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Active ingredient: 1 ampoule contains delta-sleep peptide (0.0003 g) 0.3 mg;
Bioregulator DELLIN - is produced in the form of ampoules with odorless lyophilized powder. It is highly soluble in water. The ampoule contains 0.3 mg of the delta-sleep-inducing peptide DSIP and the rest is a specially selected mixture of glycine, turine, L-carnosine and pantel (an extract from reindeer antlers).
Standard or planned therapy of the pathological process - take 1 ampoule from 10 to 30 days, if necessary, after a 10-15 day pause, repeat the course of 1 ampoule daily for 10-15 days;
Early period of rehabilitation of an acute, severe, chronic pathological process - take 2 ampoules for 15-20 days and repeat the course after a 10-day break. Further use is subject to the current state;
Early rehabilitation period for an acute but milder pathological process - take 2 ampoules for 5 days, and then 1 ampule for 15-20 days and after a 15-day pause, repeat 1 ampule daily for 10-15 days;
Complex therapy of an acute pathological process - take 2 ampoules for 10-15 days) and after a 15-day pause, repeat 1 ampoule daily for 10 days;
If the patient is undergoing resuscitation or intensive therapy, it is possible to use from 3 to 5 ampoules of the DELLIN Bioregulator per day, for 2-5 days, and then continue therapy according to the protocol for an acute, severe, chronic pathological process.
Content: Carnosine, a dipeptide consisting of two amino acids (alanine and histidine), is a natural component of human tissue: Glycine (aminoacetic acid) - refers to the nonessential amino acids, is a part of many proteins and biologically active compounds, is easily absorbed by the body. Taurine is an essential sulfoamino acid that has been found in almost all mammalian species.
Peptide complex - including delta-peptide with the last Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu, amino acids, growth factor.
Does not contain: artificial flavors or sweeteners, preservatives, sugar, starch, milk, lactose, soy, eggs, glutamate, wheat, yeast, magnesium stearate. Without GMO.
Store in a dry place at temperatures between 5 0 С and 25 0 C, away from direct sunlight.
Pantel® ( Peptide delta-sleep ) is an original complex of biologically active substances, including nervous tissue growth factors and peptides.
Free amino acids: aspartic acid (Rf = 0.51 ± 0.015); serine (Rf = 0.46 ± 0.071); glycine (Rf = 0.41 ± 0.018); histidine (Rf = 0.13 ± 0.030); arginine (Rf = 0.19 ± 0.025); tyrosine (Rf = 0.43 ± 0.020); alanine (Rf = 0.38 ± 0.043); threonine (Rf = 0.31 ± 0.011); valine (Rf = 0.56 ± 0.014); methionine (Rf = 0.27 ± 0.037); leucine (Rf = 0.64 ± 0.075); phenylalanine (Rf = 0.81 ± 0.031); lysine (Rf = 0.09 ± 0.025).
Mineral substances in the form of ionic and chelate complexes: macroelements - iron, calcium, magnesium, sodium, phosphorus and potassium; trace elements - manganese, selenium, cobalt, copper and zinc, as well as iodine.
Lipids: phospholipids, cerebroside, colaminkephalin, lecithin, etc.
Peptides: NGF-1; NGF - 3 (nerve growth factor, NGF) - small secreted proteins that maintain the viability of neurons, stimulate their development and activity. They belong to the family of neurotrophins. They are indispensable for the survival and development of sympathetic and sensory neurons. Without them, these neurons are subject to apoptosis. Nerve growth factor causes axon growth: studies have shown that it contributes to their branching and slight elongation. NGF-1 binds to at least two classes of receptors: LNGFR and TrkA. Both are associated with neurodegenerative pathologies.
There is evidence that NGF circulates throughout the body and is essential for maintaining homeostasis.
NGF prevents or reduces neuronal degeneration in animals with neurodegenerative diseases. These encouraging results in animals have led to a number of clinical trials in humans. Expression of NGF is increased in inflammatory diseases, in which it suppresses inflammation. In addition, NGF appears during the process of myelin repair. DSIP (delta-sleep-inducing peptide) - stabilizes neurons and interneuronal connections in the delta phase, activates the synthesis of neurotrophins, recreates active synaptic collaterals, prevents hyperexcitation of neurons in the process of normal adaptive reactions, preventing their self-destruction by the "Exito Cyto Toxicity" mechanism.
