Pharmacological properties of phospholipid liposomes

Toffano, G.; Bruni, A.

doi:10.1016/s0031-6989(80)80046-4

Cited by 56 publications

(5 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, it has been shown that chronic treatment with PS is able to restore the electricallyevoked acetylcholine release from cortical slices in 24 month-old rats (Pepeu et al, 1986), to increase the sensitivity of pituitary dopamine receptors to dopamine in aged rats (Di Renzo et al, 1987), and to reduce the number of ECoG power changes and epileptic spikes observed in old rats (De Sarro et al, 1987b). A reduction of prolactin secretion in rat lactotrophs during aging was also obtained after chronic treatment with PS (Toffano & Bruni, 1980;Zauli et al, 1984;Toffano, 1985). The changes in lactotrophs membrane fluidity during aging has been shown to affect phosphatidylinositol (PI) metabolism; PS was found to reduce in vitro 32P incorporation into PI and such an effect was associated with the inhibition of prolactin secretion (Bonetti et al, 1987).…”

Section: Discussionmentioning

confidence: 95%

Microinfusion of clonidine and yohimbine into locus coeruleus alters EEG power spectrum: effects of aging and reversal by phosphatidylserine

Sarro

Bagetta

Ascioti³

et al. 1988

British J Pharmacology

View full text Add to dashboard Cite

1 The behavioural and electrocortical (ECoG) power spectrum effects of clonidine, and yohimbine, an agonist and an antagonist at a2-adrenoceptors, after their unilateral microinfusion into the rat locus coeruleus (LC) in young (50-70 days old) and old (13-15 months old) rats were studied. 2 Clonidine (0.09, 0.19, 0.28 and 0.56 nmol) microinfused into the LC of young rats induced dosedependent behavioural and ECoG slow wave sleep (SWS) with a significant increase in total voltage power and power in the lower frequency bands. In contrast, yohimbine (1.3 and 2.6 nmol) infused into the LC of young rats produced ECoG desynchronization and a significant decrease in total voltage power. 3 In contrast to young rats, clonidine (0.19 and 0.28 nmol) given into the LC did not affect behaviour and the ECoG power spectrum in old rats. However, after higher doses of clonidine (0.56 and 1.2 nmol) a small and short-lasting period of behavioural and ECoG SWS was still evident. Similarly, in old rats yohimbine, at a dose (1.3 nmol) which was stimulative in young animals, did not significantly affect behaviour and ECoG power spectrum. Higher doses of yohimbine (2.6 and 5.2 nmol) were required to induce behavioural and ECoG changes similar to those observed with lower doses of yohimbine in young rats. 4 Chronic treatment with phosphatidylserine (30mgkg 1, orally, daily for 21 and 30 days), was able gradually to restore in old rats, in comparison with a vehicle-treated group, the responsiveness of a2-adrenoceptors to clonidine and yohimbine given into the LC.

show abstract

Section: Discussionmentioning

confidence: 95%

Microinfusion of clonidine and yohimbine into locus coeruleus alters EEG power spectrum: effects of aging and reversal by phosphatidylserine

Sarro

Bagetta

Ascioti³

et al. 1988

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…A myriad of proteins have been identified that require PtdSer for optimal activity (for a review consult Toffano and Bruni (1980)); of which, a number might have specific relevance to physiological function during exercise. Phosphatidylserine is the most effective phospholipid in activating the conventional isoforms of protein kinase C (Takai et al, 1979), which undertake crucial functions in diverse signal transduction pathways (Nishijima et a l, 1986).…”

