The Protective Effect of Thiamine Pryophosphate Against Sugar-Induced Retinal Neovascularisation in Rats

2018 ◽  
Vol 88 (3-4) ◽  
pp. 137-143 ◽  
Author(s):  
Emine Cinici ◽  
Renad Mammadov ◽  
Huseyin Findik ◽  
Bahadir Suleyman ◽  
Nihal Cetin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Interleukin 1 ◽  
Fasting Blood Glucose ◽  
Thiamine Pyrophosphate ◽  
Control Group ◽  
Interleukin 1 Beta ◽  
Total Glutathione ◽  
Sugar Water ◽  
Retinal Neovascularisation ◽  
Retinal Tissue

Abstract. The aim of this study was to investigate the effect of thiamine pyrophosphate (TPP), administered via sugar water, on retinal neovascularisation in rats. Animals were assigned to three groups, namely the TPP sugar-water group (TPSWG, n = 12), the control group (CG, n = 12) and the healthy group (HG, n = 12). The TPSWG was injected intraperitoneally with TPP once a day for 6 months. CG and HG rats were given distilled water in the same way. TPSWG and CG rats were left free to access an additional 0.292 mmol /ml of sugar water for 6 months. The fasting blood glucose (FBG) levels of the animals were measured monthly. After 6 months, biochemical, gene expression and histopathologic analyses were carried out in the retinal tissues removed from the animals after they were killed. The measured FBG levels were 6.96 ± 0.09 mmol/ml (p < 0.0001 vs. HG), 6.95 ± 0.06 mmol/ml (p < 0.0001 vs. HG) and 3.94 ± 0.10 mmol/ml in the CG, TPSWG and HG groups, respectively. The malondialdehyde (MDA) levels were found to be 2.82 ± 0.23 (p < 0.0001 vs. HG), 1.40 ± 0.32 (p < 0.0001 vs. HG) and 1.66 ± 0.17 in the CG, TPSWG and HG, respectively. Interleukin 1 beta (IL-1β) gene expression was increased (3.78 ± 0.29, p < 0.0001) and total glutathione (tGSH) was decreased (1.32 ± 0.25, p < 0.0001) in the retinal tissue of CG compared with TPSWG (1.92 ± 0.29 and 3.18 ± 0.46, respectively). Increased vascularisation and oedema were observed in the retinal tissue of CG, while the retinal tissues of TPSWG and HG rats had a normal histopathological appearance. A carbohydrate-rich diet may lead to pathological changes in the retina even in nondiabetics, but this may be overcome by TPP administration.

scholarly journals Keratinocyte growth factor, tumor necrosis factor-alpha and interleukin-1 beta gene expression in cultured fibroblasts and keratinocytes from burned patients

2013 ◽  
Vol 28 (8) ◽  
pp. 551-558 ◽  
Author(s):  
Alfredo Gragnani ◽  
Bruno Rafael Müller ◽  
Ismael Dale Contrim Guerreiro da Silva ◽  
Samuel Marcos Ribeiro de Noronha ◽  
Lydia Masako Ferreira
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis ◽  
Keratinocyte Growth Factor ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Necrosis Factor Alpha ◽  
Cultured Fibroblasts ◽  
Factor Alpha ◽  
Beta Gene ◽  
Necrosis Factor

scholarly journals Cholesterol Transporters ABCA1 and ABCG1 Gene Expression in Peripheral Blood Mononuclear Cells in Patients with Metabolic Syndrome

Cholesterol ◽  
2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Zahra Tavoosi ◽  
Hemen Moradi-Sardareh ◽  
Massoud Saidijam ◽  
Reza Yadegarazari ◽  
Shiva Borzuei ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Mononuclear Cells ◽  
Fasting Blood Glucose ◽  
Control Group ◽  
Regulation Mechanism ◽  
Healthy Individuals ◽  
Peripheral Blood Mononuclear ◽  
Significant Difference ◽  
Abca1 Expression

ABCA1 and ABCG1 genes encode the cholesterol transporter proteins that play a key role in cholesterol and phospholipids homeostasis. This study was aimed at evaluating and comparing ABCA1 and ABCG1 genes expression in metabolic syndrome patients and healthy individuals. This case-control study was performed on 36 patients with metabolic syndrome and the same number of healthy individuals in Hamadan (west of Iran) during 2013-2014. Total RNA was extracted from mononuclear cells and purified using RNeasy Mini Kit column. The expression of ABCA1 and ABCG1 genes was performed by qRT-PCR. Lipid profile and fasting blood glucose were measured using colorimetric procedures. ABCG1 expression in metabolic syndrome patients was significantly lower (about 75%) compared to that of control group, while for ABCA1 expression, there was no significant difference between the two studied groups. Comparison of other parameters such as HDL-C, FBS, BMI, waist circumference, and systolic and diastolic blood pressure between metabolic syndrome patients and healthy individuals showed significant differences (P<0.05). Decrease in ABCG1 expression in metabolic syndrome patients compared to healthy individuals suggests that hyperglycemia, related metabolites, and hyperlipidemia over the transporter capacity resulted in decreased expression of ABCG1. Absence of a significant change in ABCA1 gene expression between two groups can indicate a different regulation mechanism for ABCA1 expression.

scholarly journals Modulation of interleukin 1 beta gene expression by the immediate early genes of human cytomegalovirus.

