Anti-edema Effects Research Articles

Escin Sodium Improves the Prognosis of Acute Pancreatitis via Promoting Cell Apoptosis by Suppression of the ERK/STAT3 Signaling Pathway.

Acute pancreatitis (AP), an inflammatory disorder of the pancreas, can cause systemic inflammatory responses. Escin Sodium (ES), a natural mixture of triterpene saponins extracted from the dry ripe fruit of Fructus Aesculi or horse chestnut crude, has been demonstrated to have antiedematous, anti-inflammatory, and antiexudative effects. We here aim to investigate the effects of ES pretreatment on AP in vivo and in vitro and explore its potential molecular mechanism. In the present study, we demonstrated that ES pretreatment could apparently decrease amylase and lipase, downregulate inflammatory cytokines, and attenuate pancreatic damage. Additionally, the increased expression of apoptotic-related proteins and the results of flow cytometry demonstrated the effects of ES on promoting apoptosis in acinar cells. Moreover, ES could enhance mitochondrial membrane potential (MMP, ΔΨm) and reactive oxygen species (ROS) level and reduce intracellular calcium concentration, which are closely related to mitochondrial-mediated death. The effect of ES pretreatment on acinar cell apoptosis was furtherly confirmed by the regulatory pathway of the ERK/STAT3 axis. These results suggest that ES attenuates the severity of AP by enhancing cell apoptosis via suppressing the ERK/STAT3 signaling pathway. These findings provide evidence for ES which is treated as a novel and potent therapeutic for the treatment of AP.

Anti-edema effect of Aloe vera leaf extract following traumatic brain injury: Role of pro-inflammatory cytokines.

Objective:Based on anti-inflammatory effects of Aloe vera, the effect of aqueous extract of this plant on brain edema and changes in some pro-inflammatory cytokines was investigated after traumatic brain injury (TBI).Materials and Methods:In this study, adult male Wistar rats were divided into 5 groups: Sham, TBI, vehicle (Veh), and low dose (LA) and high dose (HA) Aloe vera. The vehicle and aqueous extract of Aloe vera were injected intraperitoneally 30 min after induction of diffuse TBI by Marmarou’s method. Brain edema (brain water content), and transforming growth factor beta (TGF-β), tumor necrosis factor alpha (TNFα), interleukin 6 (IL-6) and IL-1β levels in serum and brain were measured 24 hr after TBI induction.Results:Increased brain edema by TBI was reduced by both LA and HA (p<0.01 and p<0.05, respectively). IL-6 increased in the brain of TBI group compared to sham, and which was inhibited by both Aloe vera doses compared to Veh (p<0.001). The differences in the IL-6 serum levels among Veh, LA and HA groups were not significant. Increases in serum and brain IL-1β levels were reduced only in the HA group (p<0.001). Although only in the brain, TNF-α level increased after trauma, but both LA and HA inhibited it in a dose-dependent manner (p<0.01 and p<0.05, respectively) . The amount of TGF-β in the brain was reduced by both doses of the extract (p<0.001). Conclusion:These results indicated that Aloe vera has a neuroprotective effect induced by reducing brain edema. The probable mechanism particularly for HA is decreasing levels of pro-inflammatory cytokines such as TGF-β, TNF-α, IL-6 and IL-1β.

Estrogen receptor agonists induce anti‑edema effects by altering α and β estrogen receptor gene expression.

