Skip to main content

Table 3 Main outcome measures of included studies

From: Neuroprotective properties of curcumin in toxin-base animal models of Parkinson’s disease: a systematic experiment literatures review

Study (years)

Outcome measures

Neuroprotection mechanism

Virginia 2005

1. TH-positive cells in the SN were increased by curcumin. 2. Striatal concentration of DA and its metabolites DOPAC and HVA

Phenomenon research.

Pan 2007

1. TH-positive cells and protein level in the SNpc and striatum. 2. GFAP-positive cells and iNOS level in the SNpc

Anti-oxidant and anti-inflammatory.

Balusamy 2008

1. Curcumin against GSH depletion-mediated oxidative stress, significantly restored total brain GSH levels in BSO mice.

2. Accumulation of ROS was prevented only by pretreatment with curcumin.

Anti-oxidant capabilities.

Rajeswari 2008

1. Curcumin reversed the reduction in striatal DA and DOPAC levels; 2. MAO-B activity was reduced by curcumin treatment

Anti-oxidant capabilities.

Wang 2009

1. Curcumin reversed the reduction in SNpc TH and DAT mRNA levels; 2. DA and DOPAC levels were restored by curcumin

Phenomenon research.

Song 2010

1. Curcumin showed a significant increase in locomotion frequencies; 2. Curcumin increased the TH, DAT level and inhibits

astrocyte activation in terms of GFAP. 3. Inhibitory effects of curcumin on JNK, c-Jun, and caspase-3.

Anti-inflammatory and

anti-apoptosis.

Peng 2010

1. Curcumin could ameliorate rotational behaviour; 2. DA level was restored by curcumin administration.

Phenomenon research.

Zahra 2012

1. Curcumin prevented the decrease of locomotor activity. 2. The number of Nissl neurons on the left side of substantia nigra

was significantly higher in curcumin group. 3. Effect of curcumin on Bax/Bcl-2.

Anti-apoptosis.

Du 2012

1. Curcumin partly restored the levels of DA, DOPAC and HVA. 2. TH-positive neurons were restored by curcumin pretreatment.

3. Marked decrease of iron-positive cells was found in the curcumin pretreatment group.

Suppress the iron-induced

degeneration.

Yu 2012

1. Curcumin ameliorated open-field test; 2. TH, DAT levels were restored by curcumin and inhibited GFAP and TNF-a.

Anti-inflammatory.

Guo 2012

1. Motor coordination of rota-rod test and hanging test were improved in the curcumin treatment group.

2. Curcumin suppressed nuclear translocation and NF-Kβ activity. 3 TNF-a and IL-1b were restored by curcumin.

Anti-inflammatory

Tripanichkui 2013

1. Curcumin attenuated loss of TH fibers, diminished activation of GFAP and microgliosis, sustained SOD1 level.

Anti-inflammatory and anti-oxidant

Ariana 2014

1.Curcumin produced similar deleterious effects in the beam-walking test and single-pellet test. 2. Curcumin showed no

beneficial effects against Mn-induced disruption of hippocampal metal and neurotransmitter homeostasis (DA or serotonin).

No neuroprotection

  1. TH Tyrosine hydroxylase; SN Substantia Nigra; DA dopamine; DOPAC 3,4-Dihydroxyphenylacetic acid; HVA Homovanillic acid; iNOS Inducible nitric oxide synthase; GFAP Glial fibrillary acidic protein; GSH Glutathione; ROS Reactive oxygen species; MAO-B Monoamine oxidase-B; DAT dopamine transport; JNK c-Jun N-terminal kinase; SOD Superoxide Dismutase; TNF-α Tumor necrosis factor; IL- Interleukin-1β