“…40 Several studies have shown that proinflammatory cytokines can induce NOS synthesis and, consequently, NO production in high amounts. [41][42][43][44][45][46] In turn, NO has been shown to stimulate the production and activity of various MMPs in cultured rat mesangial cells 47 and both human and rabbit chondrocytes. 40,44 Paradoxically, other studies have indicated that NO can suppress cytokine-induced MMP proteolytic activity in bovine articular cartilage 48 as well as inhibit IL-1β-induced MMP-9 mRNA and TIMP-1 levels in rat mesangial cells.…”
Section: Mmp Activity Requires Tight Regional Regulation In Physiological Pregnancymentioning
The objective of this article is to review the role of matrix metalloproteinases (MMPs) in fetomaternal/neonatal complications of preterm birth. The function of MMPs as proteolytic enzymes involved in tissue remodeling/destruction is reviewed in preterm labor, preeclampsia, premature rupture of membranes, intrauterine growth restriction, chronic lung disease, necrotizing enterocolitis, intraventricular hemorrhage, cystic periventricular leukomalacia, and retinopathy of prematurity. Cytokines, steroid hormones, and reactive oxygen species all regulate MMP labor and expression/activity. In labor, activation follows an inflammatory response, which results in fetal membrane rupture and cervical dilation/ripening, particularly when premature. Expression/activation is elevated during parturition, particularly when premature. While fetal membrane rupture is preceded by increases in tissue-specific MMPs, neonatal complications also ensue from an imbalance between MMPs and their tissue inhibitors. These e fects implicate environmental triggers and a genetic predisposition. MMPs are involved in the perinatal complications of prematurity and are potential targets for therapeutic intervention. Functional MMP genetic polymorphisms may assist in identifying patients at risk of complications.
“…40 Several studies have shown that proinflammatory cytokines can induce NOS synthesis and, consequently, NO production in high amounts. [41][42][43][44][45][46] In turn, NO has been shown to stimulate the production and activity of various MMPs in cultured rat mesangial cells 47 and both human and rabbit chondrocytes. 40,44 Paradoxically, other studies have indicated that NO can suppress cytokine-induced MMP proteolytic activity in bovine articular cartilage 48 as well as inhibit IL-1β-induced MMP-9 mRNA and TIMP-1 levels in rat mesangial cells.…”
Section: Mmp Activity Requires Tight Regional Regulation In Physiological Pregnancymentioning
The objective of this article is to review the role of matrix metalloproteinases (MMPs) in fetomaternal/neonatal complications of preterm birth. The function of MMPs as proteolytic enzymes involved in tissue remodeling/destruction is reviewed in preterm labor, preeclampsia, premature rupture of membranes, intrauterine growth restriction, chronic lung disease, necrotizing enterocolitis, intraventricular hemorrhage, cystic periventricular leukomalacia, and retinopathy of prematurity. Cytokines, steroid hormones, and reactive oxygen species all regulate MMP labor and expression/activity. In labor, activation follows an inflammatory response, which results in fetal membrane rupture and cervical dilation/ripening, particularly when premature. Expression/activation is elevated during parturition, particularly when premature. While fetal membrane rupture is preceded by increases in tissue-specific MMPs, neonatal complications also ensue from an imbalance between MMPs and their tissue inhibitors. These e fects implicate environmental triggers and a genetic predisposition. MMPs are involved in the perinatal complications of prematurity and are potential targets for therapeutic intervention. Functional MMP genetic polymorphisms may assist in identifying patients at risk of complications.
“…Inhibition of NO synthesis prevents excessive inflammation in macrophages. Presence of NO is commonly used as a marker of cellular inflammation (Lyons et al., 1992). In the present study, we established an inflammation model by stimulating macrophages with 2 µg·ml −1 LPS, and investigated the NO synthesis‐inhibiting abilities of different concentrations of vegetable soybean leaf extracts prepared with different solvents.…”
To investigate ways to extract greater dietary value from the leaves of the vegetable soybean (Glycine max (L.) Merr.) cultivar ‘Kaohsiung No. 9’. Our results indicate that phenolic content and flavonoid content are highest in extracts prepared with 70% methanol and 70% ethanol. The 70% ethanol extracts also had the highest quercetin (135 ± 1.62 µg/g) and kaempferol (450 ± 1.35 µg/g) contents. These results show that flavonoids are a dominant class of compounds in these vegetable soybean leaf extracts and serve as their main source of antioxidants. At an extract concentration of 5 mg/ml, the 70% methanol extracts achieved good antioxidant effects, with a DPPH radical scavenging rate of 80%, and a reducing power of 88%. In assays of anti‐inflammatory capacity using lipopolysaccharide‐stimulated RAW 264.7 macrophages. The 70% methanol extracts displayed the most significant inhibition of nitric oxide (NO) synthesis, achieving up to 86% inhibition. As a similar trend was observed in expression levels of inducible nitric oxide synthase (iNOS), we deduced that vegetable soybean leaves may regulate NO synthesis through inhibiting iNOS. We also observed a significant decrease in cyclooxygenase (COX)‐2 gene expression. Analysis of proinflammatory cytokine synthesis revealed that the 70% methanol and 70% ethanol extracts significantly reduced TNF‐α, IL‐6, and IL‐1β synthesis, and increased the intracellular reduced glutathione/oxidized glutathione (GSH/GSSG) ratio from 8 to 12.8. These results indicate that vegetable soybean leaves possess antioxidant activities and exert inhibitory effects on inflammatory mediators, suggesting their potential for use as dietary supplements.
“…Following the discovery that NO functions physiologically as a signaling molecule, researchers set out to define and clone enzymes responsible for NO production. NO is formed in cells from the enzymatic conversion of arginine to citrulline by three nitric oxide synthases (eNOS, iNOS, and nNOS;Bredt et al, 1991;Lamas et al, 1992;Lowenstein et al, 1992;Lyons et al, 1992;Sessa et al, 1992). iNOS (or NOS-II) is inducible and plays important roles in immune defense and mediation of inflammation (reviewed in Förstermann & Sessa, 2012).…”
Nitric oxide (NO) is an important signaling molecule with many functions in the nervous system. Derived from the enzymatic conversion of arginine by several nitric oxide synthases (NOS), NO plays significant roles in neuronal developmental events such as the establishment of dendritic branching or arbors. A brief summary of the discovery, molecular biology, and chemistry of NO, and a description of important NO-mediated signal transduction pathways with emphasis on the role for NO in the development of dendritic branching during neurodevelopment are presented. Important sex differences in neuronal nitric oxide synthase expression during neuronal development are considered. Finally, a survey of endogenous and exogenous substances that disrupt dendritic patterning is presented with particular emphasis on how these molecules may drive NO-mediated sex differences in dendritic branching.
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