The present study aimed to examine whether the attenuation of estrogen receptor expression is prevented by propyl pyrazole triol (PPT), an agonist for estrogen receptor α (ERα) or and diarypropiolnitrile (DPN), an agonist for estrogen receptor β (ERβ) after traumatic brain injury (TBI). The tests performed on ovariectomized female Wistar rats included sham group, vehicle group, and treated groups: PPT, DPN, and PPT+DPN 30 minutes after TBI. Blood‑brain barrier (BBB) disruption and brain water content were estimated. RT‑PCR and\r\nwestern blotting were utilized to evaluate ESR1 and ESR2 gene and protein expression. The data indicated that PPT, DPN, and PPT+DPN attenuated TBI‑induced brain edema. Also, BBB disruption after TBI was prevented in PPT, DPN, and PPT+DPN‑treated TBI animals. Estrogen agonist‑treated animals showed a significant elevation in Esr1 mRNA and protein expression levels in the brain tissue of TBI rats. In addition, the data indicated a significant elevation of Esr2 mRNA and protein expression levels in the brain tissue of estrogen agonist‑treated TBI rats. The data shows that both ESR1 and ESR2 agonists can enhance ER mRNA and protein levels in TBI animals' brain. It appears that this effect contributes to the neuroprotective function of ER agonists.

“Reach the cells”: microcirculatory support

Background. Vessels of the microcirculatory tract provide regulatory, drainage, thermocontrol and signal functions. Disorders of these vessels are the part of the pathogenesis of coronary heart disease, endarteritis obliterans, Raynaud’s disease, etc. Common causes of microcirculation disorders include disorders of central and regional blood circulation, impaired blood volume and viscosity, impaired permeability of microvessel walls.&#x0D; Objective. To describe the features of microcirculatory support.&#x0D; Materials and methods. Analysis of literature sources on this topic.&#x0D; Results and discussion. In order to improve microcirculation, various drugs are used: antiplatelets, anticoagulants, antioxidants, and nitric oxide donors. The purpose of these drugs are to improve the rheological properties of blood, to improve the delivery of nutrients to the vascular wall, to regulate the vascular tone, and to improve endothelial function. Reosorbilact (“Yuria-Pharm”) opens precapillary sphincters, increases the area of blood contact with the target cell, improves tissue oxygenation and rheological properties of blood. Reosorbilact includes such components as sorbitol, basic cations (Na, Ca, K, Mg) and sodium lactate. Sorbitol is used for urgent energy needs, metabolized and stored as glycogen, has a disaggregating effect, improves microcirculation and tissue perfusion. The hyperosmolar action of Reosorbilact is to stimulate the flow of fluid from the intercellular space into the vascular bed. Correction of metabolic acidosis with Reosorbilact is slower than due to sodium bicarbonate buffer, so this solution does not cause severe fluctuations in pH. The detoxifying effect of Reosorbilact involves washing of metabolites and toxins out from damaged cells, tissues and organs, followed by their rapid excretion due to increased diuresis. The improvement of liver microcirculation and replenishment of glycogen depot, which normalizes the functional state of hepatocytes and enhances physiological detoxification, is an additional beneficial effect. Hemodilution is also important, because it allows to reduce the content of toxic metabolites in blood plasma. In addition, Reosorbilact gently stimulates peristalsis, has choleretic and cholekinetic effects, reduces bilirubin and creatinine, improves energy metabolism, stabilizes systemic hemodynamics, reduces the symptoms of pain due to anti-edematous effect, and accelerates wound healing. Reosorbilact can be considered a drug № 1 for low-volume infusion therapy. The positive hemodynamic effect of the drug is manifested within 2-3 hours. Reosorbilact promotes the transition of the hypokinetic type of blood circulation into eukinetic due to the redistribution of extracellular fluid into the vascular bed. The drug should be prescribed at a dose of 7 ml/kg of body weight for 5-7 days or until the symptoms of intoxication are reduced.&#x0D; Conclusions. 1. Vessels of the microcirculatory tract provide regulatory, drainage, thermoregulatory and signal functions. 2. Common causes of microcirculation disorders include disorders of central and regional blood circulation, disorders of blood volume and viscosity, impaired permeability of microvessel walls. 3. Reosorbilact improves tissue oxygenation and rheological properties of blood, promotes washing of metabolites and toxins out from damaged cells, normalizes the functional state of hepatocytes, stimulates peristalsis, stabilizes systemic hemodynamics.

