scholarly journals Effect of p38 MAPK on oxidative phosphorylation in regeneration of muscle tissue

2018 ◽  
pp. 66-70
Author(s):  
И.А. Шурыгина ◽  
М.Г. Шурыгин
Keyword(s):  
Oxidative Phosphorylation ◽  
P38 Mapk ◽  
Muscle Tissue ◽  
Active Substance ◽  
Control Group ◽  
Complex Iv ◽  
Animal Group ◽  
Oxphos Complex ◽  
Sb 203580 ◽  
Myosatellite Cells

Цель исследования: определить влияние блокады р38 МАРК на систему окислительного фосфорилирования при репарации мышечной ткани. Материалы и методы: Контрольной группе животных (n = 21) наносили рану длиннейшей мышцы спины, в рану вносили лекарственную плёнку без активного вещества, основной группе (n = 21) пленку с блокатором р38 МАР-киназы SB 203580. Выведение из эксперимента осуществляли на 1, 3, 7, 14 и 30 сутки. При гистологическом исследовании подсчитывали количество миосателлитов и количество образующихся «мышечных почек» в поле зрения в зоне травмы. Иммунофлюоресцентным методом изучали активность экспрессии OxPhos Complex IV. Результаты. Установлено, что блокада р38 МАРК каскада при помощи локального введения активного вещества в составе лекарственной пленки позволила «затормозить» деление миосателлитов в ранние сроки репаративного процесса, обусловила позднее начало образования «мышечных» почек в зоне регенерации - на 7 сутки в сравнение с 3 сутками в контрольной группе, а также привела к резкому усилению окислительного фосфорилирования в зоне регенерации мышечной ткани. The aim of the study was to determine the effect of p38 MAPK inhibition on the oxidative phosphorylation system during repair of muscle tissue. Materials and methods. In the control animal group (n = 21), a wound was inflicted on the longest back muscle; then a medicinal film free of active substance was applied to the wound. In the main group (n = 21), the applied film contained a p38 MAP-kinase inhibitor, SB 203580. The animals were euthanized on days 1, 3, 7, 14, and 30. In the histological study, the number of myosatellite cells per field of view was counted in the trauma zone. The immunofluorescence method was used to study the intensity of OxPhos Complex IV expression. Results. Inhibition of the p38 MAPK cascade by local administration of the active substance formulated into the medicated film allowed «putting the brakes» on division of myosatellite cells during the early reparative process, on day 7 vs. day 3 in the control group, and also resulted in a sharp increase in oxidative phosphorylation in the regeneration zone of muscle tissue.

Acute adenosine preconditioning is mediated by p38 MAPK activation in discrete subcellular compartments

2005 ◽  
Vol 288 (3) ◽  
pp. H1359-H1366 ◽  
Author(s):  
Cherry Ballard-Croft ◽  
Gentian Kristo ◽  
Yukihiro Yoshimura ◽  
Easton Reid ◽  
Byron J. Keith ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Adenosine Receptor ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fraction ◽  
Control Group ◽  
Mapk Activation ◽  
Subcellular Compartments ◽  
Sb 203580

Although acute adenosine preconditioning (PC) is well established, the signaling pathways mediating this cardioprotection remain unclear. Because adenosine receptor agonists activate p38 MAPK and this kinase has been implicated in ischemic and pharmacological PC, the purpose of this study was to determine the role of p38 MAPK in acute adenosine receptor PC. The role of p38 MAPK activation in discrete subcellular compartments during ischemia-reperfusion was also determined. The following groups were used in an in vivo rat ischemia-reperfusion model: 1) control (10% DMSO iv), 2) the A1/A2a adenosine receptor AMP-579 (50 μg/kg iv), 3) AMP-579 + the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 100 μg/kg iv), 4) AMP-579 + the p38 MAPK inhibitor SB-203580 (1 mg/kg iv), and 5) SB-203580 alone. p38 MAPK activation was measured by Western blot analysis in cytosolic, mitochondrial, membrane, and nuclear/myofilament fractions obtained from hearts at preischemic, ischemic, and reperfusion time points. A significant reduction in infarct size was observed with AMP-579 PC, an effect blocked by DPCPX or SB-203580 pretreatment. AMP-579 treatment was associated with a significant increase in p38 MAPK activation in the nuclear/myofilament fraction before ischemia, whereas no activation of this kinase occurred during ischemia or reperfusion. In contrast, p38 MAPK was activated in the mitochondrial fraction by ischemia and in the cytosolic, mitochondrial, and membrane fractions by reperfusion in the control group. SB-203580 blocked the AMP-579-induced increase in phosphorylation of the downstream p38 substrate activating transcription factor-2. These results suggest a role for p38 MAPK activation in discrete subcellular compartments in acute adenosine A1 receptor PC.

