Muscle Tissue Damage Research Articles

Natural antisense RNA Foxk1-AS promotes myogenic differentiation by inhibiting Foxk1 activity

BackgroundNatural antisense RNAs are RNA molecules that are transcribed from the opposite strand of either protein-coding or non-protein coding genes and have the ability to regulate the expression of their sense gene or several related genes. However, the roles of natural antisense RNAs in the maintenance and myogenesis of muscle stem cells remain largely unexamined.MethodsWe analysed myoblast differentiation and regeneration by overexpression and knockdown of Foxk1-AS using lentivirus and adeno-associated virus infection in C2C12 cells and damaged muscle tissues. Muscle injury was induced by BaCl2 and the regeneration and repair of damaged muscle tissues was assessed by haematoxylin–eosin staining and quantitative real-time PCR. The expression of myogenic differentiation-related genes was verified via quantitative real-time PCR, Western blotting and immunofluorescence staining.ResultsWe identified a novel natural antisense RNA, Foxk1-AS, which is transcribed from the opposite strand of Foxk1 DNA and completely incorporated in the 3′ UTR of Foxk1. Foxk1-AS targets Foxk1 and functions as a regulator of myogenesis. Overexpression of Foxk1-AS strongly inhibited the expression of Foxk1 in C2C12 cells and in tibialis anterior muscle tissue and promoted myoblast differentiation and the regeneration of muscle fibres damaged by BaCl2. Furthermore, overexpression of Foxk1-AS promoted the expression of Mef2c, which is an important transcription factor in the control of muscle gene expression and is negatively regulated by Foxk1.ConclusionThe results indicated that Foxk1-AS represses Foxk1, thereby rescuing Mef2c activity and promoting myogenic differentiation of C2C12 cells and regeneration of damaged muscle fibres.DfdN9uwC-a513-TBDoKHuCVideo

Effect of hydrogels on sports: how can hydrogels be implemented for sports recovery?

Due to their unique properties, hydrogels have typically been used for hygiene products, wound dressings, and drug delivery. However, as of recent, hydrogels have been noted as one of the best materials for engineering tissue due to their injectability and absorbability. This paper investigates the properties and functions of hydrogel and how its utilization in tissue engineering could be beneficial for the rehabilitation of athletes after a devastating injury. It links the discoveries of hydrogels for tissue engineering with the damaged muscle tissue of injured athletes, suggesting that the injected hydrogel would promote tissue regeneration in the location of the damaged muscle tissue much more efficiently than waiting for slow, natural regeneration and recovery. This ability of the hydrogel injection to promote tissue regeneration reduces the effects of catastrophic injuries for an athlete, allowing them to recover healthily and get back to their job quickly.

Sulforaphane Ameliorates Limb Ischemia/Reperfusion-Induced Muscular Injury in Mice by Inhibiting Pyroptosis and Autophagy via the Nrf2-ARE Pathway.

Background Limb ischemia/reperfusion (I/R) injury, as a life-threatening syndrome, is commonly caused by skeletal muscle damage resulting from oxidative stress. Additionally, inflammation-induced pyroptosis and dysregulated autophagy are vital factors contributing to the aggravation of I/R injury. Of note, sulforaphane (SFN) is a natural antioxidant, but whether it worked in limb I/R injury and the possible mechanism behind its protection for skeletal muscle has not been clearly established. Methods Effects of SFN on limb I/R-injured skeletal muscle were assessed by HE staining, followed by assessment of wet weight/dry weight (W/D) ratio of muscle tissues. Next, ELISA and biochemical tests were used to measure the inflammatory cytokine production and oxidative stress. Immunofluorescent analysis and Western blot were adopted to examine the level of pyroptosis- and autophagy-related proteins in vivo. Moreover, protein levels of Nrf2-ARE pathway-related factors were also examined using Western blot. Results SFN treatment could protect skeletal muscle against limb I/R injury, as evidenced by diminished inflammation, pyroptosis, autophagy, and oxidative stress in skeletal muscles of mice. Further mechanistic exploration confirmed that antioxidative protection of SFN was associated with the Nrf2-ARE pathway activation. Conclusions SFN activates the Nrf2-ARE pathway, and thereby inhibits pyroptosis and autophagy and provides a novel therapeutic strategy for the limb I/R-induced muscle tissue damage.

