Studies that prove that curcumin has the potential to overcome neuroinflammation.
| Researcher and year | Model | Resveratrol dosage and duration | Parameter | Key results | Conclusion |
|---|---|---|---|---|---|
| Yu et al., 2018 [49] | Microglia BV-2 cells | 5, 10, and 20 µM curcumin, 1-hour pre-incubation, then lipoteichoic acid (LTA) for 16–24 hours | 1. Cell viability (MTT assay)2. NO, PGE2, tumor necrosis factor-alpha (TNF-α) (ELISA/Griess)3. Expression of iNOS & COX-2 mRNA (qRT PCR)4. Mitogen-activated protein kinase (MAPK) phosphorylation (p38, ERK, Akt) & nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) translocation5. HO-1 & nuclear factor erythroid 2-related factor 2 (Nrf2) expression | 1. No toxic effect on cell viability2. Dose-dependent decrease in NO, PGE2, TNF-α3. Decreased iNOS and COX-2 mRNA expression4. Inhibits phosphorylation of MAPK & translocation of NF-κB5. Increases the expression of HO-1 and Nrf2; inhibition of HO-1 eliminates the anti-inflammatory effect of curcumin | Curcumin suppresses microglia activation and inflammatory mediator production by inhibiting NF-κB and MAPK pathways, as well as induction of the HO-1/Nrf2 antioxidant pathway, making curcumin a potential candidate for anti-neuroinflammatory therapy |
| Kharazmi et al., 2022 [65] | Wistar male rats | 10 mg/kg BW curcumin, oral (gavage), 35 days pretreatment before morphine injection | 1. Latency of inhibitory avoidance (IA memory)2. Motor activity (open field)3. Expression of p-CREB & total CREB in hippocampus4. NOx (nitric oxide metabolite) levels in brain tissue | 1. Pre-treatment with curcumin prevents latency decrease2. No significant change in motor activity between groups3. Increased p-CREB, supporting its protective role against memory4. Increases NOx levels, possibly activating the NO → p-CREB → memory signaling pathway | Curcumin prevents morphine-induced memory impairment in mice, likely through increased NO and activation of downstream CREB signaling |
| Namgyal et al., 2020 [63] | Swiss albino mice; Cadmium (Cd) exposure | Oral curcumin (oral gavage) at various doses; Cd exposure 2.5 mg/kg BW for 60 days | 1. Behavior (spontaneous alternation, elevated plus-maze)2. Antioxidant enzyme SOD, CAT, and GSH levels and malondialdehyde (MDA) level3. Inflammatory cytokine levels (IL-6, TNF-α, IL-10)4. Histology of prefrontal cortex neurons | 1. Working memory and anxious behavior improved in rats given curcumin2. SOD, CAT, and GSH activities increased; MDA activity decreased3. IL-6 and TNF-α decreased; IL-10 increased4. Neuron morphology in the prefrontal cortex improved | Curcumin protects cognitive function and prefrontal neuron structure by reducing oxidative stress and neuroinflammation due to Cd exposure |
| Sorrenti et al., 2018 [46] | Young adult mice | 50 mg/kg BW curcumin, orally, given 2 consecutive days before LPS injection (5 mg/kg i.p.) | 1. Microglia activation (Iba1)2. Proinflammatory cytokines3. Physical symptoms (sickness behavior)4. Long-term memory function (Morris Water Maze) | 1. Decreased microglia activation (seen from decreased Iba1 expression and improved cell morphology)2. Significant reduction in IL-1β and TNF-α expression in plasma and brain tissue3. Reduced symptoms of sickness behavior faster than the LPS group without curcumin4. Accelerated long-term memory recovery even though it was only given briefly | Short-term preventive curcumin effectively suppresses LPS-induced acute neuroinflammation and reduces long-term memory consequences |