Influence Of Methylprednisolone Research Articles

Autophagy in Femoral Head Necrosis of Broilers Bone Metabolism Parameters and Autophagy-Related Gene Expression in Femoral Head Necrosis Induced by Glucocorticoid in Broilers.

Objectives: In this study, the influence of methylprednisolone (MP) and 3-methyladenine (3-MA) on chondrocyte autophagy and bone quality were determined to investigate the mechanisms of femoral head necrosis in broilers.Methods: Chickens were divided into four groups: control, MP, 3-MA, and 3-MA+MP groups. Blood and bone samples were collected for biochemistry assay and bone quality determination. Cartilage was separated from the femoral head for histopathological analysis and gene expression detection.Results: The results indicated that MP treatment significantly affected blood levels of alkaline phosphatase, high-density lipoprotein, calcium, phosphorus, bone alkaline phosphatase, and osteocalcin in broilers. Additionally, MP treatment significantly increased blood levels of cholesterol, low-density lipoprotein, triglyceride, carboxy-terminal telopeptide of type-I collagen, and tartrate-resistant acid phosphatase 5. MP treatment also significantly decreased the levels of bone parameters compared with these values in controls, inhibited the expression of collagen-2, aggrecan, and mammalian target of rapamycin, and increased the expression of beclin1 and microtubule-associated protein 1 light chain 3, hypoxia-inducible factor 1 alpha, phosphoinositide 3-kinase, protein kinase B and autophagy-related gene 5 of the femoral head. Furthermore, following co-treatment with 3-MA and MP, 3-MA mitigated the effects of MP.Conclusions: Our findings demonstrated that autophagy may be involved in the pathogenesis of femoral head necrosis induced by MP in broilers, and this study provides new treatment and prevention ideas for femoral head necrosis caused by glucocorticoids.

Focus on radioiodine-131 biokinetics: the influence of methylprednisolone on intratherapeutic effective half-life of 131I during radioiodine therapy of Graves\u2019 disease

AimRadioiodine therapy (RIT) may trigger the development of Graves’ ophthalmopathy (GO) or exacerbate pre-existing subclinical GO. Therefore, glucocorticoid administration is recommended for patients with pre-existing GO. Aim of this study was to analyze the influence of glucocorticoid therapy with methylprednisolone on intratherapeutic effective half-life (EHL) of radioiodine-131 in patients with Graves’ disease (GD) as recent studies showed an effect for prednisolone.MethodsIn a retrospective study, 264 patients with GD who underwent RIT without any additional antithyroid medication were evaluated. Intrathyroidal EHL was determined pre- and intratherapeutically. Patients with co-existing GO (n = 43) received methylprednisolone according to a fixed scheme starting 1 day prior to RIT, patients without GO (n = 221) did not receive any protective glucocorticoid medication. The ratios of EHL during RIT and during radioiodine uptake test (RIUT) were compared.ResultsPatients receiving methylprednisolone showed a slight decrease of the mean EHL from 5.63 d (RIUT) to 5.39 d (RIT) (p > 0.05). A comparable result was obtained in patients without glucocorticoids (5.71 d (RIUT) to 5.47 d (RIT); p > 0.05). The ratios of the EHL between RIT and RIUT failed to show a significant difference between the two groups. EHL is therefore not significantly influenced by an additional protective treatment with methylprednisolone.ConclusionsIn the present study a decreased intrathyroidal EHL under glucocorticoid medication with methylprednisolone could not be detected. Therefore, co-medication with methylprednisolone in patients with GO may be preferred to avoid an intratherapeutic decrease of EHL by accompanying protective glucocorticoides.

Influence of methylprednisolone on the reversal time of sugammadex: a randomized clinical trial