Cardiovascular Risk in Myositis Patients Compared to the General Population: Preliminary Data From a Single-Center Cross-Sectional Study.

BackgroundIdiopathic inflammatory myopathies (IIM) are associated with systemic inflammation, limited mobility, and glucocorticoid therapy, all of which can lead to metabolism disturbances, atherogenesis, and increased cardiovascular (CV) risk. The aim of this study was to assess the CV risk in IIM patients and healthy controls (HC), and its association with disease-specific features.MethodsThirty nine patients with IIM (32 females; mean age 56; mean disease duration 4.8 years; dermatomyositis: n = 16, polymyositis: n = 7, immune-mediated necrotizing myopathy: n = 8, anti-synthetase syndrome: n = 8) and 39 age-/sex-matched HC (32 females, mean age 56) without rheumatic diseases were included. In both groups, subjects with a history of CV disease (angina pectoris, myocardial infarction, cerebrovascular, and peripheral arterial vascular events) were excluded. Muscle involvement, disease activity, and tissue damage were evaluated (Manual Muscle Test-8, Myositis Intention to Treat Activity Index, Myositis Damage Index). Comorbidities and current treatment were recorded. All participants underwent examinations of carotid intima-media thickness (CIMT), pulse wave velocity (PWV), ankle-brachial index (ABI), and body composition (by densitometry and bioelectric impedance). The risk of fatal CV events was evaluated by the Systematic COronary Risk Evaluation (SCORE, charts for the European population) and its modifications.ResultsCompared to HC, there was no significant difference in IIM patients regarding blood pressure, ABI, PWV, CIMT, and the risk of fatal CV events by SCORE or SCORE2, or subclinical atherosclerosis (CIMT, carotid plaques, ABI, and PWV). The calculated CV risk scores by SCORE, SCORE2, and SCORE multiplied by the coefficient 1.5 (mSCORE) were reclassified according to the results of carotid plaque presence and CIMT; however, none of them was demonstrated to be significantly more accurate. Other significant predictors of CV risk in IIM patients included age, disease duration and activity, systemic inflammation, lipid profile, lean body mass, and blood pressure.ConclusionsNo significant differences in CV risk factors between our IIM patients and HC were observed. However, in IIM, CV risk was associated with age, disease duration, duration of glucocorticoid therapy, lipid profile, and body composition. None of the currently available scoring tools (SCORE, SCORE2, mSCORE) used in this study seems more accurate in estimating CV risk in IIM.

Study on the Antifatigue Effect of Compound Amino Acid Capsules

Supplementing amino acids was proven to relieve fatigue caused by exercise. This study explored the antifatigue effects of compound amino acid capsules (CAAC) on rats undergoing the forced swimming test (FST). CAAC augmented the endurance of FST in rats and alleviated the damage of skeletal muscle tissue and reduced the content of biochemical indicators in the serum. Furthermore, CAAC prevented skeletal muscle dysfunction in FST rats by modulating inflammation and oxidation reactions. After the treatment with CAAC, apoptosis and apoptosis-related protein and p-p65 were weakened, while the levels of SIRT1 and SIRT1/PGC-1α/Nrf2 pathway-related proteins were enhanced. The antifatigue properties of CAAC were associated with its antioxidant and anti-inflammatory capabilities, which were realized by activating the SIRT1/PGC-1α/Nrf2 pathway.

Effects of Red-Fleshed Pitaya (Selenicereus polyrhizus) Ingestion after Strenuous Exercise on Creatine Kinase and Mitochondrial Function in Rat Muscle Cells