Carnosine (beta-alanyl-L-histidine) is a dipeptide consisting of amino acid residues ?-alanine[en] and histidine. Found in high concentrations in muscle and brain tissues.
The main properties of carnosine:
Numerous literary sources suggest that the antioxidant carnosine, a natural dipeptide α-alanyl-L-histidine, meets almost all the requirements for an ideal antioxidant. It is synthesized and contained in the human muscle and nervous tissue, is easily absorbed and penetrates the blood-brain barrier, has high bioavailability and membrane-stabilizing action, belongs to low-molecular-weight hydrophilic direct-acting antioxidants, although it can also have an indirect effect on the body's anti-radical defense system. The indirect effect of carnosine is evidenced by the results of experiments that showed that carnosine accelerates the metabolism of cortisol and noradrenaline released into the blood during stress. In addition, carnosine has no side effects,
The first positive biological effects of carnosine were explained by its pH-buffering properties, however, after the discovery of its direct antioxidant action, carnosine began to be considered not only as a buffer for protons, but also as a buffer for metals with variable valence and reactive oxygen species, that is, as a classic antioxidant. Subsequently, its anti-glycation, anti-crosslinking properties were revealed, which are, in fact, a reflection of antioxidant effects.
The use of carnosine in neuropsychiatric and mental disorders:
It is known that OS (oxidative stress) develops in Parkinson's and Alzheimer's diseases, in stroke, neurosis, schizophrenia, depression, in addictive disorders, in particular, in alcoholism. The cells of the nervous system are very sensitive to free radical oxidation due to many factors: high intensity of metabolic processes and a high level of oxygen consumption, a large amount of lipids with polyunsaturated fatty acids, an increased content of bound iron ions (oxidation inducers) and a low content of its carrier proteins, the formation of active forms of oxygen in the course of cellular metabolism, which perform the function of secondary messengers in neuronal cells, participation of free radicals in neuroregulation, etc.
Positive results were obtained by adding carnosine to the basic therapy of patients with chronic dyscirculatory encephalopathy. Such treatment led to an increase in the resistance of blood plasma lipoproteins to Fe2+-induced oxidation, stabilization of erythrocytes in relation to acid hemolysis, intensification of the respiratory burst of leukocytes and enhancement of the endogenous antioxidant defense of the body, and improvement of the cognitive functions of the brain of patients. That is, carnosine had antioxidant, membrane-stabilizing and immunomodulatory effects in this pathology.
A significant improvement in the clinical condition of patients was observed with the introduction of carnosine for 30 days in addition to conventional therapy in the treatment of Parkinson's disease. The use of carnosine made it possible to reduce the toxic effects of basic therapy (side effects of antiparkinsonian drugs). Patients showed a statistically significant decrease in neurological symptoms (improved coordination of movements). A positive correlation was found between the activation of the antioxidant enzyme superoxide dismutase in erythrocytes and a decrease in neurological symptoms. The addition of carnosine to the treatment regimen led to a significant decrease in hydroperoxides in blood plasma lipoproteins and significantly increased the resistance of low and very low density lipoproteins to Fe2+-induced oxidation, as well as to a decrease in the amount of oxidized proteins in the blood plasma. Thus, the addition of carnosine to basic therapy significantly improved not only clinical parameters, but also increased the antioxidant status of the body in patients with Parkinson's disease.
Carnosine is also helpful in improving brain function in autism. In one double-blind, placebo-controlled study of 301 children with autism, carnosine was found to improve expressive and receptive vocabulary and cause an objective improvement in the autism score.
