Curcumin Alleviates β Amyloid-Induced Neurotoxicity in HT22 Cells via Upregulating SOD2

In this study, the HT22 neuronal cells were exposed to Aβ to imitate neuronal injury in Alzheimer’s disease (AD). After 24-h treatment, 10 μM Aβ decreased cell viability and mitochondrial functions, including mitochondrial complex activities and mitochondrial membrane potential (MMP), and also downregulated anti-oxidants SOD2, glutathione (GSH), and catalase (CAT) levels (P <  0.05), meanwhile, increased lactic dehydrogenase (LDH) release, apoptosis level, intracellular reactive oxygen species (ROS) and mitochondrial superoxide accumulation (P <  0.05). And, co-administration of 1 μM curcumin significantly reduced the Aβ-induced cell injury and oxidative damage above (P <  0.05). Downregulating SOD2 by using small interfering RNA (siRNA), however, significantly abolished the curcumin-induced protective and anti-oxidative effects in HT22 cells (P <  0.05); the scramble (SC)-siRNA did not cause marked effects on the curcumin-induced protective effects (P >  0.05). These findings showed that curcumin can alleviate Aβ-induced injury in neuronal cells, and SOD2 protein may mediate the neuroprotective effects.
Source: Journal of Molecular Neuroscience - Category: Neuroscience Source Type: research