BACKGROUND: Free radicals formed during strenuous exercise through an increase in reactive oxygen species induce damage to tissues (e.g., muscle and liver) and cause oxidative damage to cells, resulting in mitochondrial dysfunction. AIM: As an effective method to repair mitochondrial muscle cell function, this study investigated the effects of red-fleshed pitaya (RFP) ingestion on creatine kinase (CK), which is a biomarker for muscle tissue damage, and malondialdehyde (MDA) levels during strenuous exercise. METHODS: This study involved 25 3-month-old male rats with an average weight of 200 g. The RFP extract was obtained through ethanol extraction and concentrated using an air-drying method. Rats were randomly allocated into five groups as follows: Two control groups (K1 [no-exercise, no RFP] and K2 [exercise, no RFP]) and three test groups (P1, P2, and P3; subjected to exercise and treated with 75, 150, and 300 mg kg−1 body weight of RFP, respectively). The exercise was in the form of swimming for 20 min 3 times/week for 31 days. CK and MDA were measured through an enzyme-linked immunosorbent assay, and histopathological examinations were performed through hematoxylin and eosin staining of rat muscles. RESULTS: The MDA levels after the ingestion of RFP extracts were compared between the K2 group and the P1, P2, and P3 groups. The results showed significant differences (p < 0.05 for P1 and P2, and p < 0.01 for P3), indicating the production of free radicals and CK, with features of damaged muscle cells based on histopathology. Ingestion of the RFP extract led to improvements in soleus muscle cells, resulting in cell function repair. CONCLUSION: Levels of MDA and CK increased during exercise, which caused significant muscle damage. However, after treatment with the RFP extract, the levels of both markers decreased. Thus, strenuous exercise causes an increase in reactive oxygen species, resulting in increased free radical levels. RFP ingestion decreased oxidative stress levels, thus repairing mitochondrial cell function.

Identification and profiling of Trichinella spiralis circulating antigens and proteins in sera of mice with trichinellosis.

Trichinellosis is a zoonotic disease caused by the ingestion of the Trichinella nematode. With a worldwide incidence of approximately 10,000 cases per year, Trichinella spiralis is responsible for most human infections. There are no specific signs or symptoms of this parasitic infection. Muscle biopsy is the gold diagnostic standard for trichinellosis, but the technique is invasive and unable to detect the early stage of infection. Although immunodiagnostics are also available, antibody detection usually occurs after 3 weeks and prolonged up to 19 years after the acute phase. Therefore, additional diagnostic biomarkers must be identified to improve trichinellosis diagnosis. This study aimed to measure concentration changes in mouse serum proteins prior to T. spiralis infection and 2, 4 and 8 weeks after infection, and to identify T. spiralis circulating proteins and antigens using mass spectrometry-based proteomics. Mouse muscle-related proteins including inter-alpha-trypsin inhibitor heavy chain H2, a protein involved in the response to muscle tissue damage, were up-regulated in mouse sera during the T. spiralis larvae invasion. Additionally, 33 circulatory parasite proteins were identified in infected mouse sera. Notably, T. spiralis long-chain fatty acid transport protein 1 could be detected in the early stage of infection and peroxidasin-like protein was identified 2, 4 and 8 weeks after infection. Seventeen T. spiralis circulating antigens were detected in mouse immune complexes, with PX domain protein being found 2, 4 and 8 weeks after infection. Because peroxidasin-like protein and PX domain protein were detected at all post-infection time points, sequence alignments of these proteins were performed, which showed they are conserved among Trichinella spp. and have less similarity to the human and murine sequences. Integrative analysis of T. spiralis biomarkers throughout the course of infection may reveal additional diagnostic targets to improve early diagnosis of trichinellosis.

Higher Muscle Damage Triggered by Shorter Inter-Set Rest Periods in Volume-Equated Resistance Exercise.

