Biglycan protects human neuroblastoma cells from nitric oxide-induced death by inhibiting AMPK-mTOR mediated autophagy and intracellular ROS level.
Biglycan protects human neuroblastoma cells from nitric oxide-induced death by inhibiting AMPK-mTOR mediated autophagy and intracellular ROS level. Biotechnol Lett. 2020 Jan 27;: Authors: Chen S, Guo D, Lei B, Bi J, Yang H Abstract The ubiquitous proteoglycan, biglycan (BGN) acts as an important modulator, regulating key molecular pathways of metabolism and brain function. Autophagy is documented as a defining feature of neurodegeneration in Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). In the present study, we found that BGN protected neuronal cells from nitric oxide (NO)-induced cell apoptosis. However, it is still unclear that whether the neuroprotective effect of BGN relates to autophagy. Here, we discovered that an NO donor, sodium nitroprusside (SNP) induced autophagy in human SH-SY5Y neuroblastoma cells, including activating LC3B and inhibiting p62. Inhibiting autophagy by 3MA aggravated NO-induced cell death, otherwise promoting autophagy by Rapamycin rescued NO-triggered cell death. Notably, BGN downregulated by NO, significantly protected SH-SY5Y cells against NO-induced neurotoxicity by inhibiting the activation of autophagy-dependent AMPK signaling pathway. Moreover, BGN overexpression also diminished NO-induced the elevation of intracellular reactive oxygen species (ROS) level, but not NO content. These findings suggest that BGN protects neuroblastoma cells from NO-induced death by suppressing autophagy-d...
Publication date: August 2020Source: Biomedicine &Pharmacotherapy, Volume 128Author(s): Kehinde S. Olaniyi, Oluwatobi A. Amusa
Publication date: Available online 24 May 2020Source: PhytomedicineAuthor(s): Hai-Qiao Wang, Min Liu, Liang Wang, Fen Lan, Yi-Han Zhang, Jin-Er Xia, Zhen-Dong Xu, Hai Zhang
DEMENTIA currently has no cure, but scientists have been looking into ways different types of dementia can be prevented. In a new study, three foods have been shown to have protective benefits against Alzheimer's disease.
Publication date: September 2020Source: Neurochemistry International, Volume 138Author(s): Cui Liu, Yan Xue, Mei-Fang Liu, Ying Wang, Lei Chen
Authors: Wang S, Guo P, Feng M, Qian M, Shen X, Wang G PMID: 32447268 [PubMed - as supplied by publisher]
HDAC1 is involved in a form of DNA repair, but levels decline with age, as well as in Alzheimer's disease. This leads to a greater accumulation of unrepaired oxidative DNA damage in neurons. Researchers here note that increased activation of HDAC1 appears to improve cognitive function via a reduction in this oxidative DNA damage. An HDAC1 activator drug has been tested as a treatment for dementia, but caused serious side-effects. Better compounds or other approaches may be able to obtain similar benefits without the harms. There are several members of the HDAC family of enzymes, and their primary function is to m...
Condition: Periodontal Diseases Intervention: Drug: Sodium hypochlorite gel application Sponsor: University of Messina Completed
Condition: Chorea, Huntington Intervention: Drug: Valbenazine Sponsors: Neurocrine Biosciences; Huntington Study Group Enrolling by invitation
CONCLUSION: Existing in vitro and in vivo data are promising, and highlight that naturally-occurring autophagy-regulating compounds play an important role for the prevention and treatment of neurodegenerative disorders. PMID: 31914904 [PubMed - as supplied by publisher]
In this study, we investigated whether NPY has a protective role in ER stress-induced neuronal cell death in SK-N-SH human neuroblastoma cells. An ER stress-inducing chemical, tunicamycin, increased the activities of caspase-3 and -4, whereas pretreatment with NPY decreased caspase-3 and -4 activities during the ER stress response. In addition, NPY suppressed the activation of three major ER stress sensors during the tunicamycin-induced ER stress response. NPY-mediated activation of PI3K increased nuclear translocation of XBP1s, which in turn induced expression of Grp78/BiP. Taken together, our data indicated that NPY play...