scholarly journals Absorption of iodotyrosine from iodized milk protein in animals

2020 ◽  
Vol 8 (1) ◽  
pp. 60-66
Author(s):  
Larisa Bolshakova ◽  
Dmitry Lukin
Keyword(s):  
Blood Plasma ◽  
Muscle Tissue ◽  
Potassium Iodide ◽  
Milk Protein ◽  
Control Group ◽  
Animal Group ◽  
Rat Blood ◽  
Organic Iodine ◽  
Muscle Tissues ◽  
Experimental Group

Introduction. One of the ways to the solve iodine deficiency problem is the addition of iodine to farm animal feed. It allows producing iodized livestock products. Promising sources of organic iodine are iodotyrosine-containing iodized milk proteins. Organic iodine accumulation in organs and tissues has not been sufficiently studied. Study objects and methods. We determined iodotyrosine content in rat blood plasma and in pig muscle tissue. For this purpose, high performance liquid chromatography with mass spectrometric detection and cathodic stripping voltammetry were used. Results and discussion. At the first stage of the study, we examined iodotyrosines in rat blood plasma after a single administration of iodized milk protein or potassium iodide (30 μg I/kg weight) at specific time intervals. A significant increase in the concentration of monoiodotyrosine and diiodotyrosine was recorded 4 and 24 h after the administration. At the second stage, we studied the accumulation of iodotyrosines in the muscle tissue of pigs during their fattening period (104 days). The diet of the control animal group included potassium iodide (0.6 mg I/kg of feed). The experimental groups A and B got iodized milk protein (0.3 and 0.6 mg I/kg of feed, respectively). Monoiodotyrosin content in the muscle tissue of pigs of the experimental groups was 3.0 and 5.2 times higher than that in the control group. Diiodotyrosine content was 4.9 and 8.2 times higher. In the experimental group A, iodine content in muscle tissues was 26% higher than that in the control group, in the experimental group B it was 72% higher. Calculations of iodine intake balance and its accumulation in muscle tissues showed that in animals whose diet included iodized milk protein, the iodine assimilation was much higher (0.70 and 0.53%) than in the control group (0.21%). Conclusion. Iodotyrosines from iodized milk protein are absorbed by the gastrointestinal tract in an unchanged form and accumulate in muscle tissues. The findings give more clear understanding of physiological and biochemical mechanisms of organic iodine absorption in animals.

scholarly journals EFFECT OF JNK MAPK ON THE REPAIR OF DAMAGED SKELETAL MUSCLE

2018 ◽  
Vol 3 (5) ◽  
pp. 137-140
Author(s):  
I. A. Shurygina ◽  
M. G. Shurygin
Keyword(s):  
Skeletal Muscle ◽  
Muscle Tissue ◽  
Active Substance ◽  
Slow Release ◽  
Damage Zone ◽  
Experimental Studies ◽  
Main Group ◽  
Mitogen Activated Protein Kinase ◽  
Control Group ◽  
Mapk Activity

Regeneration of muscles after injuries, as well as the development of methods that stimulate this process, is an important problem in medicine and biology. The objective of the study was to evaluate the effect of local blocking of mitogen-activated protein kinase (MAPK) activity of the JNK group (c-Jun N-terminal kinase) on the repair of muscle tissue. Materials and methods. The effect of the JNK MAPK SP600125 blocker on the repair of muscle tissue was studied on a model of a skin and muscle wound in Wistar rats. The main group (n = 30) was injected with a drug plate containing SP600125 with a slow release of the active substance, the control group (n = 30) – the plate without the active substance. The number of dividing myosatellites and muscle kidneys in the damage zone was estimated. Results. Experimental studies have shown that when using a drug plate containing a JNK SP600125 blocker with a slow release of the active substance, the number of dividing myosatellites and forming muscle kidneys in the injury zone of the muscle in the main group on the 7th, 14th and 30th days was significantly higher (p < 0.05) than in the control. Conclusion. Local blockade of JNK MAPK in the zone of muscle damage provides the ability to stimulate the repair of damaged skeletal muscle.