ObjectivesThe aim of the manuscript was to analyze the effects of two rest periods between volume-equated resistance exercise (RE) on inflammatory responses (cytokines and leukocyte) and muscle damage.MethodsTen trained men (26.40 ± 4.73 years, 80.71 ± 8.95 kg, and 176.03 ± 6.11 cm) voluntarily participated in training sessions consisting of five sets of 10 reps performed at 10-RM on (1) the barbell bench press followed by (2) leg press, with either 1- or 3-min rest between sets and exercises. Circulating concentrations of different biomarkers was measured before (Pre), and after 3 h (excepted for cytokines), 6, 12, and 24 h from exercise. The rate of perceived exertion (RPE) was recorded after each set on both planned visits.ResultsWe found greater increases triggered by the 1-min rest period in Creatine Kinase (CK), occurring from 12 to 24 h post-exercise compared to the 3-min rest condition. A significant increase in the 1-min rest condition was also observed in the total number of leukocytes, neutrophils, and monocytes. The 1-min rest period also triggered increases compared to baseline in pro-inflammatory cytokines [Interleukin 1 beta (IL-1β), p = 0.004; tumor necrosis factor α (TNF-α), p = 0.01; and granulocyte-macrophage colony-stimulating factor (GM-CSF), p = 0.01], which were more evident after 6 and 12 h post-exercise. Similarly, increases in anti-inflammatory cytokines [Interleukin 5 (IL-5), p = 0.01; Interleukin 6 (IL-6), p = 0.01; and Interleukin 10 (IL-10), p = 0.01] at all time-points were observed.ConclusionOur results indicate that a 1-min rest condition in volume-equated RE promoted greater overall muscle tissue damage with a longer duration of the inflammatory processes compared to a 3-min rest.

Integrative omics reveals subtle molecular perturbations following ischemic conditioning in a porcine kidney transplant model

BackgroundRemote Ischemic Conditioning (RIC) has been proposed as a therapeutic intervention to circumvent the ischemia/reperfusion injury (IRI) that is inherent to organ transplantation. Using a porcine kidney transplant model, we aimed to decipher the subclinical molecular effects of a RIC regime, compared to non-RIC controls.MethodsKidney pairs (n = 8 + 8) were extracted from brain dead donor pigs and transplanted in juvenile recipient pigs following a period of cold ischemia. One of the two kidney recipients in each pair was subjected to RIC prior to kidney graft reperfusion, while the other served as non-RIC control. We designed an integrative Omics strategy combining transcriptomics, proteomics, and phosphoproteomics to deduce molecular signatures in kidney tissue that could be attributed to RIC.ResultsIn kidney grafts taken out 10 h after transplantation we detected minimal molecular perturbations following RIC compared to non-RIC at the transcriptome level, which was mirrored at the proteome level. In particular, we noted that RIC resulted in suppression of tissue inflammatory profiles. Furthermore, an accumulation of muscle extracellular matrix assembly proteins in kidney tissues was detected at the protein level, which may be in response to muscle tissue damage and/or fibrosis. However, the majority of these protein changes did not reach significance (p < 0.05).ConclusionsOur data identifies subtle molecular phenotypes in porcine kidneys following RIC, and this knowledge could potentially aid optimization of remote ischemic conditioning protocols in renal transplantation.

Течение и диагностика лептоспироза у лошадей на территории Омской области

Based on the studies carried out, it was found that on the territory of the Omsk region, horse leptospirosis is recorded annually, proceeds in an asymptomatic form and has a latent course. Clinical signs: jaundice, muscle tissue damage, impaired coordination of movement, iridocyclitis, damage to the nervous system and deformity of the joints, abortion; at autopsy: yellowness of the mucous membranes, hemorrhages in the bladder, damage to the cortical layer of the kidneys. In the Omsk region, serotypes of Leptospira Icterohaemorrhagiae, Tarassovi, Hebdomadis, Canicola circulate among horses.

Foot kinematics and leg muscle activation patterns are altered in those with limited ankle dorsiflexion range of motion during incline walking

BackgroundLarger ankle dorsiflexion (DF) is required when walking on inclined surfaces. Individuals with limited DF range of motion (ROM) may experience greater tissue stress on sloped surfaces and walk in altered gait patterns compared to the those with normal DF ROM. Research questionWould the individuals with limited DF ROM walk with distinctive ankle DF patterns compared to those with normal DF ROM on the inclined surfaces? MethodsTen Limited DF ROM (passive ROM=35.3 ± 2.7°) and nine Normal DF ROM (passive ROM=46.4 ± 4.2°) participants walked on a treadmill at five slope angles (0°, 5°, 10°, 15°, 20°) for 2 min at a self-selected speed. The peak DF angles and the peak myoelectric activity levels of the tibialis anterior (TA) and soleus (SOL) muscles were quantified during the swing and stance phases of each walking trial, and they were compared between the two groups. ResultsParticipants with limited DF ROM walked with smaller peak DF (3.1° at 0° slope ~ 8.4° at 20° slope) and greater peak TA activity in swing than those of the Normal ROM participants (3.4° ~ 12.2°), with significant differences at 20° slope. The peak DF angle in stance (Limited: 9.6° ~ 19.0°; Normal: 10.1° ~ 21.0°) did not differ between the two groups at all slopes, but the peak activity of the SOL muscle was significantly greater for the Limited group at slopes of 10° and higher. SignificanceStudy results indicate that incline walking could be more challenging to the individuals with limited DF ROM as they need to approach and push-off the sloped surfaces with more efforts of the dorsiflexor and the plantar flexor muscles, respectively. Prolonged walking on inclined surfaces may produce faster development of muscle fatigue or tissue damage than those with normal DF ROM.

