scholarly journals Chlorogenic Acid Exerts Beneficial Effects in 6-Hydroxydopamine-Induced Neurotoxicity by Inhibition of Endoplasmic Reticulum Stress

2019 ◽  
Vol 25 ◽  
pp. 453-459 ◽  
Author(s):  
Shihai Shan ◽  
Lina Tian ◽  
Ruihuan Fang
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Chlorogenic Acid ◽  
Beneficial Effects ◽  
6 Hydroxydopamine

scholarly journals Bajijiasu Ameliorates β-Amyloid-Triggered Endoplasmic Reticulum Stress and Related Pathologies in an Alzheimer’s Disease Model

2018 ◽  
Vol 46 (1) ◽  
pp. 107-117 ◽  
Author(s):  
Ting-Ting Xu ◽  
Yang Zhang ◽  
Jia-Yang He ◽  
Dan Luo ◽  
Yi Luo ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Western Blotting ◽  
Disease Model ◽  
Beta Amyloid ◽  
Amyloid Peptide ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Y Maze ◽  
Improved Learning

Background/Aims: Alzheimer disease (AD) is a common neurodegenerative disease that is characterized by the deposition of beta-amyloid peptide and formation of intracellular neurofibrillary tangles. Due to the failure of various clinical trials of novel drugs for AD, effective drugs for AD treatment are urgently required. Methods: In this study, we used the classic APP/PS1 mouse model to explore the neuroprotective effects of a new compound, bajijiasu, and the mechanisms involved. Behavioral tests and western blotting were performed to assess the beneficial effects of bajijiasu in APP/PS1 mice. Results: Morris water maze and Y-maze test results showed that oral administration of bajijiasu (35 mg/kg/day and 70 mg/kg/day) improved learning and memory abilities in APP/PS1 mice. Bajijiasu reduced ROS and MDA levels in both the hippocampus and cortex. Moreover, western blotting results showed that bajijiasu protected neurons from apoptosis, elevated the expression levels of neurotrophic factors, and alleviated endoplasmic reticulum stress in both the hippocampus and cortex. Conclusion: These results indicate that the mechanisms underlying the effects of bajijiasu on AD might be related to beta-amyloid-downstream pathologies, particularly endoplasmic reticulum stress.

scholarly journals Dietary Cocoa Powder Improves Hyperlipidemia and Reduces Atherosclerosis in apoE Deficient Mice through the Inhibition of Hepatic Endoplasmic Reticulum Stress

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Hua Guan ◽  
Yan Lin ◽  
Liang Bai ◽  
Yingfeng An ◽  
Jianan Shang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Molecular Mechanisms ◽  
Plasma Cholesterol ◽  
Group Analysis ◽  
Pcr Analysis ◽  
Control Group ◽  
Cocoa Powder ◽  
Beneficial Effects ◽  
Apoe Knockout Mice

Cocoa powder is rich in flavonoids, which have many beneficial effects on human health, including antioxidative and anti-inflammatory effects. The aim of our study was to investigate whether the intake of cocoa powder has any influence on hyperlipidemia and atherosclerosis and examine the underlying molecular mechanisms. We fed apoE knockout mice a Western diet supplemented with either 0.2% (low group) or 2% (high group) cocoa powder for 12 weeks. The groups fed dietary cocoa powder showed a significant reduction in both plasma cholesterol levels and aortic atherosclerosis compared to the control group. Analysis of mRNA profiling of aortic atherosclerotic lesions revealed that the expression of several genes related to apoptosis, lipid metabolism, and inflammation was significantly reduced, while the antiapoptotic gene Bcl2 was significantly increased in the cocoa powder group compared to the control. RT-PCR analysis along with Western blotting revealed that a diet containing cocoa powder inhibited the expression of hepatic endoplasmic reticulum stress. These data suggest that cocoa powder intake improves hyperlipidemia and atherosclerosis, and such beneficial effects are possibly mediated through the suppression of hepatic endoplasmic reticulum stress.

Amelioration of bleomycin-induced pulmonary fibrosis by chlorogenic acid through endoplasmic reticulum stress inhibition

APOPTOSIS ◽  
2017 ◽  
Vol 22 (9) ◽  
pp. 1147-1156 ◽  
Author(s):  
Yi-Chun Wang ◽  
Jing Dong ◽  
Jing Nie ◽  
Ji-Xiang Zhu ◽  
Hui Wang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Pulmonary Fibrosis ◽  
Endoplasmic Reticulum Stress ◽  
Chlorogenic Acid

scholarly journals New Cardiomyokine Reduces Myocardial Ischemia/Reperfusion Injury by PI3K‐AKT Pathway Via a Putative KDEL‐Receptor Binding

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Leonardo Maciel ◽  
Dahienne Ferreira de Oliveira ◽  
Fernanda Mesquita ◽  
Hercules Antônio da Silva Souza ◽  
Leandro Oliveira ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Receptor Binding ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
In Vivo Model ◽  
Beneficial Effects ◽  
Isolated Hearts ◽  
Infarct Area ◽  
Kdel Receptor

Background CDNF (cerebral dopamine neurotrophic factor) belongs to a new family of neurotrophic factors that exert systemic beneficial effects beyond the brain. Little is known about the role of CDNF in the cardiac context. Herein we investigated the effects of CDNF under endoplasmic reticulum‐stress conditions using cardiomyocytes (humans and mice) and isolated rat hearts, as well as in rats subjected to ischemia/reperfusion (I/R). Methods and Results We showed that CDNF is secreted by cardiomyocytes stressed by thapsigargin and by isolated hearts subjected to I/R. Recombinant CDNF (exoCDNF) protected human and mouse cardiomyocytes against endoplasmic reticulum stress and restored the calcium transient. In isolated hearts subjected to I/R, exoCDNF avoided mitochondrial impairment and reduced the infarct area to 19% when administered before ischemia and to 25% when administered at the beginning of reperfusion, compared with an infarct area of 42% in the untreated I/R group. This protection was completely abrogated by AKT (protein kinase B) inhibitor. Heptapeptides containing the KDEL sequence, which binds to the KDEL‐R (KDEL receptor), abolished exoCDNF beneficial effects, suggesting the participation of KDEL‐R in this cardioprotection. CDNF administered intraperitoneally to rats decreased the infarct area in an in vivo model of I/R (from an infarct area of ≈44% in the I/R group to an infarct area of ≈27%). Moreover, a shorter version of CDNF, which lacks the last 4 residues (CDNF‐ΔKTEL) and thus allows CDNF binding to KDEL‐R, presented no cardioprotective activity in isolated hearts. Conclusions This is the first study to propose CDNF as a new cardiomyokine that induces cardioprotection via KDEL receptor binding and PI3K/AKT activation.

Inhibition of 6-hydroxydopamine-induced endoplasmic reticulum stress by l-carnosine in SH-SY5Y cells

2009 ◽  
Vol 459 (1) ◽  
pp. 7-10 ◽  
Author(s):  
Yun-Mi Oh ◽  
Eun-Hee Jang ◽  
Jeong-Hyeon Ko ◽  
Ju-Hee Kang ◽  
Chang-Shin Park ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
6 Hydroxydopamine
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