Background: Generation of reactive oxygen species together with paucity of antioxidant defense is considered as an important cause for dopaminergic neuronal death. Review of literature indicates that none of the drugs so far studied for preventing the PD were found to be promising for use. Therefore, the present study was planned to evaluate the neuroprotective effect of Paeonia emodi Wall (PEW) in 6-hydroxy dopamine induced Parkinson’s disease (PD) model.Methods: The study was conducted on Wistar rats where Parkinson’s disease was induced by producing the striatal 6-hydroxy dopamine lesions. The test animals received ethanolic extract of PEW at dose of 200 and 300mg/kg for 28 days. Circling behavior, spontaneous locomotor activity, muscular coordination and akinesia were studied. Antioxidant levels were assessed by biochemical estimation and histopathology was carried out for dopaminergic neuronal loss.Results: PEW ethanolic extract showed significant dose dependent recovery in number of circlings, line crossing, muscular coordination and akinesia. A significant increase in MDA levels and decreased GSH level in PEW treated groups was observed in test groups as compared to control group (p<0.05). Normal architecture was retained only in PEW 300mg/Kg (p<0.05). L-Dopa did not showed effect on biochemical and histological parameters.Conclusions: The ethanolic extract of PEW showed neuroprotective activity against 6-hydroxy dopamine induced Parkinson’s disease in rats in both 200 and 300mg/kg doses. The protective action of PEW in PD can be because of its ability to reduce the oxidative stress.
Purpose
Parkinson's disease (PD) is the most common age‐related neurodegenerative disease worldwide. S‐adenosyl methionine (SAMe), a methyl donor that plays an important role in DNA methylation, could replenish the cellular antioxidant glutathione (GSH). Herein, we investigated the neuroprotective effects of SAMe in 6‐hydroxydopamine (6‐OHDA) rat models of PD and elucidated the underlying mechanism.
Methods
PD model rats were developed by injecting 6‐OHDA stereotaxically into the striatum. In Phase 1 of the study, we performed the neurobehavioral tests, GSH assay, and histopathology to evaluate the neuroprotective effects of SAMe. The animals were treated with SAMe (150 or 300 mg/kg body weight) orally for 28 days. The positive control group received selegiline (5 mg/kg), whereas the disease control group received normal saline.
In Phase 2, we evaluated the striatal dopamine levels and performed DNA methylation assay to uncover the mechanism of action of SAMe. In this phase, a higher dose of SAMe (300 mg/kg) was used.
Results
SAMe (300 mg/kg) treatment for 4 weeks significantly attenuated the abnormal circling behavior in PD rats (p < 0.05). Moreover, SAMe at both doses (150 and 300 mg/kg) enhanced the performance of PD rats in the open field test and stepping test (p < 0.05). SAMe treatment significantly increased the GSH levels, and at high dose, SAMe restricted neuronal loss in the striatum of PD‐model rats (p < 0.05). Moreover, SAMe treatment led to a significant recovery in the dopamine levels and improved the DNA methylation status in the dopaminergic neurons (p < 0.05) of PD model rats.
Conclusion
SAMe exhibits antioxidant activity and DNA methylation modulating effects in 6‐OHDA model PD rats. Moreover, SAMe prevents neuronal loss in PD rats suggesting that SAMe has therapeutic potential in preventing PD development. The neuroprotective potential of SAMe is greater at high doses.
Background & objectives:Standard treatment guidelines (STGs) are the cornerstone to therapeutics. Multiple agencies in India develop STGs. This systematic review was conducted to find out STGs available in India, evaluate if these were as per World Health Organization (WHO) recommendations for STGs and compare these with National Institute for Health and Care Excellence (NICE) guidelines. Information on legal authority and responsibility for formulating STGs was also sought.Methods:PRISMA guidelines were followed. Publications from PubMed and Google Scholar were searched for STGs using terms 'Standard Treatment Guidelines AND India'. Data from STGs were compiled in excel as per the WHO and authors' criteria for STGs and compared with NICE guidelines.Results:PubMed and Google Scholar search provided 56 publications (out of 1695 search results) mentioning 27 STGs. Google search and replies from authors led us 36 STGs, totalling to 63 STGs. No STG mentioned any specific period of revision, eight STGs were not evidence-based, 55 had some Indian references, 48 STGs were for single disease and the remaining multi-disease, three STGs did not include diagnostic criteria, 16 STGs did not give prescribing information of recommended treatment and 16 STGs provide no referral criteria for patients. Fifty five STGs did not mention level of health care. While NICE is a single legal authority in England and guidelines are as per WHO recommendations for STGs, in India although Acts and rules do not vest authority, National Health Systems Resource Center is generally designated responsible for STGs.Interpretation & conclusions:In India, although there are multiple STGs developed by various authorities and professionals for the same conditions, these fulfil WHO recommendations only partially. Authority with statutory duty collaborating with professional organizations, a standard methodology for adopting international guidelines, Indian data for evidence base, attention to local needs will help in developing better STGs and their acceptance.
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