Combined application of chondroitinase ABC and photobiomodulation with low-intensity laser on the anal sphincter repair in rabbit

BackgroundPhotobiomodulation with low-intensity laser (LIL) and chondroitinase ABC (ChABC) can repair damaged muscle tissue, so the aim of this study was to investigate the effect of co-administration of these two factors on anal sphincter repair in rabbits.MethodsMale rabbits were studied in 5 groups (n = 7): Control (intact), sphincterotomy, laser, ChABC and laser + ChABC. 90 days after intervention were evaluated resting and maximum squeeze pressures, number of motor units, collagen amount, markers of muscle regeneration and angiogenesis.ResultsResting pressure in the Laser + ChABC group was higher than the sphincterotomy, laser and ChABC groups (p < 0.0001). Maximum squeeze pressure in the all study groups was higher than sphincterotomy group (p < 0.0001). In the laser + ChABC and ChABC groups, motor unit numbers were more than the sphincterotomy group (p < 0.0001). Collagen content was significantly decreased in the laser (p < 0.0001) and laser + ChABC groups. ACTA1 (p = 0.001) and MHC (p < 0.0001) gene expression in the Laser + ChABC group were more than the laser or ChABC alone. VEGFA (p = 0.009) and Ki67 mRNA expression (p = 0.01) in the Laser + ChABC group were more than the laser group, But vimentin mRNA expression (p < 0.0001) was less than the laser group.ConclusionCo-administration of ChABCs and photobiomodulation with LIL appears to improve the tissue structure and function of the anal sphincter in rabbits more than when used alone.

Замісні трансплантати в травматології та ортопедії

Робота присвячена дослідженню розвитку використання біоматеріалів для заміщення дефектів довгих кісток. Останніми десятиліттями намітилась активна тенденція, спрямована на створення матеріалів, які заміняють пошкоджені шкірні покриви, м’язову та кісткову тканину, судини та нервові волокна. На даний період такі матеріали дістали назву «біоматеріали». Одним із перспективних напрямків є виготовлення композиційних матеріалів на основі біоскла. Розглянуто особливості використання біоматеріалів різної природи, позитивні властивості та проблеми, пов’язані з їх використанням. Сформульовано вимоги до сучасних біоматеріалів, які використовуються для імплантації. Коротко охарактеризовано еволюцію даного напрямку та основні віхи. Визначено перспективні напрямки щодо подальших досліджень у даній галузі.

Особливості відновлення м’язів за умов експериментальної післятравматичної контрактури