Anti-Inflammatory and Gastroprotective Effects of Escin

Escin is a triterpenoid saponin extracted from the fruit of Aesculus wilsonii Rehd. and Aesculus hippocastanum (Hippocastanaceae). Clinically, it is widely used in the treatment of edema induced by either trauma or surgery, as well as treating chronic venous insufficiency. The anti-inflammatory and antiedema effects of escin have been extensively investigated. This article systematically reviews the effects of escin on inflammation and gastrointestinal diseases, including its role in inflammation, as an antioxidant, and in inhibiting gastric acid secretion and promoting gastrointestinal movement, especially, the molecular mechanism. The advantages and potential uses of escin have also been discussed.

Cow’s milk protein allergy and antihistamines using in infants

Allergy to cow’s milk is a frequent diagnosis in infants and amounts to 2-3%. In most cases, manifestations of allergy to cow’s milk proteins are combined polyorganic in nature with the involvement of two or more systems of the child’s body, more frequent are lesions of the skin and gastrointestinal mucosa. Supporting breastfeeding remains the first task of a pediatrician when observing a child in the first year of life, but if there is a need to appoint and choose from a variety of formulas for supplementary feeding or as a basic diet, there is a difficult question of choosing the right one. Children at risk without clinical manifestations of allergy to cow’s milk proteins should use hypoallergenic preventive formulas based on partially hydrolyzed cow’s milk proteins. In formed clinical manifestations of allergy – formulas based on highly hydrolyzed protein, and in their severe manifestations – on the basis of amino acids. Unfortunately, a significant part of infants have polyvalent sensitization, so even a properly selected formula does not fully eliminate all symptoms. Therefore, in addition to diet correction, antihistamines, both systemic and topical, as well as hormonal topical remedies, emollients, etc., are often used. Pathogenetic treatment for food allergies has not yet been developed, and the only solution we can make, in addition to elimination diets, is to apply symptomatic therapy. A special problem in pediatrics is the lack of drugs, including antihistamines, allowed for use in children under the age of 1 year. At this age, allowed to use only a few: dimetindene, ceirizine, in emergency cases – chloropyramine, starting with the age of 1 month. Optimal forms of administration for infants may be syrup, suspensions, drops, as well as topical forms - lotion, gel, emulsion or cream. Taking into account many years of experience with dimethindene, clinical data on the efficacy and safety of the drug, allow its use in pediatric practice. The drug has good antihistamine activity, antipruritic, anti-edema and antispastic effect, and is able to quickly and firmly relieve symptoms of allergy.

Ultrastructural effects of nerve growth factor and betamethasone on nerve regeneration after experimental nerve injury

ABSTRACT Peripheral nerve injuries (PNI) are an important health problem in the world. In this study, the effects of nerve growth factor (NGF) and betamethasone on nerve regeneration after sciatic nerve crush injury were examined by footprint analysis, electron microscopic, histomorphometric, and biochemical methods. Fifty Wistar rats were divided into five groups as intact control, experimental control, NGF, betamethasone, and NGF+betamethasone combined treatment groups. After the injury, betamethasone was subcutaneously injected into the lesion area of the treatment groups three times during the first day. NGF was subcutaneously injected into the lesion area of treatment groups for 14 days. Footprint analysis was made on 7, 14, 21, 28, and 35 days and after 6 weeks, tissue samples were obtained from all groups. In the experimental control group, there were severe degenerative changes in most of the axons and myelin sheaths of the nerve fibers. Moreover, an increase of MDA levels and a decrease in SOD activities were found in this group. On the other hand, malondialdehyde (MDA) levels decreased, superoxide dismutase (SOD) activities increased and significant motor functional recovery were found in the combined treatment group. The number of axons, axon diameters, and myelin thickness were significantly greater in the combined treatment group when compared with experimental control and other treatment groups. It was thought that nerve regenerative effects of NGF and anti-inflammatory and/or anti-edematous effects of betamethasone could induce functional recovery in the combined treatment group. In conclusion, combined therapy of NGF and betamethasone may be an effective approach for the treatment of PNI.