scholarly journals SPAK-p38 MAPK signal pathway modulates claudin-18 and barrier function of alveolar epithelium after hyperoxic exposure

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chih-Hao Shen ◽  
Jr-Yu Lin ◽  
Cheng-Yo Lu ◽  
Sung-Sen Yang ◽  
Chung-Kan Peng ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Knockout Mice ◽  
Barrier Function ◽  
Alveolar Epithelium ◽  
Signal Pathway ◽  
Control Group ◽  
Barrier Dysfunction ◽  
Hyperoxic Exposure ◽  
Monolayer Permeability ◽  
Mapk Signal Pathway

Abstract Background Hyperoxia downregulates the tight junction (TJ) proteins of the alveolar epithelium and leads to barrier dysfunction. Previous study has showed that STE20/SPS1-related proline/alanine-rich kinase (SPAK) interferes with the intestinal barrier function in mice. The aim of the present study is to explore the association between SPAK and barrier function in the alveolar epithelium after hyperoxic exposure. Methods Hyperoxic acute lung injury (HALI) was induced by exposing mice to > 99% oxygen for 64 h. The mice were randomly allotted into four groups comprising two control groups and two hyperoxic groups with and without SPAK knockout. Mouse alveolar MLE-12 cells were cultured in control and hyperoxic conditions with or without SPAK knockdown. Transepithelial electric resistance and transwell monolayer permeability were measured for each group. In-cell western assay was used to screen the possible mechanism of p-SPAK being induced by hyperoxia. Results Compared with the control group, SPAK knockout mice had a lower protein level in the bronchoalveolar lavage fluid in HALI, which was correlated with a lower extent of TJ disruption according to transmission electron microscopy. Hyperoxia down-regulated claudin-18 in the alveolar epithelium, which was alleviated in SPAK knockout mice. In MLE-12 cells, hyperoxia up-regulated phosphorylated-SPAK by reactive oxygen species (ROS), which was inhibited by indomethacin. Compared with the control group, SPAK knockdown MLE-12 cells had higher transepithelial electrical resistance and lower transwell monolayer permeability after hyperoxic exposure. The expression of claudin-18 was suppressed by hyperoxia, and down-regulation of SPAK restored the expression of claudin-18. The process of SPAK suppressing the expression of claudin-18 and impairing the barrier function was mediated by p38 mitogen-activated protein kinase (MAPK). Conclusions Hyperoxia up-regulates the SPAK-p38 MAPK signal pathway by ROS, which disrupts the TJ of the alveolar epithelium by suppressing the expression of claudin-18. The down-regulation of SPAK attenuates this process and protects the alveolar epithelium against the barrier dysfunction induced by hyperoxia.

scholarly journals Gene Expression Profiling of Mitochondrial Oxidative Phosphorylation (OXPHOS) Complex I in Friedreich Ataxia (FRDA) Patients

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e94069 ◽  
Author(s):  
Mohammad Hossein Salehi ◽  
Behnam Kamalidehghan ◽  
Massoud Houshmand ◽  
Goh Yong Meng ◽  
Majid Sadeghizadeh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Oxidative Phosphorylation ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Complex I ◽  
Friedreich Ataxia ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Oxphos Complex

Abstract P233: Diabetic Cardiomyopathy is Reversed by Increased Mitochondrial Bioenergetics Due to PGC-1α Activation by EET Treatment of Obese Mice

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Jian Cao ◽  
John A McClung ◽  
Shailendra P Singh ◽  
Lars Bellner ◽  
Maayan Waldman ◽  
...  
Keyword(s):  
Heart Failure ◽  
Insulin Resistance ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Dysfunction ◽  
Diabetic Cardiomyopathy ◽  
Cardiac Fibrosis ◽  
Systolic Function ◽  
Control Group ◽  
Protein Markers ◽  
Obesity And Diabetes

