Fig 1.
Schematic diagram of total experimental procedures: The treatment was continued for ten weeks.
After that, the behavioral tests were performed using Passive Avoidance (PA) and Contextual Fear Conditioning (CFC). The biomarkers were detected after completing the behavioral tasks. In-silico studies were used to determine curcumin’s binding affinity to targeted proteins.
Table 1.
Information of protein structures.
Fig 2.
Effect of curcumin on RT in D-gal and NA mice group after 24 hours of training.
The RT was calculated by performing PA tasks among Vehicle, Cur-Con, D-gal, Curcumin + D-gal, Ast + D-gal, NA, Curcumin + NA, Ast + NA groups. RT was expressed in second. Data was presented as mean ± SEM, n = 8 each group; ****p < 0.0001, ns = not significant.
Fig 3.
Effect of curcumin on the conditioning fear memory of (A) D-gal and (B) NA mice group. The memory was assessed by analyzing the FR. The FR was expressed in percentage (%). Data was presented as mean ± SEM, n = 8 each group; **p < 0.01, ***p < 0.001, ****p < 0.0001, ns = not significant.
Fig 4.
Effect of curcumin on the context and cued fear memory (Day 2b and 31b) of (A) D-gal and (B) NA mice group. The memory was assessed by analyzing the FR. The FR was expressed in percentage (%). Data was presented as mean ± SEM, n = 8 each group; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns = not significant.
Fig 5.
Effect of curcumin on GSH concentration (A and B), SOD (C and D) and CAT (E and F) activity in D-gal and NA mice group. The GSH, SOD, CAT was detected by using bioassay technique among Vehicle, Cur-Con, D-gal, Curcumin + D-gal, Ast + D-gal, NA, Curcumin + NA, Ast + NA groups. GSH level, SOD and CAT activity were expressed in μmol/mg, U/30s, and μmol/min/mg, respectively. Data was presented as mean ± SEM, n = 8 each group; *p < 0.05, **p < 0.01 ***p < 0.001, ****p < 0.0001 ns = not significant.
Fig 6.
Effect of curcumin on AOPP (A and B), NO (C and D), and MDA (E and F) concentration in D-gal and NA mice group. The AOPP level was assessed using bioassay technique among Vehicle, Cur-Con, D-gal, Curcumin + D-gal, Ast + D-gal, NA, Curcumin + NA, Ast + NA groups. AOPP, NO, and MDA level was represented in μmol/ml, mmol/mg, and nmol/ml, respectively. Data was presented as mean ± SEM, n = 8 each group; *p < 0.05, **p < 0.01, ****p < 0.0001 ns = not significant.
Fig 7.
Molecular docking of curcumin to GSTA1.
(A) Redocking of the bound ligand. (B) Docking pose of curcumin. (C) Interactions of the bound ligand with the protein. (D) Predicted interactions of curcumin with the protein.
Fig 8.
Molecular docking of curcumin to GSTO1.
(A) Redocking of the bound ligand. (B) Docking pose of curcumin. (C) Interactions of the bound ligand with the protein. (D) Predicted interactions of curcumin with the protein.
Fig 9.
Molecular docking of curcumin to KEAP1.
(A) Redocking of the bound ligand. (B) Docking pose of curcumin. (C) Interactions of the bound ligand with the protein. (D) Predicted interactions of curcumin with the protein.
Fig 10.
Relative abundance of the class of top 50 predicted molecular targets of curcumin obtained from SwissTargetPrediction.
Fig 11.
Names and target probabilities of top 10 predicted molecular targets of curcumin obtained from Swiss TargetPrediction.
Fig 12.
Molecular docking of curcumin to MAOA.
(A) Redocking of the bound ligand. (B) Docking pose of curcumin. (C) Interactions of the bound ligand with the protein. (D) Predicted interactions of curcumin with the protein.
Fig 13.
Molecular docking of curcumin to BACE1.
(A) Redocking of the bound ligand. (B) Docking pose of curcumin. (C) Interactions of the bound ligand with the protein. (D) Predicted interactions of curcumin with the protein.
Table 2.
Estimated binding energies from Vina molecular docking.