Is Topical Application of Hyaluronic Acid in Oral Lichen Planus Effective? A Randomized Controlled Crossover Study

Hyaluronic acid (HA) has anti-inflammatory and anti-edematous effects and, thus, could be promising in the treatment of oral lichen planus (OLP). The aim of the study was to evaluate the effects of topical hyaluronic acid, compared to placebo, on salivary levels of calprotectin, interleukin-6 (IL-6), and bacteria, as well as clinical and subjective parameters. Fourteen patients with confirmed OLP were included. After random selection, patients started with either 0.2% hyaluronic acid or a placebo gel for 6 weeks. Following a wash-out period, the groups changed the application. Whole saliva, clinical parameters, and questionnaires were evaluated before and after the intervention, as well as after the crossover phase. Salivary calprotectin, IL-6, and inflammation-related bacteria were determined by ELISA and PCR, respectively. There were no significant differences in clinical or subjective outcome parameters, salivary levels of IL-6, calprotectin, or bacteria after the application of hyaluronic acid, compared to placebo. However, only nine patients completed the study, as five out of seven patients starting with placebo were lost to follow-up. Significant effects of HA on inflammatory mediators and clinical parameters in OLP patients could not be proven, although a trend in clinical severity improvement could be observed.

The effectiveness of “Iodozol” in combination therapy in the treatment of postpartum vulvitis in goats

In the nosology of obstetric pathology of goats a special place is occupied by postpartum lesions of the genitals by pathogenic microflora, of which the lion's share are postpartum vulvitis. The aim of the study was to test a new treatment regimen for postpartum vulvitis in goats and to study the therapeutic efficacy of the drug “Iodozol”, “Celexib” and “Dextrodev 50” in this pathology. Clinical and anamnestic data showed that the symptoms of postpartum vulvitis of goats were characterized by inflammatory edema, high pain, local fever, impaired tissue integrity, hematomas and discharge from the genital tract. Microbiological studies of secretions from the genitals revealed the presence of E. coli, S. aureus, less often – S. saprophyticus and E. faecalis. High resistance of microorganisms to fluoroquinolones and penicillins is noted. E. coli was sensitive to only 35.7 % of antimicrobial drugs, including ceftriaxone, ceftiofur, and iodine. S. aureus is sensitive to 49.9 % of antimicrobial drugs, including ceftriaxone, cephalexin, gentamicin, ceftiofur, iodine (highest sensitivity) and chlorhexidine. S. saprophyticus was insensitive to a number of antibiotics (oxytetracycline, gentamicin, etc.), except iodine. Taking into account microbiological researches the complex scheme of treatment of postpartum vulvitis at goats is developed. Evaluation of the effectiveness of complex therapy of this pathology in animals showed that treatment with “Iodozole”, “Celexib” and “Dextrodev 50” in a short time eliminates inflammatory symptoms (pain, infiltration, redness, discharge). At the end of the course of treatment in the blood was observed an increase in hemoglobin concentration by 13.7 %, a decrease in the number of erythrocytes by 1.7 and leukocytes by 2.2 times compared with treatment. The topical intrauterine drug “Iodozol”, a non-steroidal injectable drug “Celexib”, has been found to have a broad spectrum of antimicrobial activity, and is effective and safe to use. The drugs have an anti-edematous and analgesic effect, and symptomatic treatment with intravenous solution “Dextrodev 50” is a mandatory component of complex therapy and is aimed at replenishing the body with nutrients, as well as helps to neutralize and remove toxins from the body. Further research will be to study the clinical efficacy and develop regulations for the use of this scheme in vulvitis and cervicitis of other ruminants.

Aescin Protects Neuron from Ischemia-Reperfusion Injury via Regulating the PRAS40/mTOR Signaling Pathway.

