obtaining a new functional ingredient for processed foods.
Asunto(s)
Gelatina/metabolismo , Proteínas de Vegetales Comestibles/metabolismo , Proteínas de Soja/metabolismo , Tripsina/metabolismo , Emulsiones , Humanos , Hidrólisis , Interacciones Hidrofóbicas e Hidrofílicas , Reología , Solubilidad , Viscosidad , AguaRESUMEN
We have reported the neuroprotective effect of cysteinyl leukotriene receptor 1 (CysLT1) antagonists on cerebral ischemia. Here, we further determined the protective effect of pranlukast, a CysLT1 receptor antagonist, on brain cold injury in mice. Brains were injured by placing a cooled metal probe on the skull surface for 30 s. We found that pranlukast significantly reduced cold-induced lesion volume (0.3 mg/kg) and the percentage increase in lesioned hemisphere volume (0.03-0.3 mg/kg) 24 h after injury, but did not show any effect 72 h after injury. Pranlukast also significantly inhibited neuron loss 24 h (0.1 mg/kg) and 72 h (0.1-0.3 mg/kg) after injury, and decreased the density of degenerated neurons 24 h (0.01-0.3 mg/kg) and 72 h (0.03-0.3 mg/kg) after injury. In addition, pranlukast (0.1-0.3 mg/kg) significantly reduced endogenous IgG exudation both 24 h and 72 h after injury. Thus, this study indicates the protective effect of pranlukast on brain cold injury.
Asunto(s)
Lesiones Encefálicas/prevención & control , Cromonas/farmacología , Frío/efectos adversos , Antagonistas de Leucotrieno/farmacología , Animales , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Encéfalo/patología , Edema Encefálico/etiología , Edema Encefálico/prevención & control , Lesiones Encefálicas/etiología , Lesiones Encefálicas/metabolismo , Recuento de Células , Relación Dosis-Respuesta a Droga , Exudados y Transudados/efectos de los fármacos , Exudados y Transudados/metabolismo , Inmunoglobulina G/metabolismo , Masculino , Proteínas de la Membrana/antagonistas & inhibidores , Ratones , Ratones Endogámicos ICR , Neuronas/efectos de los fármacos , Neuronas/patología , Receptores de LeucotrienosRESUMEN
OBJECTIVE: To evaluate protective effect of minocycline,a semisynthetic tetracycline derivative on different traumatic brain injuries in rats and mice. METHODS: The opened brain trauma was induced in rats and the closed head injury and cold brain injury were induced in mice. In 3 brain trauma models, minocycline (45 mg/kg, ip) was administered twice daily for 2 d before the operation, at 30 min before and 1 h after the operation, and once daily for 2 d following the operation (totally 8 doses in 5 d). After the operation, the behavioral alteration was observed daily, lesion area and survival neuron density were measured at the end of the experiments (14 d after the injuries). RESULT: For rat opened traumatic injury, minocycline promoted the recovery of hindlimb motor activity (inclined board angle), but did not alter other indexes. For mouse closed head traumatic injury, minocycline reduced the neuron loss, but did not improve behavioral dysfunction. For mouse cold injury-induced trauma, minocycline reduced death rate and lesion area, but did not remarkably improve behavior and neuron loss. CONCLUSION: Minocycline only has an incomplete neuroprotective effect on different brain traumatic injuries in rats and mice.