Introduction: Obesity and diabetes are associated with progressive cardiac fibrosis that, sequentially, results in diastolic dysfunction, reduced contractility, and ultimately heart failure. Contributing factors include hyperglycemia, insulin resistance, mitochondrial dysfunction, and a reduction in AMPK signaling. PGC-1α activates mitochondrial biogenesis and oxidative phosphorylation and is decreased in patients with diabetes mellitus (DM). We hypothesize that an epoxyeicosatrienoic acids (EETs) agonist (EET-A) will increase PGC-1α levels in a db mouse model of DM attenuate cardiomyopathy, and prevent heart failure. Methods: Db mice (4-wks), were allowed to acclimatize for 16-wks and were then divided into 3 treatment groups for an additional 16 wks: A) control, B) EET-A 1.5mg/100g BW 2 weeks and C) EET-A-Ln-PGC-1α shRNA. Ln-PGC-1α shRNA suppressed PGC-1α protein in heart tissue by 40-50%. Oxygen consumption (VO 2 ), and blood glucose was determined. Heart tissues were harvested to measure PGC-1α, HO-1, pAMPK, PGC-1α, echocardiographic fractional shortening, mitochondrial oxidative phosphorylation (OXPHOS) and mitofusion protein markers. Results: All mice developed heart failure by the end of 16 weeks and were characterized by a decrease in myocardial contractility, an increase in insulin resistance and blood pressure, decreased VO 2 , the appearance of mitochondria dysfunction and a decrease in AMPK and downstream PGC-1α signaling. Mice treated with EET-A demonstrated an increase in PGC-1α levels, improved mitochondrial function and oxidative phosphorylation (p<0.01 vs control), increased NO bioavailability (p<0.05 vs control), and normalization of glucose metabolism, insulin levels, VO 2 and LV systolic function (p<0.05 vs control). All of these findings were suppressed by PGC-1α inhibition which was accompanied by the onset of even more severe LV dysfunction than in the control group. Conclusion: Increased EET levels result in activation of PGC-1α-HO-1 which reverses diabetes induced insulin resistance, mitochondrial dysfunction, and cardiomyopathy. EET may have potential as a powerful agent for therapeutic application in the treatment of diabetic cardiomyopathy.

scholarly journals Analysis of the muscle tissue of Wistar rats submitted to the sciatic nerve compression model and cryotherapy

2018 ◽  
Vol 16 (3) ◽  
Author(s):  
Jhenifer Karvat ◽  
Camila Mayumi Martin Kakihata ◽  
Lizyana Vieira ◽  
José Luis da Conceição Silva ◽  
Lucinéia de Fátima Chasko Ribeiro ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Muscle Tissue ◽  
Wistar Rats ◽  
Nerve Compression ◽  
Control Group ◽  
Functional Evaluation ◽  
Cross Sectional ◽  
Injury Group ◽  
Significant Difference ◽  
The Right

ABSTRACT Objective: To evaluate the effects of right sciatic nerve compression and cryotherapy on muscle tissue. Methods: We used 42 male Wistar rats, subdivided in the following Groups Control, Injury 3, Injury 8 and Injury 15 submitted to nerve compression and euthanized in the 3rd, 8th and 15th day after surgery. The Cryotherapy Injury 3 was entailed treatment with cryotherapy by immersion of the animal in recipient for 20 minutes during 1 day, then animals were euthanized at the 3rd day after surgery, and the Cryotherapy Injury 8 and the Cryotherapy Injury 15 was treated for 6 days, and euthanized at the 8th and 15th day after surgery. Functional evaluation was performed by the grasping strength of the right pelvic limb. The right tibialis anterior muscles were evaluated for mass, smaller diameter and cross-sectional area. In the Cryotherapy Injury 8 and the Cryotherapy Injury 15 groups, the hydroxyproline was dosed in the right soles. Results: In the compression there was a significant difference in the Injury Groups compared with the Control Group (p<0.05). In the smaller diameter, the compression in Control Group was higher than Injury 8 (p=0.0094), Injury 15 (p=0.002) and Cryotherapy Injury 15 (p<0.001) groups. The comparison between groups with euthanasia in the same post-operative period, a significant difference (p=0.0363) was seen in day 8th after surgery, and this result in Cryotherapy Injury Group was greater than Injury Group. In the fiber area, Control Group was also higher than the Injury 8 (p=0.0018), the Injury 15 (p<0.001) and the Cryotherapy Injury 15 (p<0.001). In hydroxyproline, no significant difference was seen between groups. Conclusion: Nerve damage resulted in decreased muscle strength and trophism, the cryotherapy delayed hypotrophy, but this effect did not persist after cessation of treatment.

