Monoamine oxidase B (MAO-B) inhibition by active principles from Uncaria rhynchophylla

Wen-Chi Hou1, Rong-Dih Lin, Cheng-Tang Chen

  • 1Graduate Institute of Pharmacognosy, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan.

Insights

Two compounds from Uncaria rhynchophylla, (+)-catechin and (-)-epicatechin, inhibit monoamine oxidase B (MAO-B). This suggests potential neuroprotective benefits against oxidative neurodegeneration, warranting further investigation.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Ethnobotany

Background:

  • Monoamine oxidase B (MAO-B) activity is implicated in oxidative neurodegeneration.
  • MAO-B inhibitors are used in treating Parkinson's and Alzheimer's diseases.
  • Uncaria rhynchophylla is a traditional Chinese herb used for convulsive disorders.

Purpose of the Study:

  • To isolate and identify compounds from Uncaria rhynchophylla with MAO-B inhibitory activity.
  • To investigate the potential of these compounds in neuroprotection.

Main Methods:

  • Bioguided fractionation and purification of Uncaria rhynchophylla extracts.
  • Assay of rat brain MAO-B activity using electrophoresis.
  • Enzyme kinetics analysis using fluorescence method and Lineweaver-Burk plots.

Main Results:

  • (+)-Catechin and (-)-epicatechin were isolated from Uncaria rhynchophylla.
  • (+)-Catechin and (-)-epicatechin demonstrated dose-dependent inhibition of MAO-B.
  • IC(50) values were 88.6 microM for (+)-catechin and 58.9 microM for (-)-epicatechin.
  • K(i) values were 74 microM for (+)-catechin and 21 microM for (-)-epicatechin.

Conclusions:

  • (+)-Catechin and (-)-epicatechin are novel MAO-B inhibitors isolated from Uncaria rhynchophylla.
  • These compounds show potential for in vitro neuroprotection against oxidative stress.
  • Further research into their molecular mechanisms is warranted to explore health benefits.

Related Concept Videos

Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
Adrenergic Agonists: Chemistry and Structure-Activity Relationship01:16

Adrenergic Agonists: Chemistry and Structure-Activity Relationship

Adrenergic agonists' structure-activity relationship (SAR) determines their selectivity and efficacy. These agonists comprise a phenylethylamine moiety with an aromatic ring and an ethylamine side chain.
Aromatic ring substitutions: Substituting the aromatic ring with –OH groups at positions 3 and 4 yields catecholamines (e.g., epinephrine), which have a high affinity for adrenoceptors. Hydrogen bonding between –OH groups and receptors enhances adrenergic activity.
Separation of the aromatic...
Cholinergic Antagonists: Chemistry and Structure-Activity Relationship01:29

Cholinergic Antagonists: Chemistry and Structure-Activity Relationship

Cholinergic antagonists bind to cholinergic receptors and limit the effects of acetylcholine and other cholinergic agonists. Based on the specific cholinergic receptor affinity, these antagonists are classified as muscarinic or nicotinic. Anticholinergics interrupt parasympathetic innervations while sympathetic innervations remain uninterrupted. Muscarinic antagonists are also called 'muscarinic antagonists', 'antimuscarinics', or 'parasympatholytics'. Nicotinic antagonists are called...
Antidepressant Drugs: MAOIs and Other Agents01:23

Antidepressant Drugs: MAOIs and Other Agents

Atypical antidepressants, including bupropion (Wellbutrin), mirtazapine (Remeron), nefazodone (Serzone), trazodone (Desyrel), and vilazodone (Viibryd), offer unique mechanisms of action. Bupropion weakly inhibits dopamine and norepinephrine reuptake, aiding depression treatment and smoking cessation, with a low risk of sexual dysfunction. Mirtazapine enhances serotonin and norepinephrine neurotransmission, leading to sedation, increased appetite, and weight gain. As a result, it helps treat...
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...