Asunto(s)
Lesiones Encefálicas/tratamiento farmacológico , Minociclina/uso terapéutico , Fármacos Neuroprotectores/uso terapéutico , Animales , Masculino , Ratones , Ratones Endogámicos ICR , Ratas , Ratas Sprague-DawleyRESUMEN
Cysteinyl leukotrienes are involved in ischemic brain injury, and their receptors (CysLT(1) and CysLT(2)) have been cloned. To clarify which subtype mediates the ischemic neuronal injury, we performed permanent transfection to increase CysLT(1) and CysLT(2) receptor expressions in PC12 cells. Oxygen glucose deprivation (OGD)-induced cell death was detected by Hoechst 33258 and propidium iodide fluorescent staining as well as by flow cytometry. OGD induced late phase apoptosis mainly and necrosis minimally. Over-expression of CysLT(1) receptor decreased and over-expression of CysLT(2) receptor increased OGD-induced cell death. An agonist LTD(4) (10(-7)M) also induced apoptosis, especially in CysLT(2) receptor over-expressing cells. A selective CysLT(1) receptor antagonist montelukast did not affect OGD-induced apoptosis; while non-selective CysLT receptor antagonist Bay u9773 inhibited OGD-induced apoptosis, especially in CysLT(2) receptor over-expressing cells. Thus, CysLT(1) and CysLT(2) receptors play distinct roles in OGD-induced PC12 cell death; CysLT(1) attenuates while CysLT(2) facilitates the cell death.
Asunto(s)
Muerte Celular/fisiología , Hipoxia-Isquemia Encefálica/fisiopatología , Proteínas de la Membrana/fisiología , Receptores de Leucotrienos/fisiología , Acetatos/farmacología , Animales , Bisbenzimidazol , Muerte Celular/efectos de los fármacos , Ciclopropanos , Citometría de Flujo , Glucosa/deficiencia , Ratones , Células PC12 , Quinolinas/farmacología , Ratas , SRS-A/análogos & derivados , SRS-A/farmacología , SulfurosRESUMEN
5-Lipoxygenase (5-LOX) is a key enzyme in the metabolism of arachidonic acid to leukotrienes. The levels of leukotrienes increase after brain injury and when tumors are present. It has been reported that 5-LOX is widely expressed in the brain and that 5-LOX inhibition provides neuroprotection. However, there is still no information available for the expression patterns of 5-LOX in human brain following trauma or with astrocytomas. We investigated its expression patterns by immunohistochemistry. We found that 5-LOX is normally expressed in neurons and glial cells. In neurons, it was expressed in two patterns: in the cytosol and nucleus or only in the cytosol. In traumatic brain injury, 5-LOX expression increased in glial cells and neutrophils. Double-labeling immunohistochemistry showed that part of the 5-LOX-positive glial cells were GFAP positive. No 5-LOX expression was found in brain microvessel endothelia, except in the regenerated endothelia of a patient 8 days following brain trauma. Furthermore, 5-LOX expression increased and showed a granular pattern in high-grade (grade III/IV) astrocytoma. These results indicate that 5-LOX has multiple expression patterns, and can be induced by brain injury, which implies that 5-LOX might have pathophysiological roles in the human brain.
Asunto(s)
Araquidonato 5-Lipooxigenasa/biosíntesis , Astrocitoma/metabolismo , Lesiones Encefálicas/metabolismo , Neoplasias Encefálicas/metabolismo , Encéfalo/metabolismo , Adulto , Anciano , Anciano de 80 o más Años , Femenino , Proteína Ácida Fibrilar de la Glía/metabolismo , Humanos , Inmunohistoquímica , Masculino , Persona de Mediana Edad , Neuroglía/metabolismo , Neuronas/metabolismoRESUMEN
Cysteinyl leukotrienes (CysLTs) are potent proinflammatory mediators. CysLT receptor 1 (CysLT(1)) is one of the two CysLT receptors that has been cloned. Although the expression of CysLT(1) in the brain has been demonstrated by Northern blot and RT-PCR analyses, the location of CysLT(1) in the brain remains unknown. The objective of this study was to examine the distribution of CysLT(1) by immunohistochemical analysis in human brains with traumatic injury or tumors. CysLT(1) was expressed intensely in the microvascular endothelial cells in both normal and abnormal conditions. At 8 days after traumatic injury, microvascular regeneration was found and all of the endothelial cells highly expressed CysLT(1). In gray and white matters of the normal regions of the brain, CysLT(1) was expressed weekly or not at all. However, the CysLT(1) expression increased in the neuron- and glial-appearing cells in gray and white matters after traumatic brain injury. CysLT(1) was also detected in astrocytoma, ganglioglioma and metastatic adenocarcinoma, and the expression in the neuron- and glial-appearing cells around brain tumors increased robustly.