Ischemic stroke is one of the major causes of disability; widely use of endovascular thrombectomy or intravenous thrombolysis leads to more attention on ischemia-reperfusion injury (I/R injury). Aescin, a natural compound isolated from the seed of the horse chestnut, has been demonstrated anti-inflammatory and antiedematous effects previously. This study was aimed at determining whether aescin could induce protective effects against ischemia-reperfusion injury and exploring the underlying mechanisms in vitro. Primary cultured neurons were subjected to 2 hours of oxygen-glucose deprivation (OGD) followed by 24 hours of simulated reperfusion. Aescin, which worked in a dose-dependent manner, could significantly attenuate neuronal death and reduce lactate dehydrogenase (LDH) release after OGD and simulated reperfusion. Aescin treatment at a concentration of 50 μg/ml provided protection with fewer side effects. Results showed that aescin upregulated the phosphorylation level of PRAS40 and proteins in the mTOR signaling pathway, including S6K and 4E-BP1. However, PRAS40 knockdown or rapamycin treatment was able to undermine and even abolish the protective effects of aescin; meanwhile, the levels of phosphorylation PRAS40 and proteins in the mTOR signaling pathway were obviously decreased. Hence, our study demonstrated that aescin provided neuronal protective effects against I/R injury through the PRAS40/mTOR signaling pathway in vitro. These results might contribute to the potential clinical application of aescin and provide a therapeutic target on subsequent cerebral I/R injury.

Pituitary Adenylate Cyclase-Activating Polypeptide Attenuates Brain Edema by Protecting Blood-Brain Barrier and Glymphatic System After Subarachnoid Hemorrhage in Rats.

Brain edema is a vital contributor to early brain injury after subarachnoid hemorrhage (SAH), which is responsible for prolonged hospitalization and poor outcomes. Pharmacological therapeutic targets on edema formation have been the focus of research for decades. Pituitary adenylate cyclase-activating polypeptide (PACAP) has been shown to participate in neural development and brain injury. Here, we used PACAP knockout CRISPR to demonstrate that endogenous PACAP plays an endogenous neuroprotective role against brain edema formation after SAH in rats. The exogenous PACAP treatment provided both short- and long-term neurological benefits by preserving the function of the blood-brain barrier and glymphatic system after SAH. Pretreatment of inhibitors of PACAP receptors showed that the PACAP-involved anti-edema effect and neuroprotection after SAH was facilitated by the selective PACAP receptor (PAC1). Further administration of adenylyl cyclase (AC) inhibitor and sulfonylurea receptor 1 (SUR1) CRISPR activator suggested that the AC-cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) axis participated in PACAP signaling after SAH, which inhibited the expression of edema-related proteins, SUR1 and aquaporin-4 (AQP4), through SUR1 phosphorylation. Thus, PACAP may serve as a potential clinical treatment to alleviate brain edema in patients with SAH.

Dyslipidemia in Kidney Disorders: Perspectives on Mitochondria Homeostasis and Therapeutic Opportunities.

To excrete body nitrogen waste and regulate electrolyte and fluid balance, the kidney has developed into an energy factory with only second to the heart in mitochondrial content in the body to meet the high-energy demand and regulate homeostasis. Energy supply from the renal mitochondria majorly depends on lipid metabolism, with programed enzyme systems in fatty acid β-oxidation and Krebs cycle. Renal mitochondria integrate several metabolic pathways, including AMPK/PGC-1α, PPARs, and CD36 signaling to maintain energy homeostasis for dynamic and static requirements. The pathobiology of several kidney disorders, including diabetic nephropathy, acute and chronic kidney injuries, has been primarily linked to impaired mitochondrial bioenergetics. Such homeostatic disruption in turn stimulates a pathological adaptation, with mitochondrial enzyme system reprograming possibly leading to dyslipidemia. However, this alteration, while rescuing oncotic pressure deficit secondary to albuminuria and dissipating edematous disorder, also imposes an ominous lipotoxic consequence. Reprograming of lipid metabolism in kidney injury is essential to preserve the integrity of kidney mitochondria, thereby preventing massive collateral damage including excessive autophagy and chronic inflammation. Here, we review dyslipidemia in kidney disorders and the most recent advances on targeting mitochondrial energy metabolism as a therapeutic strategy to restrict renal lipotoxicity, achieve salutary anti-edematous effects, and restore mitochondrial homeostasis.