scholarly journals IN VITRO ANTIOXIDANT AND IN VIVO ANTIDIABETIC ACTIVITY OF TWO POTENTIAL PROBIOTIC ENTEROCOCCUS SPP. ON ALLOXAN-INDUCED DIABETIC RATS

2021 ◽  
pp. 94-98
Author(s):  
KAMNI RAJPUT ◽  
RAMESH CHANDRA DUBEY
Keyword(s):  
Diabetic Rats ◽  
Antidiabetic Activity ◽  
Control Group ◽  
Albino Rats ◽  
Bacterial Cells ◽  
Bacterial Strains ◽  
Animal Group ◽  
Enterococcus Spp

Objective: In vitro antioxidant activity, in vivo antidiabetic property and intestinal attachment by two potential probiotic bacterial strains, namely, Enterococcus faecium and Enterococcus hirae were studied using albino rats. Methods: Antioxidant the activity was assessed using 2,2-Diphenyl-1-picrylhydrazyl radicals scavenging assay. Alloxan was administered intraperitoneally to induce diabetic conditions in experimental rats. Animals were treated with oral administration of Enterococcus spp., such as E. faecium, and E. hirae isolated from goat and sheep milk. The control animal group received normal saline for the same days. Glibenclamide drug was used as a positive control against probiotic bacterial cells. Results: However, administration of probiotic bacterial strains E. faecium and E. hirae, in albino rats significantly (p<0.05) at varying doses lowered blood glucose levels in diabetic rats as compared to the diabetic control group. Both the species of Enterococcus increased the bodyweight of experimental rats. However, E. faecium was the best antidiabetic strain having the antioxidant activities also in comparison to E. hirae. The attachment of probiotic bacterial cells E. faecium on the rat’s intestine wall against pathogens was examined. Furthermore, E. faecium showed its aggregation with pathogens by attachment of the intestines of albino rats. This showed that both the bacterial strains exhibited in vivo antidiabetic effect. Conclusion: The results of this study showed that probiotic bacteria possess antioxidant, antidiabetic activities, and attachment of intestine.

scholarly journals Goat kid slaughter value and muscle quality after dietary supplementation with an alfalfa protein–xanthophyll concentrate

2017 ◽  
Vol 60 (4) ◽  
pp. 419-425 ◽  
Author(s):  
Anna Szymanowska ◽  
Anna Miduch ◽  
Tomasz Maria Gruszecki ◽  
Monika Greguła-Kania ◽  
Eugeniusz Ryszard Grela
Keyword(s):  
Muscle Tissue ◽  
Unsaturated Fatty Acids ◽  
Control Diet ◽  
Positive Influence ◽  
Carcass Composition ◽  
Muscle Quality ◽  
Control Group ◽  
Beneficial Effects ◽  
Dressing Percentage ◽  
Fattening Period

Abstract. The objective of this study was to determine the effect on goat kids of supplementation with protein–xanthophyll concentrate (PX) obtained from alfalfa (Medicago sativa). Assessments were made on carcass dressing percentage and the lipid profiles of muscle tissue. When the animals reached 30 days old (the start of the fattening period), they were allocated to two feeding groups: a control group (K), which received a standard concentrate diet, and an experimental group (D), which was fed a modified control diet where 3 % of the soybean meal was replaced with an alfalfa protein–xanthophyll preparation (PX). For the rest of the study the kids had ad libitum access to dam milk, hay and their respective diets. After 90 days of rearing (from the end of the fattening period up to when the kids were approximately 120 days of age), five (male) kids were randomly selected from each group and slaughtered. Overall, PX supplementation in goat kids does not affect any parameters of fattening, such as slaughter weight, daily weight gains or dressing percentage. However, beneficial effects of feeding with PX concentrate were found in a higher loin percentage and improved tissue composition resulting from lower fat tissue content. Moreover the PX dietary supplement improved the chemical composition of the muscle tissue by increasing the content of protein and unsaturated fatty acids. Taken together, our results suggest that supplementing the fattening diet for goat kids with the PX preparation did not affect the quantitative parameters of fattening but had a positive influence on the quality of carcass composition.

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