The frequency of traumatic injuries of the maxillofacial area and the degree of their severity, have been increasing in recent years. The introduction of modern methods of treatment made it possible to improve the results of treatment and shorten its duration. Myogenic contractures develop as a complication after facial injuries, soft tissue injuries, in particular, masticatory muscles. The gastrocnemius muscle of a rat has the same striated structure as the pterygoideus medialis muscle of a person. The purpose of the work is to study the regeneration of striatal muscles with post-traumatic contractures on the basis of combined treatment of laboratory rats. Materials and methods. The study was carried out on 45 sexually mature 12 months old outbred white male rats, which weighed 180-200 g. In animals, reflex post-traumatic muscle contractures (traumatic myositis) resulting from the slaughter of calf muscles (without violating the integrity of muscle tissue) were simulated on the posterior left leg. The rats were divided into two groups. Group 1 included 21 animals that did not receive treatment and whose wounds healed by secondary intention. Group 2 included 24 rats that received combined treatment: on the 2nd day after surgery – general (oral) administration of the drug with the active substance cyclobenzaprine hydrochloride – 0.15 mg, once a day with daily procedures of magnetic laser therapy on the affected hind limb. Results and discussion. Depending on the signs of pain behavior (changes in behavior, restriction of movement, increased sensitivity, pain), the intensity of myogenic pain syndrome was assessed (low, moderate, high, very high). It was found that the use of combined treatment (magnetic laser therapy and the use of cyclobenzaprine hydrochloride) led to the normalization of behavioral and motor reactions by the 28th day: 56% of rats didn’t feel any pain and 44% had a low level of pain. The animals with the same trauma, which weren’t treated, showed a high and moderate level of pain. On the 28th day these animals could lean on their hind limbs while they were moving. However, they could not fully move due to a sharp restriction of their left hind limb function. The obtained results are the basis for the development of new approaches to improving the methods of prevention and rehabilitation treatment of contractures using magnetic laser therapy and central muscle relaxants. Conclusion. It was found that the use of magnetic laser therapy and cyclobenzaprine hydrochloride inhibited the development of an acute inflammatory reaction in the damaged muscle tissue of the hind limb of animals, accelerated and optimized reparative processes, which prevented excessive, functionally significant growth of connective tissue

The incidence of muscle tissue damage during therapy with atorvastatin in patients after STEMI

Abstract Objective To study the incidence of side effects from muscle tissue during therapy with atorvastatin at various doses in patients with acute ST-segment elevation myocardial infarction (STEMI) during 48 weeks of follow-up. Methods The study included 115 STEMI patients aged 30 to 65 years (mean age 51.7±9.5 years). Patients were randomized to atorvastatin treatment groups. Group 1 included 59 people who took atorvastatin 80 mg / day; group 2 - 56 patients who received moderate doses of atorvastatin. The compared persons were matched by age, sex, and anthropometric data. Initially on the 7–9th days, after 24 and 48 weeks of follow-up, the CPK-MB serum level was analyzed. Muscle damage was assessed after 5–6, 24, 48 weeks of follow-up according to the development of the following symptoms: pain, fatigue, muscle weakness, decreased physical activity - on a 10-point scale. Results The CPK-MB level in the 1st group initialy was 701.5 [95% CI 391; 1012] U / L, after 24 weeks - 162.8 [95% CI 130.2; 195.4] U / L (p&amp;lt;0.001), after 48 weeks - 205.6 [95% CI 134.8; 276.4] U / L (p&amp;lt;0.001). In group 2, the dynamics of CPK-MB: on days 7–9 - 522.7 [95% CI 115.8; 755.1 U / L, after 24 weeks - 141.4 [95% CI 122.6; 160.3] U / L (p=0.0004), after 48 weeks - 150.5 [95% CI 123.9; 177.1] U / L (p=0.0003). A detailed analysis in four patients of the 1st group revealed an increase in CPK-MB &amp;gt;4 upper limit of normal (ULN) after 48 weeks of follow-up (6.8%). Moreover, symptoms of muscle damage against the background of pathological CPK-MB values were observed only in two people (3.4%). In patients of the 2nd group after 24–48 weeks of therapy with atorvastatin, there was no increase in CPK-MB &amp;gt;4 ULN. In addition, there were no cases of drug withdrawal in any of the groups due to an increase in CPK-MB&amp;gt;10 ULN. Clinical symptoms of muscle damage after 5–6th, 24th and/or 48th weeks of follow-up were diagnosed in the 1st group in 41 patients (69.5%), in the 2nd group - in 31 people (55%) (p=0.11). Conclusion In STEMI patients on the background of 48-week therapy with atorvastatin, no serious adverse effects on the muscle tissue were revealed, which testifies in favor of the safety of high-dose statin therapy. The incidence of myalgia did not depend on the dose of the drug. Funding Acknowledgement Type of funding sources: None.

The inducing of caspase and Bcl-2 pathway with royal jelly decreases the muscle tissue damage exposed with fluoride in rats.

