scholarly journals A high-cholesterol diet enriched with polyphenols from Oriental plums (Prunus salicina) improves cognitive function and lowers brain cholesterol levels and neurodegenerative-related protein expression in mice

2015 ◽  
Vol 113 (10) ◽  
pp. 1550-1557 ◽  
Author(s):  
Ping-Hui Kuo ◽  
Ching-I Lin ◽  
Yue-Hwa Chen ◽  
Wan-Chun Chiu ◽  
Shyh-Hsiang Lin
Keyword(s):  
Cognitive Function ◽  
Protein Expression ◽  
Mrna Expression ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
Related Protein ◽  
Long Term Effects ◽  
High Cholesterol ◽  
Ctrl Group ◽  
The Brain

Ageing accompanied by a decline in cognitive performance may be a result of the long-term effects of oxidative stress on neurologic processes. It has been shown that high-cholesterol contents in the blood and brain may lead to the deposition of the β-amyloid (Aβ) protein in the brain, which damages brain cells. The present study was designed to observe the effect of polyphenol-rich Oriental plums on cognitive function and cerebral neurodegeneration-related protein expression in mice that were fed a high-cholesterol diet for 5 months. The study consisted of four groups: the control (Ctrl) group, which was fed the American Institute of Nutrition (AIN)-93M diet; the high cholesterol (HC) group, which was fed the AIN-93M diet with 5 % cholesterol; the high cholesterol+low Oriental plum (LOP) group, which was fed the AIN-93M diet with 5 % cholesterol and 2 % Oriental plum powder; and the high cholesterol+high Oriental plum (HOP) group, which was fed the AIN-93M diet with 5 % cholesterol and 5 % Oriental plum powder. Measurements of cognitive function were assessed using the Morris water maze, and the mRNA expression of cholesterol hydroxylase (Cyp46), Aβ and β-secretase 1 (BACE1) were analysed. The results showed that cholesterol concentrations in both the blood and the brain were significantly higher in the HC group than in the Ctrl and HOP groups at the end of the trial. The high-cholesterol diet per se produced significant cognitive deficits, which were accompanied by a significantly increased mRNA expression of Cyp46, BACE1, Aβ and 24-hydroxycholesterol in the brain cortex and hippocampus. However, all of these variables were non-significantly increased in the HOP group as compared to the Ctrl group. In conclusion, incorporating polyphenol-enriched Oriental plum into a high-cholesterol diet can ameliorate some of the symptoms of neurodegenerative conditions.

scholarly journals High-Cholesterol Diet Decreases the Level of Phosphatidylinositol 4,5-Bisphosphate by Enhancing the Expression of Phospholipase C (PLCβ1) in Rat Brain

2020 ◽  
Vol 21 (3) ◽  
pp. 1161 ◽  
Author(s):  
Yoon Sun Chun ◽  
Sungkwon Chung
Keyword(s):  
Neurodegenerative Diseases ◽  
Rat Brain ◽  
Phospholipase C ◽  
Cultured Cells ◽  
Cell Interaction ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Amyloid Aβ ◽  
The Brain

Cholesterol is a critical component of eukaryotic membranes, where it contributes to regulating transmembrane signaling, cell–cell interaction, and ion transport. Dysregulation of cholesterol levels in the brain may induce neurodegenerative diseases, such as Alzheimer’s disease, Parkinson disease, and Huntington disease. We previously reported that augmenting membrane cholesterol level regulates ion channels by decreasing the level of phosphatidylinositol 4,5-bisphosphate (PIP2), which is closely related to β-amyloid (Aβ) production. In addition, cholesterol enrichment decreased PIP2 levels by increasing the expression of the β1 isoform of phospholipase C (PLC) in cultured cells. In this study, we examined the effect of a high-cholesterol diet on phospholipase C (PLCβ1) expression and PIP2 levels in rat brain. PIP2 levels were decreased in the cerebral cortex in rats on a high-cholesterol diet. Levels of PLCβ1 expression correlated with PIP2 levels. However, cholesterol and PIP2 levels were not correlated, suggesting that PIP2 level is regulated by cholesterol via PLCβ1 expression in the brain. Thus, there exists cross talk between cholesterol and PIP2 that could contribute to the pathogenesis of neurodegenerative diseases.

Abstract 500: Vitamin D Supplementation Attenuates ADAM-12-mediated Proliferation of Carotid Artery Smooth Muscle Cells of Hypercholesterolemic Swine

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Vikash Kansal ◽  
Eric B Patterson
Keyword(s):  
Vitamin D ◽  
Smooth Muscle ◽  
Carotid Artery ◽  
Protein Expression ◽  
Vitamin D Supplementation ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Tnf Α ◽  
Adam 12

