To the noradrenergic component of the mechanisms of stress-limiting and healing effects of dalargin

2016 ◽  
Vol 14 (4) ◽  
pp. 61-66
Author(s):  
Oleg N Zabrodin
Keyword(s):  
Gastric Mucosa ◽  
Bone Fractures ◽  
Reparative Regeneration ◽  
Synthetic Analogue ◽  
Protective Effects ◽  
Pharmacological Agents ◽  
Adrenal System ◽  
Liver And Pancreas ◽  
Sympathetic Nervous ◽  
Neurogenic Lesions

The article presents the facts of the stress-limiting and healing effects of a synthetic analogue of leucine-enkefalin dalargin (D), the analysis of literature data of the modulating effects of D on the activity of sympathetic-adrenal system (SAS) in various extraordinary influences. D prevents: hyperactivity of SAS, associated development of dystrophic-destructive changes in the organs (heart, gastric mucosa, duodenum) and the exhaustion of catecholamine’s (CA) depot in the sympathetic endings. It is noted that similar protective effects against the development of neurogenic lesions in the organs (heart, gastric mucosa, liver and pancreas) have pharmacological agents with antiadrenergic component of actions (gangliolitiks and sympatholitiks, alpha - and beta-adrenoblokers). In the article mapped the healing effects of D in relation to the gastric mucosa destructions, skin incisional wounds, bone fractures with the ability of the sympathetic nervous system to stimulate reparative regeneration in various tissues (cornea. gastric mucosa, myocardium, liver, sympathetic reinnervation). It is concluded that the stress-limiting and healing effects of D have a noradrenergic component associated with modulating effect of D on the activity of SAS. In the conditions of extraordinary influences D suppresses SAS hyperactivity, keeping the reserves of CA in the sympathetic endings. In the implementation of reparative regeneration of tissues CA, and primarily sympathetic mediator noradrenalin, promote healing of damaged organs and tissues.

scholarly journals Protective Effects of PGC-1α Activators on Ischemic Stroke in a Rat Model of Photochemically Induced Thrombosis

2021 ◽  
Vol 11 (3) ◽  
pp. 325
Author(s):  
Fatima M. Shakova ◽  
Yuliya I. Kirova ◽  
Denis N. Silachev ◽  
Galina A. Romanova ◽  
Sergey G. Morozov
Keyword(s):  
Rat Model ◽  
Nuclear Translocation ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Protein Markers ◽  
Peroxisome Proliferator Activated Receptor ◽  
Pharmacological Agents ◽  
Ischemic Brain ◽  
Neuroprotective Therapy ◽  
Dependent Protein

The pharmacological induction and activation of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), a key regulator of ischemic brain tolerance, is a promising direction in neuroprotective therapy. Pharmacological agents with known abilities to modulate cerebral PGC-1α are scarce. This study focused on the potential PGC-1α-modulating activity of Mexidol (2-ethyl-6-methyl-3-hydroxypyridine succinate) and Semax (ACTH(4–7) analog) in a rat model of photochemical-induced thrombosis (PT) in the prefrontal cortex. Mexidol (100 mg/kg) was administered intraperitoneally, and Semax (25 μg/kg) was administered intranasally, for 7 days each. The expression of PGC-1α and PGC-1α-dependent protein markers of mitochondriogenesis, angiogenesis, and synaptogenesis was measured in the penumbra via immunoblotting at Days 1, 3, 7, and 21 after PT. The nuclear content of PGC-1α was measured immunohistochemically. The suppression of PGC-1α expression was observed in the penumbra from 24 h to 21 days following PT and reflected decreases in both the number of neurons and PGC-1α expression in individual neurons. Administration of Mexidol or Semax was associated with preservation of the neuron number and neuronal expression of PGC-1α, stimulation of the nuclear translocation of PGC-1α, and increased contents of protein markers for PGC-1α activation. This study opens new prospects for the pharmacological modulation of PGC-1α in the ischemic brain.

