Filtered By:
Specialty: Food Science
Condition: Parkinson's Disease

This page shows you your search results in order of date.

Order by Relevance | Date

Total 4 results found since Jan 2013.

Chaperon-mediated autophagy can regulate diquat-induced apoptosis by inhibiting α-synuclein accumulation cooperatively with macroautophagy
In this study, we explored the role of CMA in diquat (DQ)-induced α-synucleinopathy and characterized the relationship between CMA and macroautophagy in the clearance of pathologic α-synuclein for the prevention of DQ neurotoxicity. DQ was cytotoxic to SH-SY5Y cells in a concentration-dependent manner, as shown by decreased cell viability and increased cytotoxicity. DQ treatment was also found to induce autophagy such as CMA and macroautophagy by monitoring the expression of Lamp2A and microtubule-associated protein 1A/1B light chain 3B (LC3-II) respectively. Following DQ treatment, SH-SY5Y cells were found to have induc...
Source: Food and Chemical Toxicology - December 1, 2021 Category: Food Science Authors: Hong Ju Kim Hyun Chul Koh Source Type: research

Upregulation of OPA1 by carnosic acid is mediated through induction of IKK γ ubiquitination by parkin and protects against neurotoxicity.
In conclusion, the mechanism by which CA counteracts the toxicity of 6-OHDA is through modulation of mitochondrial dynamics and upregulation of OPA1 via activation of the parkin/IKKγ/p65 pathway. PMID: 31705926 [PubMed - as supplied by publisher]
Source: Food and Chemical Toxicology - November 5, 2019 Category: Food Science Authors: Lin CY, Chen WJ, Fu RH, Tsai CW Tags: Food Chem Toxicol Source Type: research

PINK1/parkin-mediated mitophagy pathway is related to neuroprotection by carnosic acid in SH-SY5Y cells.
In conclusion, CA appears to counteract the neurotoxicity of 6-OHDA by activating PINK1/parkin-mediated mitophagy. PMID: 30707903 [PubMed - as supplied by publisher]
Source: Food and Chemical Toxicology - January 29, 2019 Category: Food Science Authors: Lin CY, Tsai CW Tags: Food Chem Toxicol Source Type: research