Blueberry anthocyanins ameliorate arsenic-induced cognitive impairment in rats: mitigating mitochondrial damage and
Xinbo Ma1, Yang Liu1, Bo Ding2
1Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, Heilongjiang Province, PR China; NHC Key Laboratory of Etiology and Epidemiology (Harbin Medical University), Harbin 150081, Heilongjiang Province, PR China; Joint Key Laboratory of Endemic Diseases (Harbin Medical University, Guizhou Medical University, Xi'an Jiaotong University), Harbin 150081, Heilongjiang Province, PR China.
Background:
Blueberry anthocyanin extract (BAE) is a natural antioxidant flavonoid found in blueberries that has the potential to alleviate oxidative stress-induced neurodegeneration. Previous studies have demonstrated the potential of BAE to mitigate arsenic-induced cognitive impairment; however, the underlying protective mechanisms remain elusive.
Purpose:
This study aimed to evaluate the effectiveness of BAE in reducing arsenic-induced cognitive impairment and explored whether BAE's neuroprotective effects are related to its antioxidant and mitochondrial protective effects.
Methods:
Sixty male rats were exposed to sodium arsenite (NaAsO2, 10 mg/kg) with or without BAE (100 and 200 mg/kg) for 12 weeks. Spatial learning and memory were evaluated using the Morris water maze (MWM). Neuronal damage in rat hippocampi was evaluated using hematoxylin and eosin (H&E) staining, electron microscopy, and terminal deoxynucleotidyl transferase-mediated nick-end labelling (TUNEL) staining. Oxidative stress markers, including malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC) were measured. Mitochondrial function was assessed by analysing peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), deacetylase sirtuin 1 (SIRT1), and proteins related to mitochondrial biogenesis and mitochondrial dynamics.
Results:
Arsenic exposure significantly impaired learning and memory in rats, as evidenced by reduced performance in the MWM, whereas BAE treatment ameliorated these deficits. Furthermore, BAE alleviated arsenic-induced hippocampal neuronal apoptosis, as well as alleviating increased oxidative stress, weakened antioxidant capacity, and imbalanced mitochondrial biogenesis and dynamics. In this study, we focused on the core of mitochondrial quality control mechanism - mitochondrial biogenesis, fusion and fission. We explored the protective mechanism of BAE against arsenic - induced nerve damage. Based on these, we proposed an innovative therapeutic strategy: using natural products to target and regulate mitochondrial quality control.
Conclusion:
This study indicated that BAE alleviates arsenic-induced neurotoxicity through its antioxidant and mitochondrial protective effects, effectively reducing arsenic-induced neurotoxicity and enhancing cognitive function.
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