In this study, 42 Wistar albino male rats (n = 42, 8 weeks old) were used. Rats were divided into 6 groups and 7 rats included each group. Groups: (i) Control group: Standard diet; (ii) RJ (royal jelly) group: Standard diet + royal jelly; (iii) F50 group: Standard diet + 50 mg/kg fluoride; (iv): F100 group: Standard diet + 100 mg/kg fluoride; (v) F50+RJ group: Standard diet + 50 mg/kg fluoride + royal jelly; (vi): F100+RJ group: Standard diet + 100 mg/kg fluoride + royal jelly. After 8 weeks, the rats were decapitated, and their muscle tissues were removed. Expression levels of Caspase-3, Caspase-6, Bax, tumor necrosis factor-α (TNF-α), interleukin 1 alpha (IL1-α) and Bcl-2 proteins in muscle tissue were determined by western blotting method. Histopathological analyses were also performed on the muscle tissue. Malondialdehyde (MDA), glutathione (GSH) and catalase (CAT) analyses were determined by a spectrophotometer. According to the obtained results, Bcl-2, TNF-α and IL1-α protein expression was increased in damage groups compared to the control and royal jelly groups, while Caspase-3, Caspase-6 and Bax protein expression levels decreased in damage groups. MDA level increased in damage groups compared to the control and royal jelly groups, while CAT and GSH levels increased with royal jelly application in royal jelly-given group in comparison to the flouride-exposed group. According to histopathological analysis results, edema and inflammatory cell formations were found in the injury groups, a tendency to decrease in these injuries was observed in the treatment groups. Based on these results, we can say that royal jelly has protective effects on muscle tissue against fluoride damage.Graphical abstract

Окислительный стресс как фактор риска развития диабетической миопатии у детей

Цель: определение патогенетической роли окислительного стресса в развитии диабетической миопатии у детей, больных сахарным диабетом. Материалы и методы. Под наблюдением находилось 60 детей, больных сахарным диабетом 1-го типа (СД1), в возрасте от 11 до 17 лет. В 1-ю группу вошло 20 пациентов с длительностью заболевания до 1 года; во 2-ю группу — 20 пациентов с течением заболевания от 1 до 5 лет; в 3-ю группу было включено 20 пациентов с течением заболевания 5 лет и более. Группу контроля составили 20 условно здоровых детей. Всем детям проводилось измерение индекса скелетной мускулатуры, ультразвуковое исследование скелетных мышц и определение уровня креатинфосфокиназы, гомоцистеина и нитротирозина в сыворотке крови. Результаты. По данным проведенной ультразвуковой диагностики установлено, что у детей, больных СД1, в динамике заболевания происходило снижение массы скелетной мускулатуры за счет уменьшения толщины мышц. Доказано, что гипергликемия у детей, больных СД1, приводила к значительному окислительному стрессу, о чем свидетельствовало увеличение содержания гомоцистеина и нитротирозина в сыворотке крови, и поражению скелетных мышц, которое подтверждалось высокими уровнями креатинфосфокиназы в сыворотке крови начиная с 1-го года заболевания. Существенные изменения были установлены в 3-й группе детей, у которых определялись высокие значения гомоцистеина и нитротирозина по сравнению как с контрольной, так и с 1-й группой исследования (р &lt; 0,05). Установлена обратная корреляционная связь между уровнями гомоцистеина, нитротирозина и индексом скелетной мускулатуры (соответственно r = –0,39 (p &lt; 0,05); r = –0,35 (p &lt; 0,05)) и зависимость данных показателей от состояния гликемического контроля. Выводы. У детей, больных сахарным диабетом 1-го типа, отмечалось прогрессивное повышение активности креатинфосфокиназы с 1-го года заболевания, что свидетельствует о раннем поражения мышечной ткани. Одной из причин поражения скелетных мышц и формирования диабетической миопатии у детей, больных сахарным диабетом, выступает окислительный стресс, который усиливался при неудовлетворительном гликемическом контроле.