Introduction: Risk of hypertension, peripheral artery disease, myocardial infarction and development of human atherosclerosis has been linked to vitamin D deficiency. Atheromatous cytokines, including IL-6, TNF-α and epidermal growth factor receptor (EGFR) family growth factors are released at the site of atherosclerosis and boost the activity of proteolytic enzymes such as ADAMs (a disintegrin and metalloproteinases). ADAM-12 cleaves proHB-EGF (Heparin-binding EGF-like growth factor) activating EGFR, resulting in increased proliferation of smooth muscle cells (SMCs). The aim of this study was to examine the effect of vitamin D on IL-6 and TNF-α-induced ADAM-12, pEGFR expression, HB-EGF release and SMC proliferation. Methods: Micro-swine were fed with vitamin D-deficient high cholesterol diet, high cholesterol diet containing 900 IU of vitamin D, and high cholesterol diet containing 3000 IU of vitamin D for total of 12 months. After six months, serum cholesterol levels of 500-600 mg/dL were achieved in all the three groups. The protein expression of ADAM-12 & pEGFR, and HB-EGF release, in presence or absence of IL-6, TNF-α and Calcitriol, in SMCs was quantified by western Blot. HB-EGF release was measured by ELISA. The proliferation was assayed by [3H]-Thymidine incorporation and cell counting method. Results: The protein expression of ADAM-12 & pEGFR, HB-EGF release were significantly reduced in carotid artery SMCs isolated from Vitamin D-supplemented swine. IL-6 and TNF-α treatment increased the protein expression of ADAM-12 & pEGFR and HB-EGF release in carotid artery SMCs. Proliferation capacity was higher in SMCs isolated from Vitamin D-deficient swine carotid artery, potentiated by IL-6 and TNF-α. Calcitriol inhibited the ADAM-12, pEGFR expression and HB-EGF released in SMCs of hypercholesterolemic swine. Calcitriol also inhibited the proliferation of carotid artery SMCs isolated from Vit D-deficient, D-sufficient and D-supplemented swine. Conclusion: Together, these results suggest that vitamin D deficiency enhances proliferation of SMCs, which is potentiated by atheromatous cytokines. Whereas, vitamin D supplementation regulates ADAM-12-mediated cleavage of proHB-EGF and activation of EGFR inhibiting SMC proliferation.

Tlr4 upregulation in the brain accompanies depression- and anxiety-like behaviors induced by a high-cholesterol diet

2015 ◽  
Vol 48 ◽  
pp. 42-47 ◽  
Author(s):  
Tatyana Strekalova ◽  
Matthew Evans ◽  
Joao Costa-Nunes ◽  
Sergey Bachurin ◽  
Naira Yeritsyan ◽  
...  
Keyword(s):  
High Cholesterol Diet ◽  
Depression And Anxiety ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
The Brain

scholarly journals Long-Term Effects of Dietary Fiber Supplementation on Serum Glucose and Lipoprotein Levels In Diabetic Rats Fed a High Cholesterol Diet.

1995 ◽  
Vol 42 (2) ◽  
pp. 187-192 ◽  
Author(s):  
TOSHIKI HOZUMI ◽  
MUNEYOSHI YOSHIDA ◽  
YOSHIHIKO ISHIDA ◽  
HIDEKI MIMOTO ◽  
JYUNKO SAWA ◽  
...  
Keyword(s):  
Dietary Fiber ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
Long Term Effects ◽  
High Cholesterol

scholarly journals Hypercholesterolemia and 27-Hydroxycholesterol Increase S100A8 and RAGE Expression in the Brain: a Link Between Cholesterol, Alarmins, and Neurodegeneration

2021 ◽  
Author(s):  
Raúl Loera-Valencia ◽  
Muhammad-Al-Mustafa Ismail ◽  
Julen Goikolea ◽  
Maria Lodeiro ◽  
Laura Mateos ◽  
...  
Keyword(s):  
Cholesterol Metabolism ◽  
Primary Cultures ◽  
Transgenic Mouse Model ◽  
Intraventricular Injection ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
The Brain ◽  
Rage Expression

AbstractAlterations in cholesterol metabolism in the brain have a major role in the physiology of Alzheimer’s disease (AD). Oxysterols are cholesterol metabolites with multiple implications in memory functions and in neurodegeneration. Previous studies have shown detrimental effects of cholesterol metabolites in neurons, but its effect in glial cells is unknown. We used a high-fat/high-cholesterol diet in mice to study the effects of hypercholesterolemia over the alarmin S100A8 cascade in the hippocampus. Using CYP27Tg, a transgenic mouse model, we show that the hypercholesterolemia influence on the brain is mediated by the excess of 27-hydroxycholesterol (27-OH), a cholesterol metabolite. We also employed an acute model of 27-OH intraventricular injection in the brain to study RAGE and S100A8 response. We used primary cultures of neurons and astrocytes to study the effect of high levels of 27-OH over the S100A8 alarmin cascade. We report that a high-fat/high-cholesterol diet leads to an increase in S100A8 production in the brain. In CYP27Tg, we report an increase of S100A8 and its receptor RAGE in the hippocampus under elevated 27-OH in the brain. Using siRNA, we found that 27-OH upregulation of RAGE in astrocytes and neurons is mediated by the nuclear receptor RXRγ. Silencing RXRγ in neurons prevented 27-OH-mediated upregulation of RAGE. These results show that S100A8 alarmin and RAGE respond to high levels of 27-OH in the brain in both neurons and astrocytes through RXRγ. Our study supports the notion that 27-OH mediates detrimental effects of hypercholesterolemia to the brain via alarmin signaling.

Hypolipidemic and antioxidant effect of Ajuga iva in rats fed a high-cholesterol diet

Planta Medica ◽  
2006 ◽  
Vol 72 (11) ◽  
Author(s):  
MA Lacaille-Dubois ◽  
A Chenni ◽  
DA Yahia ◽  
FO Boukortt ◽  
J Prost ◽  
...  
Keyword(s):  
Antioxidant Effect ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol
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