Synapto-protective effect of low-level light emitting diode (LED) therapy in an in vitro model of status epilepticus (Conference Presentation)

2018 ◽  
Author(s):  
Namgue Hong ◽  
Hee Jung Kim ◽  
Jin-Chul Ahn
Keyword(s):  
Status Epilepticus ◽  
Protective Effect ◽  
In Vitro Model ◽  
Light Emitting Diode ◽  
Light Emitting ◽  
Low Level ◽  
Led Therapy ◽  
Vitro Model

scholarly journals Blue Light Induces Down-Regulation of Aquaporin 1, 3, and 9 in Human Keratinocytes

Cells ◽  
2018 ◽  
Vol 7 (11) ◽  
pp. 197 ◽  
Author(s):  
Rosanna Avola ◽  
Adriana Graziano ◽  
Giovanna Pannuzzo ◽  
Venera Cardile
Keyword(s):  
Blue Light ◽  
Light Emitting Diode ◽  
Human Keratinocytes ◽  
Skin Aging ◽  
Nuclear Antigen ◽  
Down Regulation ◽  
Light Emitting ◽  
Proliferation And Differentiation ◽  
Vitro Model

The development in digital screen technology has exponentially increased in the last decades, and many of today’s electronic devices use light-emitting diode (LED) technology producing very strong blue light (BL) waves. Long-term exposure at LED-BL seems to have an implication in the dehydration of the epidermis, in the alterations of shape and number of the keratinocytes, and in the aging of the skin. Aquaporins (AQPs) are water membrane channels that permeate both water and glycerol and play an important role in the hydration of epidermis, as well as in proliferation and differentiation of keratinocytes. Thus, we have hypothesized that AQPs could be involved in the aging of the skin exposed to LED-BL. Therefore, we have examined the expression of AQPs in human keratinocytes exposed to LED-BL at dose of 45 J/cm2, used as an in vitro model to produce the general features of photo aging of the skin. The aim was to verify if LED-BL induces changes of the basal levels of AQPs. The keratinocytes exposure to LED-BL produced an increase of reactive oxygen species (ROS), an activation of 8-hydroxy-2’-deoxyguanosine (8-OHdG), an alteration of proliferating cell nuclear antigen (PCNA), and a down-regulation of AQP1, 3 and 9. These findings are preliminary evidences that may be used as starting points for further investigations about the mechanistic involvement of AQP1, 3, and 9 in LED-BL-induced skin aging.

Protective effect of kava constituents in an in vitro model of oral mucositis

2020 ◽  
Vol 146 (7) ◽  
pp. 1801-1811
Author(s):  
Callisthenis Yiannis ◽  
Kevin Huang ◽  
An Nhien Tran ◽  
Cathy Zeng ◽  
Emily Dao ◽  
...  
Keyword(s):  
Protective Effect ◽  
Oral Mucositis ◽  
In Vitro Model ◽  
Vitro Model

Development of an in vitro model for study of the efficacy of ischemic preconditioning in human skeletal muscle against ischemia-reperfusion injury

2006 ◽  
Vol 101 (5) ◽  
pp. 1335-1342 ◽  
Author(s):  
Glyka Martou ◽  
Catherine A. O’Blenes ◽  
Ning Huang ◽  
Sandra E. McAllister ◽  
Peter C. Neligan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Human Skeletal Muscle ◽  
In Vitro Model ◽  
Ischemia Reperfusion ◽  
Mtt Reduction ◽  
Vitro Model ◽  
Hypoxia Reoxygenation

Ischemia-reperfusion (I/R) injury causes skeletal muscle infarction and ischemic preconditioning (IPC) augments ischemic tolerance in animal models. To date, this has not been demonstrated in human skeletal muscle. This study aimed to develop an in vitro model to investigate the efficacy of simulated IPC in human skeletal muscle. Human skeletal muscle strips were equilibrated in oxygenated Krebs-Henseleit-HEPES buffer (37°C). Aerobic and reperfusion phases were simulated by normoxic incubation and reoxygenation, respectively. Ischemia was simulated by hypoxic incubation. Energy store, cell viability, and cellular injury were assessed using ATP, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2 H-tetrazolium bromide (MTT), and lactate dehydrogenase (LDH) assays, respectively. Morphological integrity was assessed using electron microscopy. Studies were designed to test stability of the preparation ( n = 5–11) under normoxic incubation over 24 h; the effect of 1, 2, 3, 4, or 6 h hypoxia followed by 2 h of reoxygenation; and the protective effect of hypoxic preconditioning (HPC; 5 min of hypoxia/5 min of reoxygenation) before 3 h of hypoxia/2 h of reoxygenation. Over 24 h of normoxic incubation, muscle strips remained physiologically intact as assessed by MTT, ATP, and LDH assays. After 3 h of hypoxia/2 h of reoxygenation, MTT reduction levels declined to 50.1 ± 5.5% ( P < 0.05). MTT reduction levels in HPC (82.3 ± 10.8%) and normoxic control (81.3 ± 10.2%) groups were similar and higher ( P < 0.05) than the 3 h of hypoxia/2 h of reoxygenation group (45.2 ± 5.8%). Ultrastructural morphology was preserved in normoxic and HPC groups but not in the hypoxia/reoxygenation group. This is the first study to characterize a stable in vitro model of human skeletal muscle and to demonstrate a protective effect of HPC in human skeletal muscle against hypoxia/reoxygenation-induced injury.

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