Ultrasonographic examination of skeletal muscles in traumatic ischemia (experimental study)

Post-traumatic muscles ischemia of the extremities is the result of severe trauma and leads to permanent dysfunction. The tactics of management and treatment of patients are decisive at all stages, so the latest methods of treatment using cellular technologies are being developed to prevent the development of complications and improve long-term results. Aim: to determine the correlation between histological and ultrasonographic parameters (qualitative and quantitative) in the muscles after traumatic ischemia and to compare the results. Material and methods. The study was performed on rabbits breed Chinchilla. The animals were placed on a tourniquet on the lower limb from the middle third of the thigh to the ankle joint, after 6 hours it was removed. Developed software to determine the texture of the sonographic image (δ-entropy) allowed to assess the qualitative and quantitative changes in the damaged muscles. Correlation analysis was performed between sonographic and histological changes in the muscles. Results. The relative amount of structurally altered tissue was morphometrically estimated and compared with entropy. A high correlation between muscle damage and vertical δ-entropy has been found, indicating that high-probability sonography can detect areas of necrosis and, to a lesser extent, fibrosis in the development of ischemic limb contracture. Conclusions. The obtained high positive correlation between the histological index of muscle tissue damage (especially atrophy of muscle fibers and fibrosis) and the results of sonographic data processing, namely vertical δ-entropy, have clinical importance in terms of establishing the severity of necrotic lesions segments of the extremities and the prediction of fibrous changes, formation of limb contracture. Key words: traumatic ischemia, necrosis, histological changes in the muscles.

The roles of betulinic acid on circulating concentrations of creatine kinase and immunomodulation in mice infected with chloroquine-susceptible and resistant strains of Plasmodium berghei.

Complete malarial therapy depends largely on the immunological and inflammatory response of the host to the invading potentials of malarial parasite. In this study, we evaluated the roles of betulinic acid on immunological response, anti-inflammatory potentials, cardiac and skeletal muscle tissue damage in mice infected with chloroquine susceptible (NK 65) and resistant (ANKA) strains of Plasmodium berghei. Serum Interleukins 1β and 6 (IL-1β, IL-6), tumour necrosis factor alpha (TNF-α), immunoglobulins G and M (IgG and IgM), C-reactive protein (CRP) and creatine kinase (CK) were determined using ELISA technique. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma glutammyl transferase (GGT) were determined using ELISA technique. The results showed that betulinic acid decreased the levels of IL-1β, IL-6, TNF-α and CRP relative to the infected control. The IgG and IgM levels significantly increased in both models while CK did not decrease significantly in both models although serum AST, ALT and GGT significantly decreased compared to the infected control. These results showed that betulinic acid possessed anti-inflammatory, immunomodulatory and remediating effects on tissue damage. Furthermore, the decrease in activity of CK brought about by betulinic acid is indicative of decrease in cardiac and skeletal muscle injury which is a major pathological concern in Plasmodium infection and treatment.

Muscle Tissue Damage and Recovery After EV71 Infection Correspond to Dynamic Macrophage Phenotypes.

Enterovirus 71 (EV71) is a positive single-stranded RNA virus from the enterovirus genus of the Picornaviridae family. Most young children infected with EV71 develop mild symptoms of hand, foot and mouth disease, but some develop severe symptoms with neurological involvement. Limb paralysis from EV71 infection is presumed to arise mainly from dysfunction of motor neurons in the spinal cord. However, EV71 also targets and damages skeletal muscle, which may also contribute to the debilitating symptoms. In this study, we have delineated the impacts of EV71 infection on skeletal muscle using a mouse model. Mouse pups infected with EV71 developed limb paralysis, starting at day 3 post-infection and peaking at day 5-7 post-infection. At later times, mice recovered gradually but not completely. Notably, severe disease was associated with high levels of myositis accompanied by muscle calcification and persistent motor end plate abnormalities. Interestingly, macrophages exhibited a dynamic change in phenotype, with inflammatory macrophages (CD45+CD11b+Ly6Chi) appearing in the early stage of infection and anti-inflammatory/restorative macrophages (CD45+CD11b+Ly6Clow/-) appearing in the late stage. The presence of inflammatory macrophages was associated with severe inflammation, while the restorative macrophages were associated with recovery. Altogether, we have demonstrated that EV71 infection causes myositis, muscle calcification and structural defects in motor end plates. Subsequent muscle regeneration is associated with a dynamic change in macrophage phenotype.