The neuroprotective effect of curcumin in a mouse model of Parkinson’s disease and its mechanism

Abstract

Objective To investigate the neuroprotective effect of curcumin on mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson’s disease (PD) and its mechanism. Methods A total of 72 male C57BL/6J mice were randomly divided into control group (group A), MPTP group (group B), and MPTP+curcumin group (group C). For the 5 d before the experiment, the mice in groups B and C were given intraperitoneal injection of MPTP every day, and those in group A were given intraperitoneal injection of an equal volume of normal saline; since day 6, the mice in group C were given intraperitoneal injection of curcumin dissolved in DMSO at a dose of 50 mg/kg, and those in groups A and B were given intraperitoneal injection of an equal volume of DMSO, every day for 7 consecutive days. After the end of administration, behavioral experiments were used to evaluate the motor, learning, and memory functions of mice in each group. On day 15 of the experiment, the samples of substantia nigra were collected from the mice in each group, and ELISA was used to measure the content of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6); Western blotting was used to measure the relative content of CD86 and NF-κB; immunohistochemical staining was used to measure the number of TH-positive neurons. Results Compared with group B, groups A and C had a significant reduction in descending time, significant increases in drop latency and percentage of alternation (F=17.29-19.28,P<0.05), significant reductions in the content of TNF-α, IL-1β, and IL-6 (F=31.73-80.97,P<0.05) and the expression of CD86 and NF-κB in the substantia nigra (F=24.93,55.61,P<0.05), and a significant increase in the number of TH-positive neurons in the substantia nigra (F=47.64,P<0.05). Conclusion Curcumin can effectively improve behavior disorder and exert a neuroprotective effect in PD mice, possibly by inhibiting the NF-κB signaling pathway, thereby leading to the inhibition of microglial cell activation, the reduction in inflammatory response, and the alleviation of dopaminergic neuron degeneration.

Keywords

• parkinson disease|disease models, animal|curcumin|microglia|nf-kappa b|neuroinflammatory diseases|neuroprotection