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. 2018 Mar 20;18(1):103.
doi: 10.1186/s12906-018-2166-0.

The antioxidant and neurochemical activity of Apium graveolens L. and its ameliorative effect on MPTP-induced Parkinson-like symptoms in mice

Pennapa Chonpathompikunlert  1 , Phetcharat Boonruamkaew  2   3 , Wanida Sukketsiri  4 , Pilaiwanwadee Hutamekalin  2 , Morakot Sroyraya  5   6
Affiliations

The antioxidant and neurochemical activity of Apium graveolens L. and its ameliorative effect on MPTP-induced Parkinson-like symptoms in mice

Pennapa Chonpathompikunlert et al. BMC Complement Altern Med. .

Abstract

Background: Apium graveolens L. is a traditional Chinese medicine prescribed as a treatment for hypertension, gout, and diabetes. This study aimed to determine the neuroprotective effects of A. graveolens extract against a Parkinson's disease (PD) model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6 mice.

Methods: Male C57BL/6 mice treated with MPTP were orally dosed with A. graveolens extract daily for 21 days. Behavioral tests, including a rotarod apparatus, a narrow beam test, a drag test, a grid walk test, a swimming test, and a resting tremor evaluation, were performed. Thereafter, the mice were sacrificed, and monoamine oxidase A and B activity, lipid peroxidation activity, and superoxide anion levels were measured. Immunohistochemical staining of tyrosine hydroxylase was performed to identify dopaminergic neurons.

Results: We found that treatment with A. graveolens at dose of 375 mg/kg demonstrated the highest effect and led to significant improvements in behavioral performance, oxidative stress parameters, and monoamine oxidase A and B activity compared with the untreated group (p < 0.05). Moreover, the extract increased the number of neurons immunopositive for tyrosine hydroxylase expression compared with MPTP alone or MPTP with a positive control drug (p < 0.05).

Conclusions: We speculated that A. graveolens ameliorated behavioral performance by mediating neuroprotection against MPTP-induced PD via antioxidant effects, related neurotransmitter pathways and an increase in the number of dopaminergic neurons.

Keywords: A. graveolens; MPTP; Monoamine oxidase; Oxidative stress; Tidomet plus; Tyrosine hydroxylase.

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Conflict of interest statement

Ethics approval

The study protocol was approved by the Animal Ethics Committee of Prince of Songkla University (Reference no. MOE0521.11/582) before the start of this study.

Consent for publication

All authors signed the paper and agreed to publish it.

Competing interests

The authors declare that they have no competing interests.

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Figures

Fig. 1
Fig. 1
Effect of AGME extract on number of forepaw touches during the drag test at 0, 1, 3, and 7 days after MPTP treatment. Each data column displays the mean ± SD (n = 8/group, o-p < 0.001 compared with the control group; #-p < 0.05 compared with the vehicle-treated group; *-p < 0.05 compared with the Tidomet Plus-treated group)
Fig. 2
Fig. 2
Effect of AGME on the number of foot faults on the grid walk test at 0, 1, 3, and 7 days after MPTP treatment. Each data column displays the mean ± SD (n = 8/group, o-p < 0.01 compared with the control group; #-p < 0.05 compared with the vehicle-treated group; *-p < 0.05 compared with the Tidomet Plus-treated group)
Fig. 3
Fig. 3
Effect of AGME on latency time (a) and foot slip errors (b) on the narrow beam test at 0, 1, 3, and 7 days after MPTP induction. Each data column represents the mean ± SD (n = 8/group, o-p < 0.01 compared with the control group; #-p < 0.05 compared with the vehicle-treated group; *-p < 0.05 compared with the Tidomet Plus-treated group)
Fig. 4
Fig. 4
Effect of AGME on resting tremor score (a) and swimming score (b) at 0, 1, 3, and 7 days after MPTP administration. Each data column represents the mean ± SD (n = 8/group, o-p < 0.01 compared with the control group; #-p < 0.05 compared with the vehicle-treated group; *-p < 0.05 compared with the Tidomet Plus-treated group)
Fig. 5
Fig. 5
Effect of AGME on retention time on the rotarod apparatus at 0, 1, 3, and 7 days after MPTP administration. Each data column represents the mean ± SD (n = 8/group, o-p < 0.001 compared with the control group; #-p < 0.05 compared with the vehicle-treated group; *-p < 0.05 compared with the Tidomet Plus-treated group)
Fig. 6
Fig. 6
Effect of AGME on the MPTP-induced decrease in TH immunostaining in the substantia nigra of mice. (A) Representative microphotographs showing the control group (a), the vehicle (NSS) + MPTP group (b), the Tidomet Plus (25 mg/kg BW) + MPTP group (c), the AGME (125 mg/kg BW) + MPTP group (d), the AGME (250 mg/kg BW) + MPTP group (e), the AGME (375 mg/kg BW) + MPTP group (f), and a negative control without anti-TH antibody (g)
Fig. 7
Fig. 7
The effect of AGME on the number of TH-immunopositive neurons in the substantia nigra after MPTP administration. The numbers of TH-positive neurons are expressed as the mean ± S.D., (n = 4/group), o-p < 0.01 compared with the control group; #-p < 0.05 compared with the MPTP/vehicle treatment group, *-p < 0.05 compared to the Tidomet Plus+MPTP treatment group
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