THE MORPHOLOGY OF THE LUNGS AT THE EXPERIMENTAL ACUTE INJURY AND ITS PHARMACOCORRECTION

The study of lung morphology under the influence of various environmental factors is of great interest for various areas of medicine and biology. The study of pathological changes in the respiratory part of the lung of rats with aspiration acute injury and the action of pharmacological correction was carried out. Acetone was used as a damaging agent, and HyperHAES was used as a means of pharmacological correction, containing 7.2% NaCl solution in combination with 6% hydroxyethyl starch, as well as a liposomal form of N-acetylcysteine, which was administered to experimental animals once intravenously after induction of acute lung injury. The control group of animals received antibiotic therapy. The staining of the slides was carried out using hematoxylin and eosin. A quantitative assessment of the histological signs of lung tissue damage was carried out. As a result of the study of preparations of the lungs, the degree of pulmonary edema was established, as well as the anti-edema effect of pharmacological corrections. On the 6th day of the experiment, the anti-edematous effect was retained only after the introduction of N-acetylcysteine. Histological examination of the lungs showed generalized destruction of the organ architectonics in response to the impact of a damaging factor and its reduction under the influence of pharmacological corrections. In the control group, the signs of acute lung injury were most extensive. One day after the administration of the HyperHAEC solution, there were no hemorrhages in the histological picture of the lungs. In a quantitative assessment of the histological signs of acute lung injury, it was shown that the maximum positive effect from the administration of HyperHAES develops 24 hours after application. N-acetylcysteine primarily led to a decrease in leukocyte infiltration and prevented the development of a suppurative process. The lung-protective effect of N-acetylcysteine was realized in 24 hours from the moment of administration and persisted until the 6th day of the experiment. The use of pharmacological correction agents in acute lung injury was reflected in the picture of the lethality of the experimental animals. When HyperHAES was applied, 37.5% of animals died by day 6, in the group with N-acetylcysteine - 28.6%, while in the control group all animals died.

Leech therapy (Jalaukavacharana) - A gift of ayurveda for treatment of medico-surgical diseases

The first description of Jalaukavacharana (leech therapy) is available in Sushruta Samhita written in 800 B.C. Recently, many pieces of research have proved that leech saliva has a variety of bioactive compounds including anti-thrombin (Hirudin, bufrudin), antiplatelet (calin), factor Xa inhibitors, antibacterial and other property. The main objective of the present article is to explore the procedures of leech therapy and research works done over a few decades on the application of leech therapy in different medico-surgical diseases. The procedure of leech therapy is documented from authors' observations and information, and its application in different diseases is gathered from various published works of the last ten years. Many clinical pieces of research show that leech therapy is beneficial in various medico-surgical diseases. A total of eight publications were included in the final selection after systematic analysis. Leech therapy or Jalaukavacharan is an ancient Ayurvedic bloodletting technique that has the great potential to manage many inflammatory, ischemic, and infectious diseases. Leech’s saliva contains many biologically and pharmacologically active compounds that exert anticoagulant, antiplatelet, anti-inflammatory, and anti-edema effects in the host's body. Arthritis, venous congestion, vascular diseases, abscess, ischemic heart disease, etc. can be successfully managed by leech therapy.

Macular edema: Understand mechanisms to develop treatments

Macular edema is an increase in volume of the central area of the retina, responsible for visual acuity. Visual symptoms handicap the lives of millions of patients with macular edema secondary to chronic and sometimes acute retinal disease. Proteins that neutralize the vascular endothelial growth factor (VEGF) pathway or glucocorticoids, at the cost of repeated intraocular injections over years, limit visual symptoms. A better understanding of why and how edema forms and how therapeutic molecules exert an anti-edematous effect will help prevent this disabling and blinding retinal complication from occurring.

Attenuation of Inflammatory Symptoms by Icariside B2 in Carrageenan and LPS-Induced Inflammation Models via Regulation of MAPK/NF-κB Signaling Cascades.