Radix Dipsaci extract protects against Rosiglitazone induced bone loss

2021 ◽  
Vol 8 (9) ◽  
pp. 15-21
Author(s):  
Khalid A Asseri ◽  
◽  
Yahya I Asiri ◽  
Ali Alqahtani ◽  
Krishnaraju Venkatesan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Loss ◽  
Bone Fractures ◽  
Scientific Evidence ◽  
Streptozotocin Diabetes ◽  
Diabetic Control ◽  
Albino Rats ◽  
Protective Effects ◽  
Diabetes Group ◽  
Diabetic Osteoporosis

The dried root of Dipsacus asperoides is known as Radix Dipsaci extract(RDE). It's a kidney-toning herbal medication with a lengthy track record of safe usage in the treatment of bone fractures and joint disorders. The drug rosiglitazone (RSG) causes an imbalance in bone remodelling, which results in increased apoptotic death of osteogenic cells and decreased bone production. The goal of this study was to investigate the effects of RDE on RSGinduced bone loss in diabetic rats in a systematic way. Five groups of six Wistar albino rats were studied: control (vehicle therapy), Streptozotocin (diabetes) group, RDE group, Rosiglitazone, and Rosiglitazone +RDE group. Insulin, oxidative stress, and bone turnover markers in the blood were all detected using ELISA tests. When compared to diabetic control rats, RDE therapy significantly raised insulin and osteocalcin levels. RDE may be able to prevent diabetic osteoporosis by boosting osteogenesis and lowering oxidative stress in the bone.These findings support the use of RDE as a bone loss inhibiting in diabetics. Well-designed clinical trials are likely to yield further scientific evidence on its bone-protective effects and safety. Keywords: Radix Dipsaci, Diabetic osteoporosis, Rosiglitazone.

scholarly journals Mechaqnism of protective effects of Ouren-Gedoku-To and San'ou-Syashin-To on the gastric mucosa.

1991 ◽  
Vol 98 (4) ◽  
pp. 319-325 ◽  
Author(s):  
Toshiaki SUENAGA ◽  
Toshio SHIRAKAWA ◽  
Nobue HARADA ◽  
Chie TAO ◽  
Masashi YAMASAKI ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Protective Effects

scholarly journals Sphingosine-1-Phosphate: Its Pharmacological Regulation and the Treatment of Multiple Sclerosis: A Review Article

Biomedicines ◽  
2020 ◽  
Vol 8 (7) ◽  
pp. 227
Author(s):  
Stanley Cohan ◽  
Elisabeth Lucassen ◽  
Kyle Smoot ◽  
Justine Brink ◽  
Chiayi Chen
Keyword(s):  
Multiple Sclerosis ◽  
G Protein ◽  
Cell Types ◽  
Protective Effects ◽  
Preclinical Research ◽  
Pharmacological Agents ◽  
Inflammatory Damage ◽  
Sphingosine 1 Phosphate ◽  
The Central Nervous System ◽  
Lymphocyte Egress

Sphingosine-1-phosphate (S1P), via its G-protein-coupled receptors, is a signaling molecule with important regulatory properties on numerous, widely varied cell types. Five S1P receptors (S1PR1-5) have been identified, each with effects determined by their unique G-protein-driven downstream pathways. The discovery that lymphocyte egress from peripheral lymphoid organs is promoted by S1P via S1PR-1 stimulation led to the development of pharmacological agents which are S1PR antagonists. These agents promote lymphocyte sequestration and reduce lymphocyte-driven inflammatory damage of the central nervous system (CNS) in animal models, encouraging their examination of efficacy in the treatment of multiple sclerosis (MS). Preclinical research has also demonstrated direct protective effects of S1PR antagonists within the CNS, by modulation of S1PRs, particularly S1PR-1 and S1PR-5, and possibly S1PR-2, independent of effects upon lymphocytes. Three of these agents, fingolimod, siponimod and ozanimod have been approved, and ponesimod has been submitted for regulatory approval. In patients with MS, these agents reduce relapse risk, sustained disability progression, magnetic resonance imaging markers of disease activity, and whole brain and/or cortical and deep gray matter atrophy. Future opportunities in the development of more selective and intracellular S1PR-driven downstream pathway modulators may expand the breadth of agents to treat MS.

Dimethyloxalylglycine (DMOG) and the Caspase Inhibitor “Ac-LETD-CHO” Protect Neuronal ND7/23 Cells of Gluocotoxicity

2019 ◽  
Author(s):  
Debasmita Mukhopadhyay ◽  
Mohammad Hammami ◽  
Amani Khalouf ◽  
Yazan Al Shaikh ◽  
Abdul Khader Mohammed ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Viability ◽  
Dependent Manner ◽  
Ros Production ◽  
Protective Effects ◽  
Caspase Inhibitor ◽  
Novel Therapy ◽  
Pharmacological Agents ◽  
Micro Rnas ◽  
The Impact

