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Beta-Boswellic Acid Reverses 3-Nitropropionic Acid-Induced Molecular, Mitochondrial, and Histopathological Defects in
Thamer H Albekairi1, Arzoo Kamra2, Sudeep Bhardwaj2
1Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia.
Insights
Beta Boswellic acid (β-BA) and vitamin E show neuroprotective effects in Huntington
Area of Science:
- Neuroscience
- Neuropharmacology
- Biochemistry
Background:
- Huntington's disease (HD) is a neurodegenerative disorder characterized by CAG repeat expansion in the Htt gene, leading to neuronal loss in the striatum and cortex.
- Mitochondrial dysfunction, specifically involving the electron transport chain (ETC) complexes, is a key factor in HD pathogenesis, contributing to neuronal energy deficits, inflammation, and cell death.
- Beta Boswellic acid (β-BA), a natural phytochemical, has demonstrated neuroprotective properties relevant to various neurological conditions.
Purpose of the Study:
- To investigate the neuroprotective potential of β-BA, alone and in combination with vitamin E, in a 3-nitropropionic acid (3-NP)-induced rat model of Huntington's disease.
- To evaluate the effects of β-BA on mitochondrial ETC complex activity, neurotransmitter levels, oxidative stress, and neuroinflammation in the context of HD.
Main Methods:
- Adult Wistar rats were administered 3-NP (10 mg/kg) daily for 14 days to induce HD-like pathology.
- Experimental groups received varying oral doses of β-BA (5, 10, 15 mg/kg) and/or vitamin E (8 mg/kg).
- Evaluations included behavioral assessments, biochemical analysis of brain homogenates (ETC complex activity, neurotransmitters, oxidative stress markers), and histopathological examination of striatum and cortex.
Main Results:
- 3-NP administration exacerbated HD symptoms, including impaired motor function, cognitive deficits, and suppressed ETC-complex-II activity.
- Co-administration of β-BA and vitamin E significantly improved behavioral impairments and restored levels of ETC complexes I, II, and V.
- β-BA treatment normalized neurotransmitter levels, reduced inflammatory cytokines and oxidative stress biomarkers, and mitigated neuronal loss in the striatum and cortex.
Conclusions:
- Beta Boswellic acid (β-BA), particularly when combined with vitamin E, demonstrates significant neuroprotective effects against 3-NP-induced neurodegeneration in rats.
- β-BA ameliorates HD pathology by restoring mitochondrial function, balancing neurotransmitter levels, reducing oxidative stress and inflammation, and preventing neuronal death.
- These findings highlight the therapeutic potential of natural phytochemicals like β-BA as a preventative strategy for neurological disorders such as Huntington's disease.
Abstract:
Huntington's disease (HD) is distinguished by a triple repeat of CAG in exon 1, an increase in poly Q in the Htt gene, and a loss of GABAergic medium spiny neurons (MSN) in the striatum and white matter of the cortex. Mitochondrial ETC-complex dysfunctions are involved in the pathogenesis of HD, including neuronal energy loss, synaptic neurotrophic decline, neuronal inflammation, apoptosis, and grey and white matter destruction. A previous study has demonstrated that beta Boswellic acid (β-BA), a naturally occurring phytochemical, has several neuroprotective properties that can reduce pathogenic factors associated with various neurological disorders. The current investigation aimed to investigate the neuroprotective potential of β-BA at oral doses of 5, 10, and 15 mg/kg alone, as well as in conjunction with the potent antioxidant vitamin E (8 mg/kg, orally) in 3-NP-induced experimental HD rats. Adult Wistar rats were separated into seven groups, and 3-NP, at a dose of 10 mg/kg, was orally administered to each group of adult Wistar rats beginning on day 1 and continuing through day 14. The neurotoxin 3-NP induces neurodegenerative, g, neurochemical, and pathological alterations in experimental animals. Continuous injection of 3-NP, according to our results, aggravated HD symptoms by suppressing ETC-complex-II, succinate dehydrogenase activity, and neurochemical alterations. β-BA, when taken with vitamin E, improved behavioural dysfunctions such as neuromuscular and motor impairments, as well as memory and cognitive abnormalities. Pharmacological treatments with β-BA improved and restored ETC complexes enzymes I, II, and V levels in brain homogenates. β-BA treatment also restored neurotransmitter levels in the brain while lowering inflammatory cytokines and oxidative stress biomarkers. β-BA's neuroprotective potential in reducing neuronal death was supported by histopathological findings in the striatum and cortex. As a result, the findings of this research contributed to a better understanding of the potential role of natural phytochemicals β-BA in preventing neurological illnesses such as HD.