Prolonged inflammatory responses can lead to the development of several chronic diseases, such as autoimmune disorders and the development of natural therapeutic agents is required. A murine model was used to assess the anti-inflammatory effects of the megastigmane glucoside, icariside B2 (ICSB), and the assessment was carried out in vitro, and in vivo. The in vitro anti-inflammatory effects of ICSB were tested using LPS-stimulated BV2 cells, and the protein expression levels of inflammatory genes and cytokines were assessed. Mice were subcutaneously injected with 1% carrageenan (CA) to induce acute phase inflammation in the paw. Inflammation was assessed by measuring paw volumes hourly; subsequently, the mice were euthanized and the right hind paw skin was expunged and processed for reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analyses. ICSB inhibits LPS-stimulated nitric oxide (NO) and prostaglandin E2 (PGE2) generation by reducing the expression of inducible NO synthase (iNOS) and cyclooxygenase 2 (COX-2). ICSB also inhibits the COX-2 enzyme with an IC50 value of 7.80 ± 0.26 µM. Molecular docking analysis revealed that ICSB had a strong binding affinity with both murine and human COX-2 proteins with binding energies of −8 kcal/mol and −7.4 kcal/mol, respectively. ICSB also reduces the manifestation of pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β, at their transcriptional and translational level. ICSB hinders inhibitory protein κBα (IκBα) phosphorylation, thereby terminating the nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) nuclear translocation. ICSB also represses the mitogen-activated protein kinases (MAPKs) signaling pathways. ICSB (50 mg/kg) showed an anti-edema effect in CA-induced mice and suppressed the CA-induced increases in iNOS and COX-2 protein levels. ICSB attenuated inflammatory responses by downregulating NF-κB expression through interference with extracellular signal-regulated kinase (ERK) and p38 phosphorylation, and by modulating the expression levels of iNOS, COX-2, TNF-α, IL-1β, and IL-6.

Mannitol Reduces Spinal Cord Edema in Rats with Acute Traumatic Spinal Cord Injury

Background: The research about anti-edema effects of mannitol on acute traumatic spinal cord injury (SCI) in rats is rare. Objective: This study aimed to explore the effect of mannitol on spinal cord edema after SCI in rats. Methods: Seventy-eight adult female rats were assigned to three groups randomly: a sham control group (n = 18), a contusion and normal saline contrast group (n=30), and a contusion and mannitol treatment group (n=30). We used the open-field test to estimate the functional recovery of rats weekly. Spinal cord water content was measured to determine the spinal cord edema. The ultrastructure features of the injured dorsolateral spinal cord were determined on the 7th day after SCI by HE staining. Results: The mannitol group had greatly improved Basso-Beattie-Bresnahan (BBB) scores when compared with the saline contrast group. The spinal cord water content was increased significantly after SCI, and there was no significant difference in the water content between the NaCl and mannitol groups 1 day after SCI. The water content at 3 and 7 days after SCI was significantly lower in the mannitol group than in the NaCl group (p &lt; 0.05). Mannitol can reduce spinal cord edema by increasing the number of red blood cells in the injured spinal cord and decrease the ratio (dorsoventral diameter/ mediolateral diameter) of spinal cord 7 days post-SCI. Conclusion: Mannitol increases recovery of motor function in rats, reduces spinal cord edema and increases the number of red blood cells in the injured spinal cord, decreasing the ratio of spinal cord to reduce pressure.

Abilities of physical rehabilitation in pneumonia

The use of physical rehabilitation methods, in particular respiratory rehabilitation for pneumonia, allows to increase the tolerance to physical activity, improve oxygen consumption and endurance of patients compared to the initial level, reduce the frequency and duration of their hospitalization, as well as significantly improve the effectiveness of drug therapy. In the first stage of assisting patients with pneumonia of various genesis, therapeutic exercises are recommended that improve drainage function of the bronchi and promotes the discharge of bronchial mucous. Prescription of physiotherapeutic methods of treatment, which have a bactericidal, anti-inflammatory, anti-edema and resorption effects, significantly increase the effectiveness of complex therapeutic measures. A comprehensive approach to the treatment of pneumonia can produce better results by using all therapeutic physical exercise and physiotherapy options that have proven effective over many decades.

