Extract of Hypericum perforatum blocks caffeine-induced locomotor activity in mice: a possible role of nitric oxide

I Tayfun Uzbay1, Ilke Coskun, Hakan Kayir

  • 1Department of Medical Pharmacology, Psychopharmacology Research Unit, Faculty of Medicine, Gulhane Military Medical Academy, Ankara, Turkey. tuzbay@gata.edu.tr

Insights

Herbal পদার্থ নির্যাস (HPE) caffeine-induced locomotor hyperactivity in mice-কে বাধা দেয়। এই প্রভাবটি nitric oxide synthase (NOS) inhibition-এর সাথে সম্পর্কিত হতে পারে, কারণ l-arginine এটি বিপরীত করে।

Area of Science:

  • Pharmacology
  • Neuroscience
  • Ethnobotany

Background:

  • Caffeine is a widely consumed stimulant known to increase locomotor activity.
  • Understanding the mechanisms behind caffeine's effects and potential modulators is crucial for pharmacology.
  • Herbal preparations are often explored for their bioactive compounds and physiological effects.

Purpose of the Study:

  • To investigate the effects of Herbal পদার্থ নির্যাস (HPE) on caffeine-induced locomotor activity in mice.
  • To determine if HPE can counteract the stimulant effects of caffeine.
  • To explore the potential role of nitric oxide synthase (NOS) in HPE's action.

Main Methods:

  • Adult male Swiss-Webster mice were used in the study.
  • Locomotor activity was measured after administration of caffeine, HPE, or saline.
  • HPE was administered both alone and before caffeine, with and without l-arginine pretreatment.

Main Results:

  • Caffeine significantly increased locomotor activity in mice.
  • HPE (6-24 mg/kg) demonstrated a significant inhibitory effect on caffeine-induced hyperactivity.
  • Pretreatment with l-arginine reversed the inhibitory effect of HPE, suggesting a role for NOS.

Conclusions:

  • Herbal পদার্থ নির্যাস (HPE) effectively blocks caffeine-induced locomotor hyperactivity in mice.
  • The inhibitory action of HPE on caffeine's effects may be linked to its nitric oxide synthase (NOS) inhibitory properties.
  • Further research into HPE's pharmacological profile and NOS interaction is warranted.

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...
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
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...
Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates,  such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...
Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants


Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
Drugs Acting on Autonomic Ganglia: Blockers01:28

Drugs Acting on Autonomic Ganglia: Blockers

Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups: