| Literature DB >> 30426393 |
Venkatesan Manigandan1, Jagatheesan Nataraj2, Ramachandran Karthik1, Thamilarasan Manivasagam2, Ramachandran Saravanan3, Arokyasamy Justin Thenmozhi2, Musthafa Mohamed Essa4,5, Gilles J Guillemin6.
Abstract
The present investigation was an attempt to study the effect of low molecular weight sulfated chitosan (LMWSC) on in vitro rotenone model of Parkinson's disease (PD) by evaluating cell viability, oxidative stress, mitochondrial membrane potential, DNA fragmentation, and apoptosis. Incubation of SH-SY5Y cells with 100 nm rotenone resulted in neuronal cell death, redox imbalanced mitochondrial dysfunction, DNA fragmentation, condensation, and apoptotic cellular morphology. Rotenone exposure enhanced the expression of preapoptotic (cytochrome C (cyto c), caspase-3, -8, -9, and Bax) and down-regulated the expression of anti-apoptotic (Bcl-2) markers. Reduction of the intracellular reactive oxygen species (ROS) levels ensued due to pretreatment of LMWSC along with consequent normalization of antioxidant enzymes, mitigation of rotenone induced mitochondrial dysfunction and apoptosis. Our current findings suggested that LMWSC exhibit the pronounced neuroprotective effects, which could be due to its antioxidant, mitochondrial protection, and anti-apoptotic properties. We thus conclude that LMWSC could be developed as a novel therapeutic molecule for the benefit of reducing the consequences of PD. However, further extensive preclinical and clinical studies are warranted.Entities:
Keywords: Apoptosis; Mitochondrial dysfunction; Neuronal damage; Oxidative stress; Rotenone; Sulfated chitosan
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Year: 2018 PMID: 30426393 DOI: 10.1007/s12640-018-9978-z
Source DB: PubMed Journal: Neurotox Res ISSN: 1029-8428 Impact factor: 3.911