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Neuroprotective effects of Embelin in an ethidium bromide-induced multiple sclerosis in rats: Modulation of p38 MAPK
Anika1, Shamsher Singh1, Rimpi2
1Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab 142001, India.
Background:
Multiple sclerosis (MS) is a debilitating inflammatory disease characterized by demyelination, varied remyelination conservation, and partial axonal retention in central nervous system (CNS) lesions. The p38 mitogen-activated protein kinase (MAPK) pathway has been implicated in the pathophysiology of MS. Embelin (EMB), derived from the Embelia ribes plant, possesses diverse biological activities, including anti-inflammatory properties.
Objective:
This study aimed to investigate the neuroprotective effects of EMB in an ethidium bromide (EB)-induced model of MS in Wistar rats.
Methods:
Wistar rats were randomly divided into five groups (n = 8). MS-like manifestations were induced by injecting EB (0.1 %/10 µl) into the intracerebropeduncle (ICP) region of the rat brain for seven consecutive days. EMB was administered at doses of 1.25, 2.5, and 5 mg/kg. Behavioral assessments, neuroinflammatory cytokine analysis like tumor necrosis factor-α, interleukin-1-β, interleukin-6 (TNF-α, IL-1β, IL-6), oxidative stress marker measurements malondialdehyde, reduced glutathione, superoxide dismutase (MDA, GSH, SOD), and nitrite (NO), Acetylcholinesterase enzyme (AchE), and neurotransmitter level analysis, dopamine, serotonin, and norepinephrine (DA, 5-HT, and NE) were conducted.
Results:
The study assessed behavioral, neurochemical, biochemical, and neuroinflammatory parameters, along with the modulation of p38 MAPK signaling. EMB administration significantly ameliorated neurological consequences induced by EB, improving motor coordination and gait abnormalities in rats. Furthermore, EMB effectively reduced neuroinflammatory cytokines (TNF-α, IL-1β, IL-6) and oxidative stress markers (AchE, SOD, MDA, GSH, nitrite). Notably, EMB exhibited a modulatory effect on neurotransmitter levels, increasing GABA, DA, and 5-HT, while reducing glutamate in EB-treated groups.
Conclusion:
This study demonstrates the neuroprotective potential of EMB against the EB-induced model of MS in rats. EMB administration mitigated neurological impairments, attenuated neuroinflammation, alleviated oxidative stress, and restored neurotransmitter balance. These findings highlight the promise of EMB as a therapeutic candidate for MS treatment, providing insights into its potential mechanism of action involving the modulation of p38 MAPK signaling.
Insights
Embelin (EMB) shows neuroprotective effects in a rat model of multiple sclerosis (MS). EMB treatment reduced neurological deficits, inflammation, and oxidative stress, offering potential for MS therapy.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Multiple sclerosis (MS) is a central nervous system (CNS) inflammatory disease impacting myelin and axons.
- The p38 mitogen-activated protein kinase (MAPK) pathway is implicated in MS pathophysiology.
- Embelin (EMB), from Embelia ribes, exhibits anti-inflammatory properties.
Purpose of the Study:
- To investigate the neuroprotective effects of Embelin (EMB).
- To evaluate EMB's efficacy in an ethidium bromide (EB)-induced rat model of MS.
Main Methods:
- Wistar rats were induced with MS-like symptoms using EB.
- Rats received varying doses of EMB (1.25, 2.5, 5 mg/kg).
- Evaluated behavioral, neuroinflammatory (TNF-α, IL-1β, IL-6), oxidative stress (MDA, GSH, SOD, NO), and neurotransmitter (GABA, DA, 5-HT, glutamate) markers.
Main Results:
- EMB administration significantly improved motor coordination and gait in EB-treated rats.
- EMB reduced key neuroinflammatory cytokines and oxidative stress markers.
- EMB modulated neurotransmitter levels, increasing GABA, dopamine, and serotonin while decreasing glutamate.
Conclusions:
- Embelin (EMB) demonstrates significant neuroprotective potential in an MS rat model.
- EMB mitigated neurological impairments, neuroinflammation, and oxidative stress.
- EMB may offer a therapeutic strategy for MS by modulating p38 MAPK signaling and restoring neurotransmitter balance.
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