Background and objectivesSugammadex is a modified gamma-cyclodextrin that reverses the effects of aminosteroidal neuromuscular blocking agents. Likewise, some steroid molecules, such as toremifene, fusidic acid, and flucloxacillin, can also be encapsulated by sugammadex. Methylprednisolone, which is a synthetic steroid used commonly for airway edema prophylaxis, can also be encapsulated by sugammadex. The objective of this study was to compare the recovery times of sugammadex for reversing rocuronium-induced moderate neuromuscular blockade in those who received intraoperative 1mgkg−1 methylprednisolone or saline. MethodThis single-centered, randomized, controlled, prospective study included 162 adult patients undergoing elective ear-nose-throat procedures (aged from 18 to 65, an ASA physical status I-II, a BMI less than 30kgm−2, and not taking steroid drug medication) with propofol, remifentanyl, rocuronium and sevoflurane. Neuromuscular monitoring was performed using calibrated acceleromyography. The Control Group (Group C) received 5mL of saline, while the Methylprednisolone Group (Group M) received 1mgkg−1 of methylprednisolone in 5mL of saline just after induction. After the completion of surgery, regarding the TOF count, two reappeared spontaneously and 2mgkg−1 sugammadex was administered to all patients. Recovery of the TOF ratio to 0.9 was recorded for both groups, and the estimated recovery time to reach a TOF ratio (TOFr) of 0.9 was the primary outcome of the study. ResultsMedian time to TOFr=0.9 was for 130.00s (range of 29–330) for Group C and 181.00s (100–420) for Group M (p<0.001). The differences between the two groups were statistically significant. ConclusionWhen using 2mgkg−1 of sugammadex to reverse rocuronium-induced neuromuscular blockade in patients who received 1mgkg−1 of intraoperative methylprednisolone, demonstrated delayed recovery times.

Influence of Methylprednisolone on Late Stages of Differentiation of Memory CD4+ T Cells in Rheumatoid Arthritis: In Vitro Study

We studied the effects of methylprednisolone (MP) on the late stages of differentiation of activated memory T cells in healthy donors and in patients with the diagnosis of rheumatoid arthritis (RA) in vitro. It was found that MP exerts a suppressing effect on the number of CD4+ T cells expressing the activation (CD25) and co-stimulation (CD28) molecules in CD3+CD45RO+ cultures of healthy donors and patients with rheumatoid arthritis (RA). Assessment of the level of expression of the U2af1l4 and Gfi1 genes controlling the alternative splicing of the Ptprc gene demonstrated unidirectional but quantitatively different changes in health and in RA. Association between the level of expression of the U2af1l4 and Gfi1 genes and the number of CD3+CD4+CD45RO–CD28– cells in the populations of TCR-activated memory T cells in RA patients treated with MP confirms the hypothesis that glucocorticoids can stimulate the formation of terminally differentiated lymphocytes (CD4+CD28–CD45RO–, TEMRA), which are supposed to play the key role in the pathogenesis of RA.

Application and effect of methylprednisolone in clinical anesthesia

Background There is still no good prevention strategy about postoperative adverse reactions. Methylprednisolone is one kind of glucocorticoid drug with anti-inflammatory, immunosuppressive, and anti-shock effects. Now more and more anesthesiologists use methylprednisolone treat postoperative adverse reactions such as postoperative nausea and vomiting (PONV), pain, airway stability and inflammatory reactions. Objective To provide the clinical reference for clinical application of methylprednisolone in the perioperative period. Content This review summarized the influence of methylprednisolone on PONV, pain, airway stability and inflammatory reactions. Trend Methylprednisolone combined with other drugs have broad prospects in clinical anesthesia application. Key words: Methylprednisolone; Clinical anesthesia; Perioperative period

The influence of methylprednisolone on the ability of CD4+CD95+HLA-DR+ T-cells to produce proinflammatory medators in cultures of TCR-activated CD3+CD45RO+ T-lymphocytes from patients with rheumatoid arthritis

The effect of different concentrations of the glucocorticoid (GC) methylprednisolone (MP) on CD4+CD95+HLA-DR+ T-cells and their ability to produce proinflammatory mediators in cultures of TCR-stimulated CD3+CD45RO+ T-lymphocytes in the in vitro system was investigated. T cells were obtained from healthy donors and patients with rheumatoid arthritis (RA).Under conditions of TCR-activation, MP increased the number of CD4+HLA-DR+CD95+ cells in CD3+CD45RO+ cultures obtained from RA patients and did not change their content in the control group. In general, MP decreased production of proinflammatory factors (IFN-, IL-2, IL-17, IL-21 and TNF-) by TCR-activated CD3+CD45RO+ cells from healthy donors and RA, consistent with the overall immunosuppressive mechanism of GC action. The correlation between CD4+CD45RO+HLA-DR+CD95+ T-cell contents and parameters reflecting production of proinflammatory mediators (IL-17, IL-21 and TNF-) in RA patients indicates maintenance of the pro-inflammatory potential of this T-cell population exposed to GC action. We suggest that relative resistance of CD4+CD45RO+CD95+HLA-DR+ T-cells of RA patients to the suppressor effect of GC leads to maintenance and even enhancement in the functional capacities of autoreactive cells in the pathogenesis of RA.

