Research Article
Received: 2023-01-22 | Revised:2023-02-20 | Accepted: 2023-02-22 | Published: 2023-03-01
Pages: 26-33
DOI: https://doi.org/10.58985/jddb.2023.v01i01.05
Abstract
Alzheimer’s disease (AD) is a progressive loss of neurons, caused by impaired activity of many enzymes involved in normal brain physiology. Active research has shown promising counter effects on AD symptoms by medicinal plant extracts. Our current study investigates the disease-modifying potential of Chlorogenic acid against multiple targets involved in AD by inhibiting the key enzymes in AD pathophysiology, such as acetylcholinesterase (AChE), Butyrylcholinesterase (BuChE), β-APP cleaving enzyme 1 (BACE1) and monoaminoxidase-B (MAO-B). UPLC-QTOF analysis of the hydroalcoholic root extract of Nardostachys jatamansi showed the presence of polyphenols mainly. The most abundant m/z 359.03 corresponds to the peak of chlorogenic acid. It was further validated and quantified using novel RP-HPLC method. The chlorogenic acid inhibited AChE and BuChE to 58% and 40% respectively in concentration dependent manner. The percentage inhibition for BACE1 was reported to be 41% at 50μM whereas, chlorogenic acid inhibited MAO-B enzyme very strongly and significantly at 40μM (88%). The in vitro experimentation showed complementarity with in silico results, where strong molecular interactions of chlorogenic acid with target proteins- AChE, BuChE, BACE1, MAO-B and Aβ 42 was observed. Thus chlorogenic acid could be developed as MTDL candidate against factors implicated in AD.
Keywords
Chlorogenic acid; Nardostachys jatamansi; Alzheimer’s disease; BACE1;
Neuroprotection; MAO-B; Molecular docking
Abstract
Alzheimer’s disease (AD) is a progressive loss of neurons, caused by impaired activity of many enzymes involved in normal brain physiology. Active research has shown promising counter effects on AD symptoms by medicinal plant extracts. Our current study investigates the disease-modifying potential of Chlorogenic acid against multiple targets involved in AD by inhibiting the key enzymes in AD pathophysiology, such as acetylcholinesterase (AChE), Butyrylcholinesterase (BuChE), β-APP cleaving enzyme 1 (BACE1) and monoaminoxidase-B (MAO-B). UPLC-QTOF analysis of the hydroalcoholic root extract of Nardostachys jatamansi showed the presence of polyphenols mainly. The most abundant m/z 359.03 corresponds to the peak of chlorogenic acid. It was further validated and quantified using novel RP-HPLC method. The chlorogenic acid inhibited AChE and BuChE to 58% and 40% respectively in concentration dependent manner. The percentage inhibition for BACE1 was reported to be 41% at 50μM whereas, chlorogenic acid inhibited MAO-B enzyme very strongly and significantly at 40μM (88%). The in vitro experimentation showed complementarity with in silico results, where strong molecular interactions of chlorogenic acid with target proteins- AChE, BuChE, BACE1, MAO-B and Aβ 42 was observed. Thus chlorogenic acid could be developed as MTDL candidate against factors implicated in AD.
Keywords
Chlorogenic acid; Nardostachys jatamansi; Alzheimer’s disease; BACE1;
Neuroprotection; MAO-B; Molecular docking
References
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Abstract
Alzheimer’s disease (AD) is a progressive loss of neurons, caused by impaired activity of many enzymes involved in normal brain physiology. Active research has shown promising counter effects on AD symptoms by medicinal plant extracts. Our current study investigates the disease-modifying potential of Chlorogenic acid against multiple targets involved in AD by inhibiting the key enzymes in AD pathophysiology, such as acetylcholinesterase (AChE), Butyrylcholinesterase (BuChE), β-APP cleaving enzyme 1 (BACE1) and monoaminoxidase-B (MAO-B). UPLC-QTOF analysis of the hydroalcoholic root extract of Nardostachys jatamansi showed the presence of polyphenols mainly. The most abundant m/z 359.03 corresponds to the peak of chlorogenic acid. It was further validated and quantified using novel RP-HPLC method. The chlorogenic acid inhibited AChE and BuChE to 58% and 40% respectively in concentration dependent manner. The percentage inhibition for BACE1 was reported to be 41% at 50μM whereas, chlorogenic acid inhibited MAO-B enzyme very strongly and significantly at 40μM (88%). The in vitro experimentation showed complementarity with in silico results, where strong molecular interactions of chlorogenic acid with target proteins- AChE, BuChE, BACE1, MAO-B and Aβ 42 was observed. Thus chlorogenic acid could be developed as MTDL candidate against factors implicated in AD.
Abstract Keywords
Chlorogenic acid; Nardostachys jatamansi; Alzheimer’s disease; BACE1;
Neuroprotection; MAO-B; Molecular docking
This work is licensed under the
Creative Commons Attribution
4.0
License (CC BY-NC 4.0).
This work is licensed under the
Creative Commons Attribution 4.0
License.(CC BY-NC 4.0).