1990 ◽  
Vol 85 (6) ◽  
pp. 1853-1857 ◽  
Author(s):  
G K Iwamoto ◽  
M M Monick ◽  
B D Clark ◽  
P E Auron ◽  
M F Stinski ◽  
...  
Keyword(s):  
Gene Expression ◽  
Human Cytomegalovirus ◽  
Interleukin 1 ◽  
Immediate Early Genes ◽  
Immediate Early ◽  
Interleukin 1 Beta ◽  
Early Genes ◽  
Beta Gene

scholarly journals A labile transcriptional repressor modulates endotoxin tolerance.

1994 ◽  
Vol 180 (6) ◽  
pp. 2269-2275 ◽  
Author(s):  
K E LaRue ◽  
C E McCall
Keyword(s):  
Gene Expression ◽  
Interleukin 1 ◽  
Endotoxin Tolerance ◽  
Potential Candidate ◽  
Interleukin 1 Beta ◽  
Transcription Inhibition ◽  
Cytokine Mrna ◽  
I Kappa B Alpha ◽  
Cellular Expression ◽  
Beta Gene

Tolerance to bacterial lipopolysaccharide (LPS, endotoxin) is an adaptive cellular process whereby exposure to endotoxin induces a subsequent hyporesponsive state characterized by decreased levels of LPS-induced cytokine mRNA and protein. We demonstrate, in a human promonocytic cell line, THP-1, that endotoxin tolerance is manifested by decreased LPS-induced interleukin 1 beta (IL-1 beta) transcription. Inhibition of protein synthesis reverses the tolerant phenotype by inducing transcription of IL-1 beta in the absence of a second stimulus. These results indicate that a labile protein contributes to the endotoxin-tolerant phenotype, and that this factor acts in a dominant repressive manner to inhibit the activity of existing transcription factors. We provide further data that cellular expression of I kappa B-alpha correlates with downregulated IL-1 beta gene expression during endotoxin tolerance, implicating I kappa B-alpha as a potential candidate for the labile repressor identified herein.

An Interleukin-1 beta (IL1B) haplotype linked with psychosis transition is associated with IL1B gene expression and brain structure

2019 ◽  
Vol 204 ◽  
pp. 201-205 ◽  
Author(s):  
Md Shaki Mostaid ◽  
Stefanos Dimitrakopoulos ◽  
Cassandra Wannan ◽  
Vanessa Cropley ◽  
Cynthia Shannon Weickert ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Structure ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Il1b Gene

Interleukin-1 beta and tumor necrosis factor-alpha synergistically stimulate nerve growth factor synthesis in rat mesangial cells

1991 ◽  
Vol 261 (5) ◽  
pp. F792-F798 ◽  
Author(s):  
P. Steiner ◽  
J. Pfeilschifter ◽  
C. Boeckh ◽  
H. Radeke ◽  
U. Otten
Keyword(s):  
Gene Expression ◽  
Nerve Growth Factor ◽  
Tumor Necrosis ◽  
Mesangial Cells ◽  
Interleukin 1 ◽  
Tnf Alpha ◽  
Interleukin 1 Beta ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Recent evidence indicates that cytokines are potent inducers of nerve growth factor (NGF) expression both in peripheral tissues and the central nervous system and that NGF, in addition to its neurotrophic action, also acts as an immunoregulatory agent. It was of interest to investigate whether inflammatory cytokines affect NGF production in renal mesangial cells, which play a crucial role in the modulation of the local immune function in the glomerulus. Our results show that the simultaneous addition of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) elicited a marked (13-fold) increase of NGF protein released by cultured rat glomerular mesangial cells within 24 h, whereas IL-1 alpha in combination with TNF-alpha, as well as the cytokines alone, did not promote the synthesis of NGF. The synergistic effect was dose dependent (maximal at 1 nM) and due to enhanced gene expression, since the cytokine treatment caused a fivefold increase in NGF mRNA after 8 h. Stimulation of NGF synthesis was abolished by mepacrine and dexamethasone, indicating that phospholipase A2 may be involved in NGF regulation. Moreover, pretreatment of the cells with the lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA) abolished induction of NGF by cytokines; in contrast, the specific cyclooxygenase inhibitors indomethacin and diclofenac failed to modify NGF production. These data suggest that a lipoxygenase metabolite produced in response to IL-1 beta and TNF-alpha acts as a mediator in NGF gene expression. In conclusion, these findings support a model in which a cytokine cascade including NGF may play an important role in the pathophysiology of inflammatory renal diseases.

Interleukin-1-beta Gene Expression in Human Monocytes and Alveolar Macrophages from Normal Subjects and Patients with Sarcoidosis

1988 ◽  
Vol 137 (5) ◽  
pp. 1180-1184 ◽  
Author(s):  
Jeffrey A. Kern ◽  
Roberta J. Lamb ◽  
John C. Reed ◽  
Jack A. Elias ◽  
Ronald P. Daniele
Keyword(s):  
Gene Expression ◽  
Alveolar Macrophages ◽  
Interleukin 1 ◽  
Normal Subjects ◽  
Human Monocytes ◽  
Interleukin 1 Beta ◽  
Beta Gene
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