Section: Enzyme Cofactormentioning

confidence: 99%

Effects of Phosphatidylserine Supplementation on Exercising Humans

Kingsley

2006

Sports Medicine

View full text Add to dashboard Cite

Phosphatidylserine (PtdSer) is a ubiquitous phospholipid species that is normally located within the inner leaflet of the cell membrane. PtdSer has been implicated in a myriad of membrane-related functions. As a cofactor for a variety of enzymes, PtdSer is thought to be important in cell excitability and communication. PtdSer has also been shown to regulate a variety of neuroendocrine responses that include the release of acetylcholine, dopamine and noradrenaline. Additionally, PtdSer has been extensively demonstrated to influence tissue responses to inflammation. Finally, PtdSer has the potential to act as an effective antioxidant, especially in response to iron-mediated oxidation. The majority of the available research that has investigated the effects of PtdSer supplementation on humans has concentrated on memory and cognitive function; patients experiencing some degree of cognitive decline have traditionally been the main focus of investigation. Although investigators have administered PtdSer through intravenous and oral routes, oral supplementation has wider appeal. Indeed, PtdSer is commercially available as an oral supplement intended to improve cognitive function, with recommended doses usually ranging from 100 to 500 mg/day. The main sources that have been used to derive PtdSer for supplements are bovine-cortex (BC-PtdSer) and soy (S-PtdSer); however, due to the possibility of transferring infection through the consumption of prion contaminated brain, S-PtdSer is the preferred supplement for use in humans. Although the pharmacokinetics of PtdSer have not been fully elucidated, it is likely that oral supplementation leads to small but quantifiable increases in the PtdSer content within the cell membrane.A small number of peer-reviewed full articles exist that investigate the effects of PtdSer supplementation in the exercising human. Early research indicated that oral supplementation with BC-PtdSer 800 mg/day moderated exercise-induced changes to the hypothalamo-pituitary-adrenal axis in untrained participants. Subsequently, this finding was extended to suggest that S-PtdSer 800 mg/day reduced the cortisol response to overtraining during weight training while improving feeling of well-being and decreasing perceived muscle soreness. However, equivocal findings from our laboratory might suggest that the dose required to undertake this neuroendocrine action may vary between participants.Interestingly, recent findings demonstrating that short-term supplementation with S-PtdSer 750 mg/day improved exercise capacity during high-intensity cycling and tended to increase performance during intermittent running might suggest an innovative application for this supplement. With the findings from the existing body of literature in mind, this article focuses on the potential effects of PtdSer supplementation in humans during and following exercise.

show abstract

“…On the other hand, there is extensive preclinical and clinical evidence that hypothalamic phospholipid liposomes increase monoaminergic neurotransmission, as shown by the activation of tyrosine hydroxylase (the rate-limiting enzyme in the synthetic pathway of dopamine and other catecholamines); the increase in monoamines turnover and release; the stimulation of the dopamine-dependent adenylyl cyclase and the increase in dopamine metabolite levels in human cerebrospinal fluid (CSF); the decrease in prolactin secretion through dopamine agonist activity (dopamine being the main inhibitor of the prolactin synthesis and release); and, finally, the modification of the receptor adaptation of central aminergic neurons to chronic treatment with antidepressants [47,48,[58][59][60][61]. The monoaminergic effect of hypothalamic phospholipid liposomes renders them highly relevant for the treatment of fatigue, where a dopaminergic effect is particularly needed, as well as for the treatment of other COVID-19 neuropsychiatric sequalae, such as anxiety and depression.…”

Section: The Monoaminergic Hypothesismentioning

confidence: 99%

The Potential Role of Hypothalamic Phospholipid Liposomes in the Supportive Therapy of Some Manifestations of Post-COVID-19 Condition: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Brain Fog

Menichetti

2023

JCM

View full text Add to dashboard Cite

Post-COVID-19 condition (commonly known as Long COVID) is a heterogeneous clinical condition in which Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and brain fog stand out among the different clinical symptoms and syndromes. Cerebral metabolic alterations and neuroendocrine disorders seem to constitute an important part of the pathophysiology of Post-COVID-19 condition (PCC). Given the substantial lack of specific drugs and effective therapeutic strategies, hypothalamic phospholipid liposomes, which have been on the market for several years as adjuvant therapy for cerebral metabolic alterations resulting from neuroendocrine disorders, might represent a potential option in an overall therapeutic strategy that aims to control PCC-associated symptoms and syndromes. Their pharmacological mechanisms and clinical effects strongly support their potential effectiveness in PCC. Our initial clinical experience seems to corroborate this rationale. Further controlled clinical research is warranted in order to verify this hypothesis.

show abstract

Pharmacological properties of phospholipid liposomes

Cited by 56 publications

References 42 publications

Microinfusion of clonidine and yohimbine into locus coeruleus alters EEG power spectrum: effects of aging and reversal by phosphatidylserine

Microinfusion of clonidine and yohimbine into locus coeruleus alters EEG power spectrum: effects of aging and reversal by phosphatidylserine

Effects of Phosphatidylserine Supplementation on Exercising Humans

The Potential Role of Hypothalamic Phospholipid Liposomes in the Supportive Therapy of Some Manifestations of Post-COVID-19 Condition: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Brain Fog

Contact Info

Product

Resources

About