Protective effects of bajijiasu in a rat model of Aβ25-35-induced neurotoxicity

Chen, Diling; Zhāng, Peng; Lin, Li; Zhang, Heming; Deng, Shaodong; Wu, Zeqing; Shuai, Ou; Liu, Songhao; Wang, Jin-Yu

doi:10.1016/j.jep.2014.04.004

Cited by 38 publications

(40 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Bajijiasu were isolated and purified as described previously (Chen et al, 2014b). The HPLC-ELSD fingerprint of bajijiasu ensured its purity (Z98%).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Effect of bajijiasu isolated from Morinda officinalis F. C. how on sexual function in male mice and its antioxidant protection of human sperm

Chen

Lin

et al. 2015

Journal of Ethnopharmacology

Self Cite

View full text Add to dashboard Cite

“…Bajijiasu were isolated and purified as described previously (Chen et al, 2014b). The HPLC-ELSD fingerprint of bajijiasu ensured its purity (Z98%).…”

Section: Methodsmentioning

confidence: 99%

“…The acute toxicity of bajijiasu was investigated in our previous study (Chen et al, 2014b), and the doses used here were below the toxic dose. Every group contained 10 animals and the dosing regimen was performed daily for 30 days.…”

Section: Experimental Designmentioning

confidence: 99%

Effect of bajijiasu isolated from Morinda officinalis F. C. how on sexual function in male mice and its antioxidant protection of human sperm

Chen

Lin

et al. 2015

Journal of Ethnopharmacology

Self Cite

View full text Add to dashboard Cite

“…Moreover, it also inhibits neuronal apoptosis AD [136] Taurine Attenuates Aβ-induced mitochondrial dysfunction by activating of SIRT1 in SK-N-SH cells AD…”

Section: Methazolamide (Mtz)mentioning

confidence: 99%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

Mounting evidence suggests a link between metabolic syndrome (MetS) such as diabetes, obesity, non-alcoholic fatty liver disease in the progression of Alzheimer's disease (AD), Parkinson's disease (PD) and other neurodegenerative diseases (NDDs). For instance, accumulated Aβ oligomer is enhancing neuronal Ca release and neural NO where increased NO level in the brain through post translational modification is modulating the level of insulin production. It has been further confirmed that irrespective of origin; brain insulin resistance triggers a cascade of the neurodegeneration phenomenon which can be aggravated by free reactive oxygen species burden, ER stress, metabolic dysfunction, neuorinflammation, reduced cell survival and altered lipid metabolism. Moreover, several studies confirmed that MetS and diabetic sharing common mechanisms in the progression of AD and NDDs where mitochondrial dynamics playing a critical role. Any mutation in mitochondrial DNA, exposure of environmental toxin, high-calorie intake, homeostasis imbalance, glucolipotoxicity is causative factors for mitochondrial dysfunction. These cumulative pleiotropic burdens in mitochondria leads to insulin resistance, increased ROS production; enhanced stress-related enzymes that is directly linked MetS and diabetes in neurodegeneration. Since, the linkup mechanism between mitochondrial dysfunction and disease phenomenon of both MetS and NDDs is quite intriguing, therefore, it is pertinent for the researchers to identify and implement the therapeutic interventions for targeting MetS and NDDs. Herein, we elucidated the pertinent role of MetS induced mitochondrial dysfunction in neurons and their consequences in NDDs. Further, therapeutic potential of well-known biomolecules and chaperones to target altered mitochondria has been comprehensively documented. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.

show abstract

“…The purity of the compound was analyzed by high-performance liquid chromatography as previously described [22]. Primary antibodies—PKR-like ER kinase (PERK), phosphorylated PERK (P-PERK), inositol-requiring enzyme (IRE-1α), phosphorylated IRE-1α (P-IRE-1α), phosphorylated eukaryotic initiation factor 2 (P-eIF-2α), eukaryotic initiation factor 2 (eIF-2α), binding immunoglobulin protein (BIP), protein-disulphide isomerase (PDI), C/EBP homologous protein (CHOP), nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), Bcl-2, and caspase-3—were purchased from Cell Signaling Technology, Inc. Anti-Bax antibody was purchased from Santa Cruz Biotechnology, Inc. Anti-β-actin was purchased from Sigma-Aldrich.…”

Section: Methodsmentioning

confidence: 99%

“…1). Bajijiasu has been shown to be effective in ameliorating disease and pathological mechanisms such as oxidative stress [22, 23], reinforcing population spikes and long-term potentiation [19], attenuating D-galactose-induced cognitive dysfunction in mice, and protecting against neuronal damage or death induced by ischemia. Bajijiasu can also protect against Aβ 25-35 -induced neurotoxicity in PC12 cells [24].…”

Section: Introductionmentioning

confidence: 99%

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

Zhang

et al. 2018

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Protective effects of bajijiasu in a rat model of Aβ25-35-induced neurotoxicity

Cited by 38 publications

References 38 publications

Effect of bajijiasu isolated from Morinda officinalis F. C. how on sexual function in male mice and its antioxidant protection of human sperm

Effect of bajijiasu isolated from Morinda officinalis F. C. how on sexual function in male mice and its antioxidant protection of human sperm

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

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

Contact Info

Product

Resources

About