Impact of methylprednisolone in priming solution of cardiopulmonary bypass on anti-inflammatory CD163 receptor during cardiac surgery

We evaluated the influence of methylprednisolone in cardiopulmonary bypass fluid on scavenger receptor for hemoglobin CD163 molecule expression on monocytes of patients who underwent elective coronary artery bypass grafting with cardiopulmonary bypass with either exposure to methylprednisolone present in the cardiopulmonary bypass fluid (20 patients), or without methylprednisolone in the cardiopulmonary bypass fluid (22 patients) and operated on without cardiopulmonary bypass (42 patients). The dynamics of CD163 expression was also followed in patients operated on without cardiopulmonary bypass. This study was a retrospective analysis of a comparison of two studies. The expression of CD163 was determined quantitatively by standardized flow cytometry technique. The similarities in the dynamics of CD163 monocyte expression, comparing the patients operated on with or without cardiopulmonary bypass, were found. Compared to the preoperative level, CD163 monocyte expression was significantly elevated on the 1(st) postoperative day. Monocyte CD163 expression on the 1(st) postoperative day was evidently similar in both groups of patients operated without cardiopulmonary bypass (median value of mean fluorescence intensity (MFI) 18,896; interquartile range from 27,538 to 57,711; median value of MFI 18,863; interquartile range from 16,514 to 26,559; n.s.), suggesting high reproducibility of our flow cytometric method; the monocyte CD163 expression was significantly higher (median value of MFI 37,902; interquartile range from 27,538 to 57,711) on the 1(st) postoperative day in patients exposed to methylprednisolone compared to patients without this exposure (median value of MFI 20,995; interquartile range from 16,321 to 29,623) (p<0.001). We concluded that the expression of hemoglobin scavenger receptor CD163 on monocytes of cardiac surgical patients is induced by methylprednisolone present in cardiopulmonary bypass fluid.

Influence of methylprednisolone on magnetic resonance and histological measures during cuprizone-induced demyelination

MRI is widely used for routine assessment of the progression of white matter injury while patients receive therapeutic agents, such as the glucocorticoid agonist methylprednisolone (MP). Given this, it is important to determine whether MRI parameters are altered by MP treatment in the absence of changes in cellular and myelin pathology. In this study, we compared magnetic resonance and histological measures during myelin injury in mice with and without short duration MP administration. Mice were scanned with a 4.7 T MRI scanner before and after MP or vehicle injections using T2WI and DTI sequences and histology was performed on the brains following the second scan. Comparison of post-injection to pre-injection MRI showed a reduced T2WI intensity in the CC and an attenuated response in ADC|| and ADC⊥ in the MP group in comparison with the vehicle group. However, quantitative analyses of myelin staining, neurofilament intensity and oligodendrocyte and microglial density were not different between the MP and the vehicle groups, indicating that the short duration MP treatment did not alter cellular and myelin pathology. These data suggest that MP could confound the validity of paraclinical measures such as ADC|| and ADC⊥ that are otherwise being touted as markers of either axonal integrity or myelin repair.

Influence of Methylprednisolone on Levels of Neuron-Specific Enolase in Cardiac Surgery: A Corticosteroid Derivative to Decrease Possible Neuronal Damage

Cerebral injury is a well-known complication after cardiac surgery with cardiopulmonary bypass (CPB), especially in adult patients. Specific biochemical markers like neuron-specific enolase (NSE) and S-100beta protein were developed previously for early detecting neuronal damage after CPB. Corticosteroids are shown to reduce multisystemic deleterious effects of cardiopulmonary bypass due to their anti-inflammatory characteristics. The aim of this study is to demonstrate the decrease of serum neuron-specific enolase levels in patients who received corticosteroids before CPB. Thirty patients scheduled for elective coronary bypass surgery were included in the study. Patients were divided randomly into two groups as the control group (n = 15) who underwent a standard coronary bypass surgery without any additional medication and the study group (n = 15) who received 1 gm of methylprednisolone before CPB. Blood samples for analysis of serum NSE, interleukin-6 (IL-6), and IL-10 were drawn before CPB, 4 and 24 hours after the end of extracorporeal circulation. Serum cytokine and NSE levels were significantly increased after CPB above their normal range in both groups. In the study group, IL-6 and NSE levels were significantly reduced while IL-10 levels were much higher after CPB. High NSE levels significantly correlated with IL-6 levels in the control group. The lower levels of NSE in patients who received methylprednisolone may suggest that corticosteroids might be useful in decreasing possible neuronal damage during heart surgery. However, we were not able to demonstrate an adverse neurological outcome.

