Low Molecular Weight Sulfated Chitosan: Neuroprotective Effect on Rotenone-Induced In Vitro Parkinson's Disease.
Venkatesan ManigandanJagatheesan NatarajRamachandran KarthikThamilarasan ManivasagamRamachandran SaravananArokyasamy Justin ThenmozhiMusthafa Mohamed EssaGilles J GuilleminPublished in: Neurotoxicity research (2018)
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.
Keyphrases
- cell death
- oxidative stress
- cell cycle arrest
- diabetic rats
- induced apoptosis
- reactive oxygen species
- poor prognosis
- dna damage
- drug delivery
- high glucose
- ischemia reperfusion injury
- cell free
- endoplasmic reticulum stress
- single molecule
- anti inflammatory
- photodynamic therapy
- binding protein
- cerebral ischemia
- climate change
- wound healing
- signaling pathway
- risk assessment
- mesenchymal stem cells
- cell therapy
- long non coding rna
- brain injury