AbstractIt well known that long-lasting hyperglycaemia disrupts neuronal function and leads to neuropathy and other neurodegenerative diseases. The α-ketoglutarate analogue (DMOG) and the caspase-inhibitor “Ac-LETD-CHO are potential neuroprotective molecules. Whether their protections may also extend glucotoxicity-induced neuropathy is not known. Herein, we evaluated the possible cell-protective effects of DMOG and Ac-LETD-CHO against hyperglycaemia-induced reactive oxygen species and apoptosis in ND7/23 neuronal cells. The impact of glucotoxicity on the expression of HIF-1α and a panel of micro-RNAs of significance in hyperglycaemia and apoptosis was also investigated.ND7/23 cells cultured under hyperglycaemic conditions showed decreased cell viability and elevated levels of ROS production in a dose- and time-dependent manner. However, presence DMOG (500 µM) and/or Ac-LETD-CHO (50 µM) counteracted this effect and increase cell viability concomitant with reduction in ROS production, DNA damage and apoptosis. AcLETD-CHO suppressed hyperglycaemia-induced caspase 3 activation in ND7/23 cells. Both DMOG and Ac-LETD-CHO increased HIF-1α expression paralleled with the suppression of miR-126–5p, miR-128–3p and miR-181 expression and upregulation of miR-26b, 106a-5p, 106b-5p, 135a-5p, 135b-5p, 138–5p, 199a-5p, 200a-3p and 200c-3p expression.We demonstrate a mechanistic link for the DMOG and Ac-LETD-CHO protection against hyperglycaemia-induced neuronal dysfunction, DNA damage and apoptosis and thereby propose that pharmacological agents mimicking these effects may represent a promising novel therapy for the hyperglycaemia-induced neuropathy.

scholarly journals The use of anabolic androgenic steroids: A focus on polypharmacy

2018 ◽  
Vol 71 (11-12) ◽  
pp. 413-417
Author(s):  
Bozana Nikolic ◽  
Dusica Rakic
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adverse Effects ◽  
Anabolic Steroids ◽  
The Body ◽  
Anabolic Androgenic Steroids ◽  
Synthetic Analogue ◽  
Pharmacological Agents ◽  
Nonmedical Use ◽  
Androgenic Steroids

Introduction. Anabolic androgenic steroids, such as testosterone and its synthetic analogue, nandrolone, have clear clinical indications. However, their abuse is practiced to enhance physical performance in professional, recreational and non-professional athletes; outside of sports, their nonmedical use is associated with different social groups (criminal activities, substance abuse). Polypharmacy. Testosterone and its synthetic analogues are also used for nonmedical purposes, mainly administered in supraphysiological doses in cycles lasting a few weeks. In order to potentiate the anabolic properties and control the adverse effects, the users also administer other pharmacological agents. Thus, growth hormone and insulin are complement to anabolic steroids; clenbuterol, amphetamine and thyroid hormones stimulate body fat loss; diuretics reduce the body weight and improve muscle definition; and erythropoietin increases the training capacity and accelerates the recovery after hard competitions. To control adverse effects, cardiovascular drugs, central nervous system depressants, central nervous system stimulants, human chorionic gonadotropin, sexual enhancement drugs, estrogen antagonists, analgesics/opioids, nonsteroidal anti-inflammatory drugs and others, are administered. Probenecid, finasteride and diuretics mask the administration of other doping agents. Additionally, during the last two decades, attention has increasingly been focused on the relationship between the use of anabolic androgenic steroids and psychoactive substances (alcohol, cannabis, amphetamines, cocaine, hallucinogens). Conclusion. Supraphysiological doses and polypharmacy additionally increase the risk of adverse effects, including withdrawal syndrome; therefore, prevention of nonmedical use of anabolic androgenic steroids should be a public health priority.

Mechanisms of prevention postoperative immunosuppression by regional anesthesia

2021 ◽  
Vol 19 (3) ◽  
pp. 345-353
Author(s):  
Oleg N. Zabrodin ◽  
Viktor I. Strashnov
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Epidural Analgesia ◽  
Regional Anesthesia ◽  
Epidural Anesthesia ◽  
Preventive Action ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal System ◽  
Sympathetic Nervous ◽  
Postoperative Epidural Analgesia

The data on the factors of development of postoperative immunosuppression (PI) are presented. Among them, an important role in the development of PI belongs to hyperactivity during operations of the sympathetic nervous system (SNS) and hypothalamic-pituitary-adrenal system. It has been shown that PI is prevented by regional anesthesia, primarily epidural anesthesia and postoperative epidural analgesia, as well as prolonged ganglioplegia. It is concluded that the preventive action of regional anesthesia in relation to the development of PI is largely associated with the sympatholytic component of action.

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