Effect of Qingxinkaiqiao compound on cortical mRNA expression of the apoptosis-related genes Bcl-2, BAX, caspase-3, and Aβ in an Alzheimer's disease rat model

Objective: The objective of this study is to analyze caspase-3 mRNA gene expression in a Wistar rat model of Alzheimer’s disease (AD) treated with Musa paradisiaca L. (MPL) ethanol extract or banana extract (BE)Methods: MPL was evaluated for its effect on the caspase-3 mRNA gene expression of rat amyloid beta (Aβ) induced, an AD model. Each model included twenty Wistar rats were randomized into five groups: K0, without AD induction and no BE; K1, AD induction and no BE; K2, AD induction+BE 250 mg/kg body weight (BW); K3, AD induction+BE 500 mg/kg; and K4, AD induction+BE 1000 mg/kg. AD induction was performed by Aβ1-42 (0.2 ug) injection at the intracerebroventricular area. mRNA caspase-3 level measurements were performed by real time-polymerase chain reaction.Results: Paired t-test analysis showed no significant differences of caspase-3 mRNA level before Aβ induction among five groups (p>0.05). At 6 weeks post-Aβ induction, there was significantly increased caspase-3 mRNA in all groups except K0 (p<0.05). Notably, after 3 weeks of BE administration, caspase-3 mRNA expression was significantly decreased in all BE-treated groups; in the K1 placebo group, caspase-3 mRNA expression increased. The maximum decreased caspase-3 mRNA expression was in group K4 (-BE 1000 mg/kg BW), and the minimum was in group K2 (-BE 250 mg/kg BW).Conclusion: The results revealed that the ethanolic extract of MPL fruit could decrease caspase-3 mRNA gene expression in AD rat.

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Effect of Bee Venom on an Experimental Cellular Model of Alzheimer’s Disease

The American Journal of Chinese Medicine ◽

10.1142/s0192415x20500901 ◽

2020 ◽

Vol 48 (08) ◽

pp. 1803-1819

Author(s):

Yong Ho Ku ◽

Jae Hui Kang ◽

Hyun Lee

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Mrna Expression ◽

Caspase 3 ◽

Bee Venom ◽

Control Group ◽

Cellular Model ◽

Expression Levels ◽

Cox 2 ◽

Mrna Expression Levels

Alzheimer’s disease (AD) is a neurodegenerative disease and is characterized by the deposition of the [Formula: see text]-Amyloid peptide ([Formula: see text]A), which causes the inflammation of neurons. Bee venom (BV) elicits a strong anti-inflammatory response, and therefore we conducted an in vitro experiment to study the efficacy of BV in an AD cellular model. To mimic AD, the U87MG cell line was incubated for 168 hours with 2.5 [Formula: see text]M [Formula: see text]A. Changes were confirmed by microscopy, and peptides were measured under stain-free conditions using homo-tomography. Sulforhodamine B analysis was performed to analyze the cell viability. Real-Time quantitative polymerase chain reaction (qPCR) analysis was conducted to analyze mRNA expression levels of pro-inflammatory cytokines (NF-[Formula: see text]B, COX-2, TNF-[Formula: see text], IL-1), and Western blot was performed to measure the Caspase-3 protein levels. BV showed no cytotoxicity at concentrations below 10 [Formula: see text]g/mL. The NF-[Formula: see text]B mRNA levels were not significantly different between the BV group and the control group. The amount of [Formula: see text]A accumulation in the BV group decreased significantly. The mRNA expression levels of COX-2, TNF-[Formula: see text], and IL-1 were significantly reduced using 10 [Formula: see text]g/mL of BV compared to those in the control group. Additionally, Caspase-3 levels were also reduced compared to those of the control group when BV was used at a concentration of 10 [Formula: see text]g/mL. BV could inhibit apoptosis and inflammatory responses in an AD cellular model. In addition, it prevented cell accumulation of [Formula: see text]A, an important pathogenic mechanism in AD.

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Effects of treadmill exercise on hippocampal cell proliferation and memory in streptozotocin rat model for sporadic Alzheimer's disease

Exercise Science ◽

10.15857/ksep.2007.16.1.11 ◽

2007 ◽

Vol 16 (1) ◽

pp. 11-22

Author(s):

ILGYU JEONG ◽

Chang-Ju Kim ◽

Jin hwan Yoon ◽

Lee Hee Hyuk

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cell Proliferation ◽

Rat Model ◽

Treadmill Exercise ◽

Sporadic Alzheimer’S Disease ◽

Hippocampal Cell ◽

Streptozotocin Rat Model

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A PPAR-alpha agonist gemfibrozil ameliorates cognitive and memory impairments in a sporadic Alzheimer’s disease rat model

10.26226/morressier.5b681761b56e9b005965c37b ◽

2018 ◽

Author(s):

