Stem cells isolated from human TM and expanded in vitro exhibit the ability to home to the TM and differentiate into TM cells in vivo. Such cells present a potential for development of a novel cell-based therapy for glaucoma.
Oleanolic acid (OA) is a triterpenoid known for its anti-inflammatory and anti-cancer properties; however, the anti-inflammatory effects of OA on lipopolysaccharide (LPS)-mediated pro-inflammatory responses have not been studied. Here, we first investigated the possible anti-inflammatory effects of OA against pro-inflammatory responses in human umbilical vein endothelial cells (HUVECs) induced by LPS and the associated signaling pathways. We found that OA inhibited LPS-induced barrier disruption, expression of cell adhesion molecules (CAMs), and adhesion/transendothelial migration of monocytes to HUVECs. OA also suppressed acetic acid-induced hyperpermeability and carboxymethylcellulose-induced leukocyte migration in vivo. Further studies revealed that OA suppressed the production of tumor necrosis factor-α and activation of nuclear factor-κB by LPS. Collectively, these results suggest that OA has anti-inflammatory effects by inhibiting hyperpermeability, the expression of CAMs, and the adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapeutic agent for vascular inflammatory diseases.
The effects of nitric oxide (NO) on ethylene synthesis and softening of ripening-initiated banana slice were investigated. Fruit firmness, color, and contents of starch and acid-soluble pectin (ASP) were measured. In addition, ethylene production, 1-aminocyclopropane-1-carboxylic acid (ACC) content, expression and activities of ACC synthase (ACS) and ACC oxidase (ACO), and activities of cell-wall-modifying enzymes, polygalacturonase (PG), pectin methylesterase (PME), and endo-beta-1,4-glucanase, were analyzed. Application of NO reduced ethylene production, inhibited degreening of the peel and delayed softening of the pulp. The decrease of ethylene production was associated with the reduction in the activity of ACO and the expression of the MA-ACO1 gene. Moreover, the NO-treated fruit showed a lower expression of the MA-ACS1 gene but higher ACS activity and ACC content. In addition, NO treatment decreased the activities of PG, PME, and endo-beta-1,4-glucanase and maintained higher contents of ASP and starch, which may account for the delay of softening. We proposed that the inhibition of ACO activity and transcription of gene MA-ACO1 by NO resulted in decreased ethylene synthesis and the delay of ripening of banana slice.
It is thought that the neuronal cell loss caused by oxidative stress is the primary mechanism underlying the pathogenesis of several neurodegenerative disorders. Glutamate is an endogenous neurotransmitter, but at high concentrations it can act as a neurotoxicant by increasing the intracellular levels of reactive oxygen species (ROS). Therefore, the development of factors that can attenuate glutamate-induced oxidative stress in neuronal cells is a good strategy by which new drugs could be discovered that may treat or prevent neurodegenerative diseases. Here, the neuroprotective effects of kaempferol (KF) isolated from the stems of butterbur (Petasites japonicus) were examined in glutamate-treated hippocampal neuronal cells (HT22). The administration of KF (25 μM) resulted in a significant increase in cell viability (105.18 ± 7.48%) compared with the control (100.00 ± 3.05%), while glutamate (5 mM) reduced cell viability by 39.94 ± 1.61%. The glutamate-induced calcium (Ca(2+)) influx (1.93 ± 0.08-fold) was significantly reduced by 0.89 ± 0.02-fold following the administration of 25 μM KF. Additionally, when HT22 cells were stressed with excessive glutamate, there was a 3.70 ± 0.01-fold increase in intracellular ROS generation, even though this was effectively attenuated by KF (25 μM, 0.72 ± 0.01-fold). The protective effects of KF in HT22 cells were later confirmed using a lactate dehydrogenase (LDH) assay and a FITC-annexin V/propidium iodide double staining procedure. These findings also revealed that the neuroprotective effects of KF are a result of the regulation of the expression levels of proteins, such as Bcl-2, Bid, apoptosis-inducing factor (AIF), and mitogen-activated protein kinase (MAPK). This is the first report to investigate the neuroprotective influence of KF in glutamate-treated HT22 cells. These data demonstrate that KF may be a useful candidate for pharmacological therapies that can prevent and treat neurodegenerative diseases such as Alzheimer's disease (AD).
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