Title:Restoring Impaired Neurogenesis and Alleviating Oxidative Stress by
Cyanidin against Bisphenol A-induced Neurotoxicity: In Vivo and In Vitro
Evidence
Volume: 21
Issue: 2
Author(s): Swathi Suresh and Chitra Vellapandian*
Affiliation:
- Department of Pharmacology, SRM College of Pharmacy, SRM Institute of Science and Technology, Kattankulathur,
Chengalpattu, 603 203, Tamil Nadu, India
Keywords:
Neurotoxicity, neurogenesis, anthocyanin, cyanidin, Wnt, bisphenol A, antioxidant, neurodegeneration.
Abstract:
Background: Bisphenol A (BPA) is a known neurotoxic compound with potentially harmful
effects on the nervous system. Cyanidin (CYN) has shown promise as a neuroprotective agent.
Objective: The current study aims to determine the efficacy of CYN against BPA-induced neuropathology.
Methods: In vitro experiments utilized PC12 cells were pre-treated with gradient doses of CYN and
further stimulated with 10ng/ml of BPA. DPPH radical scavenging activity, catalase activity, total
ROS activity, and nitric oxide radical scavenging activity were done. In vivo assessments employed
doublecortin immunohistochemistry of the brain in BPA-exposed Sprague-Dawley rats. Further, In silico molecular docking of CYN with all proteins involved in canonical Wnt signaling was performed
using the Autodock v4.2 tool and BIOVIA Discovery Studio Visualizer.
Results: IC50 values of CYN and ascorbic acid were determined using dose-response curves, and it
was found to be 24.68 ± 0.563 μg/ml and 20.69 ± 1.591μg/ml, respectively. BPA-stimulated cells
pre-treated with CYN showed comparable catalase activity with cells pre-treated with ascorbic acid
(p = 0.0287). The reactive species production by CYN-treated cells was significantly decreased compared
to BPA-stimulated cells (p <0.0001). Moreover, CYN significantly inhibited nitric oxide production
compared to BPA stimulated and the control cells (p < 0.0001). In vivo CYN positively
affected immature neuron quantity, correlating with dosage. During molecular docking analysis,
CYN exhibited a binding affinity > -7 Kcal/mol with all the key proteins associated with the Wnt/β-
catenin signaling cascade.
Conclusion: Conclusively, our finding suggests that CYN exhibited promise in counteracting BPAinduced
oxidative stress, improving compromised neurogenesis in hippocampal and cortical regions,
and displaying notable interactions with Wnt signaling proteins. Thereby, CYN could render its neuroprotective
potential against BPA-induced neuropathology.