Yildiz Sila ◽

Rumeysa Keles ◽

Cam Muhammet Emin

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Rat Model ◽

Ppar Alpha ◽

Sporadic Alzheimer’S Disease ◽

Memory Impairments ◽

Alpha Agonist

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MiR-335-5p Inhibits β-Amyloid (Aβ) Accumulation to Attenuate Cognitive Deficits Through Targeting c-jun-N-terminal Kinase 3 in Alzheimer’s Disease

Current Neurovascular Research ◽

10.2174/1567202617666200128141938 ◽

2020 ◽

Vol 17 (1) ◽

pp. 93-101 ◽

Cited By ~ 3

Author(s):

Dan Wang ◽

Zhifu Fei ◽

Song Luo ◽

Hai Wang

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Transgenic Mice ◽

Western Blot ◽

Mrna Expression ◽

Cognitive Deficits ◽

Protein Levels ◽

Amyloid Aβ ◽

Β Amyloid ◽

The Relationship

Objectives: Alzheimer's disease (AD), also known as senile dementia, is a common neurodegenerative disease characterized by progressive cognitive impairment and personality changes. Numerous evidences have suggested that microRNAs (miRNAs) are involved in the pathogenesis and development of AD. However, the exact role of miR-335-5p in the progression of AD is still not clearly clarified. Methods: The protein and mRNA levels were measured by western blot and RNA extraction and quantitative real-time PCR (qRT-PCR), respectively. The relationship between miR-335-5p and c-jun-N-terminal kinase 3 (JNK3) was confirmed by dual-luciferase reporter assay. SH-SY5Y cells were transfected with APP mutant gene to establish the in vitro AD cell model. Flow cytometry and western blot were performed to evaluate cell apoptosis. The APP/PS1 transgenic mice were used as an in vivo AD model. Morris water maze test was performed to assess the effect of miR- 335-5p on the cognitive deficits in APP/PS1 transgenic mice. Results: The JNK3 mRNA expression and protein levels of JNK3 and β-Amyloid (Aβ) were significantly up-regulated, and the mRNA expression of miR-335-5p was down-regulated in the brain tissues of AD patients. The expression levels of miR-335-5p and JNK3 were significantly inversely correlated. Further, the dual Luciferase assay verified the relationship between miR-335- 5p and JNK3. Overexpression of miR-335-5p significantly decreased the protein levels of JNK3 and Aβ and inhibited apoptosis in SH-SY5Y/APPswe cells, whereas the inhibition of miR-335-5p obtained the opposite results. Moreover, the overexpression of miR-335-5p remarkably improved the cognitive abilities of APP/PS1 mice. Conclusion: The results revealed that the increased JNK3 expression, negatively regulated by miR-335-5p, may be a potential mechanism that contributes to Aβ accumulation and AD progression, indicating a novel approach for AD treatment.

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Failure of the Brain Glucagon-Like Peptide-1-Mediated Control of Intestinal Redox Homeostasis in a Rat Model of Sporadic Alzheimer’s Disease

Antioxidants ◽

10.3390/antiox10071118 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1118

Author(s):

Jan Homolak ◽

Ana Babic Perhoc ◽

Ana Knezovic ◽

Jelena Osmanovic Barilar ◽

Melita Salkovic-Petrisic

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Rat Model ◽

Redox Homeostasis ◽

Brain State ◽

Gastrointestinal Hormone ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

The Brain

The gastrointestinal system may be involved in the etiopathogenesis of the insulin-resistant brain state (IRBS) and Alzheimer’s disease (AD). Gastrointestinal hormone glucagon-like peptide-1 (GLP-1) is being explored as a potential therapy as activation of brain GLP-1 receptors (GLP-1R) exerts neuroprotection and controls peripheral metabolism. Intracerebroventricular administration of streptozotocin (STZ-icv) is used to model IRBS and GLP-1 dyshomeostasis seems to be involved in the development of neuropathological changes. The aim was to explore (i) gastrointestinal homeostasis in the STZ-icv model (ii) assess whether the brain GLP-1 is involved in the regulation of gastrointestinal redox homeostasis and (iii) analyze whether brain-gut GLP-1 axis is functional in the STZ-icv animals. Acute intracerebroventricular treatment with exendin-3(9-39)amide was used for pharmacological inhibition of brain GLP-1R in the control and STZ-icv rats, and oxidative stress was assessed in plasma, duodenum and ileum. Acute inhibition of brain GLP-1R increased plasma oxidative stress. TBARS were increased, and low molecular weight thiols (LMWT), protein sulfhydryls (SH), and superoxide dismutase (SOD) were decreased in the duodenum, but not in the ileum of the controls. In the STZ-icv, TBARS and CAT were increased, LMWT and SH were decreased at baseline, and no further increment of oxidative stress was observed upon central GLP-1R inhibition. The presented results indicate that (i) oxidative stress is increased in the duodenum of the STZ-icv rat model of AD, (ii) brain GLP-1R signaling is involved in systemic redox regulation, (iii) brain-gut GLP-1 axis regulates duodenal, but not ileal redox homeostasis, and iv) brain-gut GLP-1 axis is dysfunctional in the STZ-icv model.

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