Prevention of Oxidative Stress-induced Metabolic Aberrations in the Neural Retina by Caffeine
Kavita Rajeev Hegde,
Kristen Deacon
Issue:
Volume 4, Issue 4, July 2019
Pages:
53-58
Received:
5 September 2019
Accepted:
23 September 2019
Published:
12 October 2019
Abstract: Oxyradical-induced damage to the retina has been implicated as one of the contributing factors in the pathogenesis of vision-impairing diseases such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). It is hypothesized that caffeine, a nutraceutical antioxidant, will be effective in preventing metabolic aberrations in the neural retina exposed to oxygen radicals. This hypothesis is based on our previous studies demonstrating its effectiveness in preventing oxidative damage to the lens, and in protecting the neural retina against UV-A- and peroxide-induced biochemical damage. Bovine neural retinas were incubated in medium 199 at 37°C for 6 hours. Xanthine (XA)-xanthine oxidase (XO) were used to generate reactive oxygen species (ROS). Incubations were conducted in 3 groups- control, experimental (with XA+XO), and caffeine group (XA + XO+ 5mM caffeine). Retinas were then processed for determining protein, lactate and pyruvate concentrations. Lactate concentration in the controls was 2.62±0.43mM/mg protein, decreasing to 1.04±0.3 mM/mg protein in the presence of XA+XO. Its level in the caffeine group was significantly higher, 2.44±0.65 mM/mg protein, close to the controls. Pyruvate concentration in the controls was 0.16±0.05mM/mg protein, which declined significantly with XA+XO to 0.066±0.02 mM/mg protein. Such decrease was substantially prevented in the caffeine group, wherein its concentration was 0.156±0.03mM/mg protein. Caffeine was thus found to be highly effective in preventing metabolic aberrations, due to its ability to scavenge oxyradicals and thereby possibly prevent inactivation of key enzymes. Such effect of caffeine in maintaining metabolism of the neural retina exposed to ROS has been shown for the first time.
Abstract: Oxyradical-induced damage to the retina has been implicated as one of the contributing factors in the pathogenesis of vision-impairing diseases such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). It is hypothesized that caffeine, a nutraceutical antioxidant, will be effective in preventing metabolic aberrations in the neur...
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Expression of Interleukins (ILs) mRNA in Otitis Media
Sung Ho Kang,
Dae Joon Lim,
Bo Hyung Kim,
Myung Sang Yu,
Shinseok Kang
Issue:
Volume 4, Issue 4, July 2019
Pages:
59-66
Received:
3 October 2019
Accepted:
21 October 2019
Published:
25 October 2019
Abstract: The purpose of this study was to investigate the expression of interleukins (ILs) cytokine in postauricular skin, mastoid mucosa, inflamed mastoid mucosa and middle ear mucosa from Otitis patients. Specimens were obtained from patients with otitis media who visited the Department of Otorhinolaryngology, Chungju Hospital, Kunkuk University School of Medicine, Chungju, Republic of Korea between August 2015 and July 2017. We examined human 38 kinds of human interleukins in this experiment. The total RNA was extracted from specimens using RNAiso Plus (Takara, Japan) according to the manufacturer's instructions. 38 ILs primers were used. IL-4, IL-8, IL-9, IL-21, IL-24 were not expressed at postauricular skin, mastoid mucosa, inflamed mastoid mucosa, and middle ear mucosa. IL-1a, IL-17, IL-17d, IL-17e and IL-17f were strongly expressed in mastoid mucosa and middle ear mucosa. The degree of IL-7 gene expression may be an indicator gene in otitis media. IL-1a, IL-17, IL-17d, IL-17e and IL-17f were involved in the inflammatory and immune processes of otitis media.
Abstract: The purpose of this study was to investigate the expression of interleukins (ILs) cytokine in postauricular skin, mastoid mucosa, inflamed mastoid mucosa and middle ear mucosa from Otitis patients. Specimens were obtained from patients with otitis media who visited the Department of Otorhinolaryngology, Chungju Hospital, Kunkuk University School of...
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