Therapeutic potential of topical naturopathic remedies in otorhinolaryngology

Introduction. Тhe search for drugs that accelerate the process of resolving post-traumatic reactive changes, which have both sufficient anti-edema and anti-inflammatory effects, and reparative properties, is relevant.Goal of reserch. The purpose of this review is to find a means to speed wound healing after nasal traumas.Materials and methods. The researchers conducted an analysis of scientific research data to evaluate the efficacy of naturopathic mountain arnica-based remedies for the treatment of patients with an external nose trauma accompanied by the formation of edema, hematoma of lateral nasal wall and/or skin abrasions of external nose.Results. This work shows that topical plant remedies based on Аrnicamontana has a pronounced anti-inflammatory and antiedema effect, comparable to the traditionally used for this purpose heparin-containing ointments and gels. However, unlike the latter, products based on Arnica montana have a pronounced wound- healing effect, which allows to significantly reduce the time to resolve traumatic injuries of the skin of the external nose. The analysis of the work also demonstrates the absence of adverse reactions when using this drug.Conclusion. The obtained data allow us to recommend topical naturpathic remedies based on Arnicamontana for use as a firstchoice drug for wound healing after nasal traumas. In addition, the drug is effective in the complex treatment of patients with nasal trauma requiring surgical intervention: at the preoperative stage - to reduce post-traumatic reactions and prepare for surgery, and at the postoperative stage - for the early recovery, reducing edema and inflammation.

Preliminary assessment of low-intensity transcranial magnetic stimulation (TMS) during the treatment for brain glioblastomas.

2545 Background: The standard treatment of malignant brain gliomas, including surgical and radiation therapies, does not provide recovery and a long-time favorable prognosis. The development of technologies and international guidelines on the introduction of electric (TTF) and electromagnetic (TMS) fields in combination treatment for glioblastomas aims to improve immediate results, as shown in experiments on human glioblastoma cell culture. The TMS protocol requires further refinement in parameters of frequency, intensity, and exposure with an assessment of the immediate results of combined treatment. Methods: The study included 60 patients diagnosed with MBG receiving osteoplastic craniotomy with radical (within visible unchanged tissues) tumor removal. Starting from the second day after the surgery, patients of group 1 (n = 30) received 10 sessions of magnetotherapy in the double exposure mode. For the first morning exposure, we used an ultra-low-frequency magnetic field (ULFMF) (0.03 to 9.0 Hz) on the hypothalamus projection area to induce a general antistress reaction. After 2.5-3 hours, local (on the surgical site) TMS exposure with the Neuro-MSD system (Russia) was applied in the pulse algorithm, up to 1 GHz and 5 Hz, 15 mT, 3 min. The induction was reduced exponentially (C = 0.8). The control group 2 (n = 30) did not receive ULFMF or TMS. Magnetic resonance imaging (MRI) was used to determine the volume of tumors (Vt, cm3) and perifocal edema (Ve, cm3) calculated according to the Shrek’s formula for an ellipsoid (V = a×b×c×π/6). Results: Before surgery, Vt = 54.7±5.7cm3 in group 1, in group 2 - Vt = 60.9±8.5cm3 (no statistical differences). After surgery and the subsequent course of ULFMF and TMS, residual tumor volumes in group 1 were 2.5 times lower than in controls (p &lt; 0.05). The difference between Ve values before and after treatment was on average 80.7 cm3 in group 1 and 41.8 cm3 in group 2 (p &lt; 0.05). Conclusions: The inclusion of sequential ULFMF and TMS exposures into postoperative therapy for gliomas, taking into account various vectors of the influence on the projection of centers of homeostasis regulation and the surgical field, as well as the development of programmed modes of biotropic exposure parameters, improves antitumor and anti-edematous effects.