Table 3.
The basic study of vitamins in PD.
| Vitamin | Authors | Object of study | Treatment | Conclusions |
|---|---|---|---|---|
| Vitamin B3 (nicotinamide) | Lu et al. [31] | Rotenone-PC12 cells | NMN (0.1 mM, 1.0 mM, 5 mM, and 10 mM) coculture | Attenuated apoptosis and improved energy metabolism |
| Xu et al. [114] | MPTP-C57BL/6 mice | 500 mg/kg/day for 5 days i.p. | Nicotinamide can alleviate MPTP-induced damage to dopaminergic neurons through antioxidant stress | |
| Jia et al. [115] | MPP(+)-SK-N-MC human neuroblastoma cells and alpha-synuclein transgenic Drosophila PD model | Nicotinamide concentration (21, 51, 101, 301, and 501 mg/L and 3, 15, 30, and 60 mg/100 g) | High doses of nicotinamide can reduce oxidative stress and improve mitochondrial function | |
| Anderson et al. [116] | MPTP-adult male C57Bl/6 mice | Nicotinamide (125, 250, or 500 mg/kg i.p.) | Recovered the striatal DA levels and SNc neurons after accepting nicotinamide | |
| Vitamin C (ascorbic acid) | Khan et al. [117] | PD Drosophila model | L-Ascorbic acid (AA, 11.35 × 10−5 M, 22.71 × 10−5 M, 45.42 × 10−5 M, and 68.13 × 10−5 M for 21 days) | Except 11.35 × 10−5 M, other concentrations of AA attenuated the loss of climbing ability of PD model flies in a dose-dependent manner |
| Yan et al. [52] | Mesencephalic precursors from the E12 rat | Ascorbic acid (0.1 μM, 1 μM, 10 μM, 100 μM, and 1 mM) | Ascorbic acid promoted the dopaminergic differentiation | |
| Seitz et al. [49] | Human neuroblastoma cell line SK-N-SH | Short-term incubation (100–500 μM for 2 h) and long-term incubation (200 μM for 5 days) | Ascorbic acid increased the DOPA production and tyrosine hydroxylase gene expression | |
| Pardo et al. [47] | Human neuroblastoma cell NB69 | 10−3 M ascorbic acid or 23 and 115 × 10−3 M alpha-tocopherol | Ascorbic acid prevents the levodopa toxicity and quinone formation, but alpha-tocopherol did not | |
| Sershen et al. [48] | MPTP-BALB/cBy mice | Ascorbic acid 100 mg/kg i.p. | Ascorbic acid may protect against the MPTP neurotoxicity | |
| Vitamin E | Nakaso et al. [75] | MPTP-C57BL/6 mice | δ-Tocotrienol (100 μg/kg for 4 days, p.o.) | δ-Tocotrienol administration inhibited the loss of dopaminergic neurons and improved the motor performance |
| Sharma and Nehru [70] | Rotenone-Sprague-Dawley rats | Vitamin E (100 IU/kg/day for 35 days i.m.) | Vitamin E administration significantly improved locomotor activity and increased the dopamine level, GSH, and SOD | |
| Ortiz et al. [118] | MPTP-C57BL/6 mice | Vitamin E (50 mg/kg/day p.o.) | Vitamin E administration has decreased the COX-2 activity, LPO, and nitrite/nitrate level | |
| Pasbakhsh et al. [119] | 6-OHDA-rat | Alpha-tocopherol acid succinate (24 IU/kg, i.m.) | Vitamin E treatment can protect locus coeruleus neurons in the PD model | |
| Roghani and Behzadi [69] | 6-OHDA – Sprague-Dawley rats | d-α-Tocopheryl acid succinate (24 I.U./kg, i.m.) | Vitamin E treatment improved the rotational behaviour and prevented the reduction of tyrosine hydroxylase-immunoreactive cells | |
| Vitamin D | Lima et al. [120] | 6-OHDA-Wistar rats | 1,25-(OH)2D3 (1 μg/kg for 7 days or for 14 days, p.o.) | Vitamin D can protect the dopaminergic neurons by its anti-inflammatory and antioxidant properties |
| Calvello et al. [121] | MPTP-male C57BL/6 N mice | Vitamin D (1 μg/kg for 10 days, i.g.) | Vitamin D administration attenuates neuroinflammation and dopaminergic neurodegeneration | |
| Li et al. [122] | MPTP-C57BL/6 mice | Calcitriol (0.2, 1, and 5 μg/kg/day for 7 days p.o.) | Calcitriol can significantly attenuate the neurotoxicity induced by MPTP | |
| Jang et al. [104] | Rotenone-SH-SY5Y cells | Calcitriol (0.0 μM, 0.63 μM, 1.25 μM, 2.5 μM, 5 μM, and 10 μM) | 1,25-Dyhydroxyvitamin D3 can induce the autophagy to protect against the rotenone-induced neurotoxicity | |
| Cass et al. [123] | 6-OHDA-male Fischer-344 rats | Calcitriol (0.3 or 1.0 μg/kg/day for 8 days, i.h.) | Calcitriol can promote functional recovery of dopaminergic neurons and release of dopamine | |
| Sanchez et al. [100] | 6-OHDA-Sprague-Dawley rats | 1,25(OH)(2)D(3) (1 μg/mL/kg/day for 7 days i.p.) | 1,25(OH)(2)D(3) treatment increased the GDNF protein expression and partially restored TH expression | |
| Kim et al. [102] | 6-OHDA Sprague-Dawley rats and MPTP-C57BL/6 mice | 1,25-(OH)2D3 (1 μg/mL at 1 mL/kg/day for 7 days, i.p.) | 1,25-(OH)2D3 can inhibit the microglial activation and protect against nigrostriatal degeneration |
LPO: lipid peroxides; COX-2: ciclooxigenase-2; TH: tyrosine hydroxylase; i.p.: intraperitoneal; i.m.: intramuscular; i.g.: intragastrical; i.h.: hypodermic injection; p.o.: peros.