Abstract
BackgroundMulti-factorial etiology exists in pathophysiology of neurodegenerative diseases. The imbalance of anti-oxidant enzymes and dopamine level leads to Parkinsonism. The objective of this study was to assess the protective effect of Spirulina fusiform alone and in combination with amantadine against Parkinsonism effect in 6-hydroxydopamine (6-OHDA) induced rat model.MethodsS. fusiform was administered in different groups (500 mg/kg, once daily and twice daily) and a combination of spirulina (500 mg/kg, once daily) with amantadine (20 mg/kg once daily) for 30 days before and 14 days after a single injection of 6-OHDA into the dorsal striatum. Post lesion produced rotational behavior which was measured at two week intervals (37th and 44th day). Locomotors activity was also done at 44th and muscle coordination at 48th day. Dorsal striatum was isolated from rat brain for evaluating the antioxidant assays and dopamine content at 49th day.ResultsBoth the body rotations (ipsilateral and contralateral) were found to have a statistically significant (p < 0.001) decrease by 34.26 and 52 % after treatment with spirulina (Twice a day) in spirulina treated lesioned group. A higher percentage of improvement was shown in the reduction of ipsilateral (57.34 %) and contralateral (78.3 %) rotations in combination of spirulina with amantadine treated lesioned group rather than spirulina alone treated lesioned groups when compared with positive control lesioned group. Body movements and locomotor activity were improved statistically (p < 0.0001) significant in both treated lesioned groups (Combination of spirulina with amantadine and spirulina twice daily). Similar results were also seen in anti-oxidant levels which later on reached to the normal value. The levels of dopamine content had a statistically significant (p < 0.0001) increase by 78.3 % only in case of spirulina with amantadine treated lesioned group.ConclusionSpirulina is a potent nutraceutical supplement all over the world, so my preclinical study may contribute to give an additional adjuvant drug therapy in aging related disorders (Neurodegenerative as well as diabetes associated neurodegenerative disorders).Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-015-0815-0) contains supplementary material, which is available to authorized users.
Highlights
Multi-factorial etiology exists in pathophysiology of neurodegenerative diseases
Effect of Parkinsonism on behavior activity and its restoration by Spirulina fusiformis After post lesion, at 37th day, ipsilateral body rotations were increased by 70.62 % with amphetamine and 80.62 % contra lateral body rotations were produced by apomorphine on 44th day in the lesioned positive control group (Fig. 1) when compared with normal saline sham operated group
In activity chamber, lesioned positive control group showed a significantly declined in percentage (73.81 %) of locomotion activity when compared with normal saline sham operated group (Fig. 2)
Summary
The imbalance of anti-oxidant enzymes and dopamine level leads to Parkinsonism. Neurodegenerative disorders encompass a condition where nerve cells of different parts of brain and spinal cord vanish leading to either functional loss or sensory dysfunction [1]. Parkinson’s disease (PD) is second most prevalent neurological disorder that is characterized by progressive neurodegeneration affecting dopaminergic neurons in the negrostriatal pathway [2]. Some of the common causes which are responsible for etiology of this disorder include oxidative stress, mitochondrial damage, protein dysfunctions, and inflammation [1]. Parkinson’s disease is characterized by the significant degeneration of dopaminergic neurons in the substantia nigra pars compacta, which leads to the depletion of dopamine in its striatal projections and other brain stem neurons, with consequent disruption of the cerebral neuronal systems responsible for motor functions. Many studies claim that excessive generation of reactive oxygen species (ROS) and inflammation may play a central role in the neuropathology of PD [5]
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