Abstract
The present study was designed to explore the neuroprotective properties of Aconitum napellus (Ranunculaceae). The plant detoxification was done using either water, or cow or goat milk as per the Ayurvedic shodhana method. The evaluation of the neuroprotective role of A. napellus was performed on diabetic neuropathy induced by streptozotocin in Sprague Dawley (SD) rats. Body mass, blood sugar level, oral glucose tolerance test, hyperalgesia, cold allodynia, motor co-ordination test, and locomotor activity, oxidative biomarkers (TBARS, reduced glutathione, catalase and superoxide dismutase) and sciatic nerve histomorphology were assessed. The in vitro studies were done on human neuroblastoma cell line SHSY-5Y and used an MTT assay to assess the antiproliferative activity of different extracts. Results suggest that the goat milk treated chloroform extract has less percentage of aconitine. After administration of the detoxified chloroform extract to the diabetic animals, there was a significant improvement in the myelination and degenerative changes of the nerve fibers along with behavioral changes (p < 0.05 as compared with diabetic control group). The findings of the in vitro research show an effective neuroprotective role of A. napellus. This suggests that A. napellus should be further investigated for its effect in diabetic pathology.
Highlights
Neurodegeneration is the serious side effect of acute injuries or chronic irregular incidents of ischemia and hypoxia, which can generate oxidative stress and neuro-inflammation, eventually leading to neuropathy [1]
The current study shows that in HG-induced neuropathy the SHSY-5Y cells shows a significant elevation in reaction oxygen species level which leads to apoptosis and death as compared with normal glucose cells, our observation was in agreement with earlier studies [36]
GMT-treated groups have indicated a neuroprotective role by improving the nerve dysfunctioning in STZ induced diabetic neuropathy in an experimental animal model
Summary
Neurodegeneration is the serious side effect of acute injuries or chronic irregular incidents of ischemia and hypoxia, which can generate oxidative stress and neuro-inflammation, eventually leading to neuropathy [1]. Neuronal degradation after a long-term of non-treated or uncontrolled diabetes may lead to diabetic neuropathy (DN). DN is a disorder mainly coupled with diabetes mellitus, which may result in numerous clinical manifestations. There is a symmetrical degeneration of nerve fibers that. Plants 2020, 9, 356 affects motor and autonomic system. About 50% of the diabetic population develops neuropathy if left untreated or blood sugar levels are not controlled [2]. Oxidative nervous tension and construction of cytokines along with dysfunction in vascular tissues are significant aspects responsible for DN [3]
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