Introduction
Moringa oleifera (Lam), commonly known as “Kelor” in Indonesia, is a member of the Moringaceae family that has been utilized for both nutritional and medicinal purposes across Asia, particularly in Indonesia. Every part of this plant—including leaves, seeds, pods, roots, stems, and bark—can be processed into various forms such as powders, suspensions, oils for oral consumption, and creams for topical application. The leaves of M. oleifera are particularly valued for their high nutritional content, making them a staple in many diets.
Research has highlighted the numerous health benefits associated with M. oleifera, including its antioxidant and neuroprotective properties. These effects are largely attributed to the diverse phytochemical constituents found in the plant, such as tannins, sterols, saponins, terpenoids, phenolics, alkaloids, and flavonoids. While much of the existing literature focuses on the leaves, there is a growing interest in the pharmacological potential of other parts of the plant, particularly the seeds.
Recent studies have indicated that extracts from M. oleifera leaves can ameliorate cognitive deficits and enhance memory function, particularly in models of neurodegeneration. However, there is a notable gap in comparative studies examining the neuropharmacological effects of different M. oleifera formulations. This article aims to explore the neuroprotective effects of both M. oleifera leaf extract (MOE) and M. oleifera seed oil (MOO) in the context of memory impairment induced by scopolamine (Sco), a common model for studying cognitive dysfunction.
Methods
Plant Material
The MOE was obtained from PT Javaplant (Solo, Indonesia) and prepared using an aqueous extraction method. The MOO was sourced from PT Kelorina (Medan, Indonesia), where fresh seeds were dried, blended, and subjected to oil extraction under controlled temperature and pressure conditions.
Phytochemical Screening
Qualitative phytochemical analyses were conducted on MOE to identify the presence of various compounds, including alkaloids, flavonoids, saponins, anthraquinones, and tannins. The methods employed were based on established protocols to ensure reliability.
Gas Chromatography-Mass Spectrometry (GC-MS) Analysis
GC-MS analysis of MOO was performed to identify and quantify the active phytochemical compounds present in the oil. The analysis revealed a diverse array of compounds, including fatty acids and sterols, which are believed to contribute to the oil’s pharmacological properties.
Animal Study
A total of twenty male BALB/c mice were used for the study. The mice were divided into four groups: a normal control group, a Sco group receiving only Sco, a Sco+MOE group receiving MOE, and a Sco+MOO group receiving MOO. Behavioral tests, including the Y-maze and Novel Object Recognition (NOR) tests, were conducted to assess memory function.
Behavioral Studies
The Y-maze test evaluated spatial memory, while the NOR test assessed recognition memory. Both tests were designed to exploit the natural exploratory behavior of mice, allowing for an objective measure of cognitive function.
Biochemical Analysis
Post-behavioral testing, the mice were sacrificed, and their hippocampi were collected for biochemical analysis. Acetylcholinesterase (AChE) activity, total antioxidant capacity (TAC), and protein expression levels of key neurotrophic factors were measured to elucidate the underlying mechanisms of action.
Results
Phytochemical Analysis
The qualitative analysis of MOE confirmed the presence of several bioactive compounds, including flavonoids and saponins, which are known for their antioxidant and neuroprotective properties. The GC-MS analysis of MOO identified 26 active compounds, with palmitic acid, oleic acid, and stigmasterol being the most prevalent.
Memory Impairment and Recovery
The administration of Sco resulted in significant memory impairment in the Y-maze and NOR tests, as evidenced by reduced spontaneous alternation and investigation time of novel objects. However, pretreatment with MOO significantly restored memory function, suggesting its superior neuroprotective effect compared to MOE.
Biochemical Mechanisms
MOO treatment effectively reduced AChE activity, indicating a restoration of cholinergic function. Additionally, MOO was associated with a decrease in TAC levels, suggesting a potential antioxidant effect. Notably, MOO also tended to downregulate NF-κB expression, a key player in neuroinflammation, while enhancing TrkB and CREB signaling pathways, which are crucial for neurogenesis and memory function.
Discussion
This study provides compelling evidence for the neuroprotective effects of Moringa oleifera, particularly its seed oil, in mitigating memory impairment induced by scopolamine. The findings highlight the importance of exploring different formulations of M. oleifera to fully understand their therapeutic potential. The distinct phytochemical profiles of MOE and MOO may contribute to their varying effects on cognitive function, with MOO demonstrating a more pronounced ability to restore memory and reduce neuroinflammation.
The results underscore the need for further research to elucidate the specific mechanisms by which M. oleifera exerts its neuroprotective effects, particularly in the context of oxidative stress and cholinergic dysfunction. Future studies should also investigate the pharmacokinetics of these formulations to determine their efficacy in crossing the blood-brain barrier and achieving therapeutic concentrations in the brain.
Conclusion
In conclusion, Moringa oleifera seed oil shows significant promise as a neuroprotective agent, particularly in the context of memory impairment. Its ability to modulate cholinergic activity, reduce oxidative stress, and inhibit neuroinflammatory pathways positions it as a potential therapeutic candidate for cognitive disorders. Further exploration of its pharmacological properties and mechanisms of action is warranted to fully harness its benefits in neuroprotection and cognitive enhancement.
Data Availability Statement
The original contributions presented in this study are included in the article/supplementary material. Further inquiries can be directed to the corresponding author.
Ethics Statement
The animal study was reviewed and approved by the Komite Etik Penelitian Kesehatan Faculty of Medicine of Universitas Indonesia.
Author Contributions
WA, HL, AB, and AM designed the experiment, analyzed the data, and wrote the manuscript. WA, EP, HL, and AB conducted the experiments and contributed to the data analysis. All authors contributed to the article and approved the final submitted version.
Funding
This research was supported by grants from HIBAH PUTI DOKTOR 2020, Universitas Indonesia, Indonesia (NKB-573/UN.2.RST/HKP.05.00/2020), and Kangwon National University (2019), Republic of Korea.
Conflict of Interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Publisher’s Note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors, and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Acknowledgments
The authors thank Puspita E. Wuyung, Chiswita Halida, and Annisa for their excellent technical assistance.
References
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