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Centella asiatica Attenuates Amyloid-β-Induced Oxidative Stress and Mitochondrial Dysfunction
Nora E Gray1, Harini Sampath2, Jonathan A Zweig3
1Department of Neurology, Oregon Health and Science University, Portland, OR, USA.
Journal of Alzheimer'S Disease : JAD
|January 31, 2015
Summary
Centella asiatica water extract (CAW) protects against amyloid-beta (Aβ) toxicity by boosting antioxidant responses and improving mitochondrial function. This study identifies key biochemical pathways involved in CAW's neuroprotective effects.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Centella asiatica water extract (CAW) shows promise in mitigating amyloid-beta (Aβ)-induced cognitive deficits and cytotoxicity.
- The precise neuroprotective mechanisms of CAW remain largely unelucidated.
Purpose of the Study:
- To investigate the biochemical pathways modulated by CAW in in vitro models of Aβ toxicity.
- To identify how CAW influences antioxidant response, calcium homeostasis, and mitochondrial function.
Main Methods:
- Utilized MC65 and SH-SY5Y neuroblastoma cell lines to assess CAW's effects on Aβ-induced cellular damage.
- Evaluated intracellular reactive oxygen species, calcium levels, mitochondrial respiration, ATP production, and gene/protein expression.
Main Results:
- CAW reduced Aβ-induced increases in reactive oxygen species and calcium levels.
- CAW enhanced mitochondrial respiration, ATP production, and expression of antioxidant and mitochondrial genes.
- Caffeoylquinic acids within CAW demonstrated similar protective effects on gene expression.
Conclusions:
- CAW likely exerts neuroprotection against Aβ toxicity through enhanced mitochondrial biogenesis.
- Activation of antioxidant response genes and normalization of calcium homeostasis are key contributing factors.
- CAW represents a potential therapeutic agent for neurodegenerative conditions associated with Aβ pathology.
