Table 2.
Recently reported curcumin (CU) activities in in vitro and in vivo models of neurodegenerative diseases [41,42,43,44,45,46,47,48,49,50].
| Disease | Model/Administration Route | Mechanism | Outcomes |
|---|---|---|---|
| AD | In vitro: human neuroblastoma SH-SY5Y and IMR-32 cells | Enhancement of the expression of DNA repair enzymes (APE1, pol β, and PARP1 1) to halt the oxidative DNA base damage via base excision repair (BER) pathway; Activation of the antioxidant response element (ARE) via Nrf2 upregulation |
Revitalization of the neuronal cells from Aβ 2 induced oxidative stress [41]. |
| AD | In vitro: mouse hippocampal clone neuronal cell line HT-22 cells treated with Aβ 1-42, In vivo: mice with APP/PS1 transgenes |
Decrease of the autophagosomes number, Increase of the lysosomal Ca2+ regulation of PI(3,5)P2 and Transient Receptor Potential Mucolipin-1 Expression (TRPME) |
Neuronal cell growth, Protective role of CU on memory and cognition impairments [42]. |
| AD | In vivo: rat, oral supplementation |
Increase of GPx 3, CAT 4, GSH 5 activities and Ach 6 levels | Improving memory and cognitive abilities [43]. |
| PD | In vivo: Drosophila model of PD with dUCH 7 knockdown | Effects on dUCH 7 knockdown, a homolog of human UCH-L1 | Decrease of ROS levels, Improved locomotive abilities, Reduction of dopaminergic neurons degeneration [44]. |
| PD | In vivo: male Sprague-Dawley rats injured by 6-OHDA 8 in the left striatum | Activation of the Wnt/β-catenin signaling pathway, Higher Wnt3a and β-catenin mRNA and protein expressions, c-myc and cyclin D1 mRNA expression, enhanced SOD 9 and GPx 3 contents, decreased MDA 10 content and elevated mitochondrial membrane potential |
Protective effect of CU against oxidative stress-induced injury, Enhanced viability, survival, and adhesion, attenuated apoptosis of deutocerebrum primary cells [45]. |
| PD | In vivo: MPTP 11 mice, intranasal mode of administration of CU (mucoadhesive system) | Increase of dopamine concentration in brain, which improves muscular coordination and gross behavioral activities of the test animal, Significant reduction of the MPTP11-mediated dopamine depletion |
Improvement in motor performance, Symptomatic neuroprotection against MPTP-induced neurodegeneration in the striatum [46]. |
| HD | In vivo: CAG140 mice, a knock-in (KI) mouse model of HD | Decreased huntingtin aggregates, increased striatal DARPP-32 and D1 receptor mRNAs | Partial improvement of transcriptional deficits, partial behavioral improvement [47]. |
| Diazepam-induced cognitive impairment | In vivo: diazepam-treated rats, oral supplementation | Downregulation of the extracellular signal-regulated kinase (ERK 1/2)/nuclear transcription factor-(NF-)κB/pNF-κB pathway in the hippocampus and the iNOS 12 expression in the hippocampus and frontal cortex | Improvement of the cognitive performance, Decrease of blood and brain oxidative stress levels [48]. |
| Alcohol-induced neurodege neration | In vivo: rat, oral supplementation |
Decrease of the reduced form of GSH 5, SOD 9, GPx 3, GR 13, change in the Bcl-2 levels, Activation of the CREB-BDNF signaling pathway |
Neuroprotection against alcohol-induced oxidative stress, apoptosis and inflammation [49]. |
| Nicotine-induced neurodege neration | In vivo: rat, oral supplementation |
Activation of the CREB-BDNF signaling pathway | Neuroprotection against nicotine-induced inflammation, apoptosis and oxidative stress, Reduction of the motor activity disturbances [50]. |
1 Poly [ADP-ribose] polymerase 1; 2 Aβ-amyloid; 3 Glutathione Peroxidase; 4 Catalase; 5 Glutathione; 6 Acetylcholine; 7 Ubiquitin carboxy-terminal hydrolase; 8 6-Hydroxydopamine; 9 Superoxide dismutase; 10 Malondialdehyde; 11 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; 12 Induced Nitric Oxide Synthase; 13 Glutathione Reductase.