In terms of general anti-aging effects, several clinical studies have identified the potential effect of carnosine in slowing down the aging process by preventing oxidative damage and glycosylation. In addition, carnosine has been shown to directly and indirectly inhibit the release of inflammatory mediators such as cytokines. Reducing asymptomatic inflammation is becoming another key goal not only as part of an anti-aging strategy, but also helps prevent the development of chronic degenerative diseases such as heart disease and diabetes, and neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. Given the unique action of carnosine within the brain,
In addition, Glycine supports cell bioenergetics and belongs to antihypoxants. Being a non-essential amino acid, it, together with other amino acids, is part of the polypeptide chain that forms the primary structure of proteins. Glycine is directly involved in the synthesis of purines, porphyrins, creatine and phospholipids that form cell membranes. Particular attention should be paid to the participation of glycine in the synthesis of the tripeptide glutathione ? source of SH-groups and natural antioxidant. It stands in the first echelon of cell protection from free radicals, which are constantly formed in the body. Activation of glutathione, in addition, leads to an increase in the compensatory capacity of the cell during the period of oxidative stress. An equally important aspect of the metabolic action of glycine? its ability to direct non-specific conjugation of xenobiotics, resulting in substances toxic to the cell, interact with it and form less dangerous metabolites. The drug, being a detoxicant, binds aldehydes and ketones, which are formed in large quantities during acute stroke.
Recently, it has been established that in the brain taurine plays the role of a neurotransmitter amino acid that inhibits synaptic transmission and has anticonvulsant activity. Taurine helps to improve energy processes, stimulates healing processes in dystrophic diseases and processes accompanied by a significant metabolic disorder of eye tissues. There is evidence that taurine promotes the formation of new cells in the hippocampus, an area of the brain associated with memory. It also promotes brain regeneration in closed head injuries.
The mechanisms of action of taurine are not yet fully understood. Taurine reduces the release of D-aspartate (analogous to L-glutamate). It appears to protect neurons from glutamate-induced neuronal excitotoxicity by reducing intracellular free Ca2+ levels. In addition, by influencing the opening of chloride channels, it prevents depolarization of the cell membrane caused by glutamate, thereby stopping the unfolding of the pathological cascade. Perhaps he plays the role of an agent that establishes a balance between the excitatory and depressant systems of the brain.
Being a structural analogue of the main inhibitory transmitter GABA, it interacts with GABA receptors, activating them, but to a lesser extent than GABA itself. Among all GABAA receptors, taurine most strongly affects those containing the b2 subunit, localized in mammals in the dentate gyrus, nigra substance, the cerebellar molecular layer, the medial nucleus of the thalamus, and the CA3 field of the hippocampus. The release of taurine from neurons also reduces cell edema and thus helps regulate osmosis in a state of excitotoxicity.
The processes of free radical oxidation in the body are controlled by the antioxidant system. The leading role in maintaining the antioxidant status of the cell belongs to glutathione peroxidase and glutathione reductase. The main function of these enzymes is the reduction of hydroperoxides to alcohols. As the results of the study showed, with cerebral edema, a decrease in the content of glutathione and the activity of glutathione peroxidase and glutathione reductase is observed.
In animals and humans, glutathione is present in both oxidized (GSSG; about 10% of the total amount) and reduced (GSH) form. The main antioxidant effect of glutathione is realized through its participation in the work of enzymatic antioxidants; being a substrate for glutathione peroxidases, it actually acts as a donor of hydrogen atoms for the reduction of H2O2 and lipid peroxides.
Due to the fact that the decrease in the level of glutathione and antioxidant enzymes is one of the leading factors in the development of various pathological processes, substances that increase the content of glutathione and activate glutathione-dependent reactions are of great interest. The amino acid taurine acts as such a substance. There are convincing data on the role of taurine as an active osmoregulator, which is especially important for brain neurons. A correlation was shown between the content of water and taurine in the brain tissue. In hepatic encephalopathy, a decrease in the content of taurine in the central nervous system may be one of the causes of cerebral edema. It is also involved as a neuromodulator in the control of respiratory function, especially during acute hypoxia.
As the results of studies have shown, the introduction of taurine for 15–20 days led to the elimination of lipid peroxidation products, the normalization of oxidative modification of proteins in the mitochondrial fraction of the brain of individuals with cerebral edema.
In 1970, about 20 reports were published on the properties of taurine to attenuate epileptic seizures in various animal models. Some success in attenuating seizures with the administration of taurine in animal models of epilepsy has given impetus to human clinical studies. Clinical trials have shown that lowering the concentration of taurine in the brain can increase the overall excitation of neurons and thus participate in the onset of epileptic seizures. This question has recently, namely, after the publication of publications by French and Finnish scientists, arouses the keenest interest among specialists. One such work by SS Ojaa, P. Saransaari, which summarized the knowledge accumulated by the authors, was published in the journal Epilepsy Research (2013; 104: 187-194).