Influence of Methylprednisolone on Plasma Homocysteine Levels in Cadaveric Renal Transplant Recipients

The aim of the present study was to investigate plasma homocysteine levels in renal transplant recipients in the course of steroid-based or steroid-free immunosuppression. Data from 32 patients were retrospectively analyzed according to the steroid immunosuppressive regimen. The 20 recipients on methylprednisolone (MP) plus cyclosporine (CyA) or tacrolimus (TRL) ( n = 20) showed similar creatinine levels when compared with those on calcineurin inhibitors plus mycophenolate mofetil (MMF; n = 12), (1.6 ± 1.5 vs 1.6 ± 0.4 mg/dL; P = NS) but significantly higher total plasma homocysteine (tHcy) levels (28.5 ± 12.5 vs 16.3 ± 5.5 μmol/L; P < .05). No differences of tHcy levels have been observed when patients were analyzed according to CyA- or TRL-based immunosuppression regardless of MP or MMF associations. Our data suggest that recipients, particularly those on steroid-based immunosuppression, should receive homocysteine-lowering treatment early after transplantation.

Influence of methylprednisolone on the healing of intestinal anastomoses in rats

Although steroids are generally thought to impair intestinal anastomotic healing, this effect has never been proven unequivocally in either clinical or experimental studies. We have investigated the influence of methylprednisolone (2.5 or 10.0 mg kg-1 day-1) given from 2 days before operation onwards, on 3-day-old and 7-day-old ileal and colonic anastomoses in rats. Anastomotic abscesses occurred more frequently in the ileum, but not in the colon, after steroid medication. However, methylprednisolone did not lower anastomotic bursting pressures in either of the bowel segments. Comparison of the hydroxyproline content of the anastomotic segment yielded no significant difference between control and methylprednisolone groups in either small or large bowel. Thus, healing of experimental colonic anastomoses remains unaffected by short-term administration of this corticosteroid.

Influence of methylprednisolone on the healing of intestinal anastomoses in rats

Although steroids are generally thought to impair intestinal anastomotic healing, this effect has never been proven unequivocally in either clinical or experimental studies. We have investigated the influence of methylprednisolone (2.5 or 10.0 mg kg-1 day-1) given from 2 days before operation onwards, on 3-day-old and 7-day-old ileal and colonic anastomoses in rats. Anastomotic abscesses occurred more frequently in the ileum, but not in the colon, after steroid medication. However, methylprednisolone did not lower anastomotic bursting pressures in either of the bowel segments. Comparison of the hydroxyproline content of the anastomotic segment yielded no significant difference between control and methylprednisolone groups in either small or large bowel. Thus, healing of experimental colonic anastomoses remains unaffected by short-term administration of this corticosteroid.

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Effect of steroid treatment on the migration behaviour of neutrophils in patients with early rheumatoid arthritis.

The influence of methylprednisolone on the migratory characteristics of neutrophil granulocytes was investigated in 10 patients with early rheumatoid arthritis (RA) and compared to 12 controls. The migration of neutrophils was measured with a whole-blood membrane filter assay with and without stimulation by the chemoattractant N-formyl-methionyl-leucyl-phenylalanine (fMLP). Total migration index (TMI), distribution characteristics (DC) and the product of TMI and DC (neutrophil migratory activity; NMA) served to characterize the migratory behaviour of neutrophils. The data demonstrated an increased polymorphonuclear leucocyte (PMN) migration in patients with early RA, indicating a bystander role of PMNs in inflammatory joint injury. Treatment with methylprednisolone reduced significantly the penetration depth (DC) of neutrophils, but did not influence the number of migrating cells (TMI). The unstimulated NMA was significantly reduced due to the marked DC reduction, whereas steroids did not influence the stimulated NMA of neutrophils. A significant reduction in PMN penetration depth was demonstrated only after a steroid therapy of at least 10 days, suggesting that a longer period of steroid therapy is necessary to provide effective inflammatory control.

4-31-13 The influence of methylprednisolone with prednisone treatment on sIL-2 receptor levels and TNF-alpha in patients with multiple sclerosis. Correlation with MRI

4-31-13 The influence of methylprednisolone with prednisone treatment on sIL-2 receptor levels and TNF-alpha in patients with multiple sclerosis. Correlation with MRI

Effects of methylprednisolone on extracellular lactic acidosis and amino acids after severe compression injury of rat spinal cord.

We evaluated in rats with severe spinal cord compression at T8-9 the influence of methylprednisolone (MP) on lactic acidosis and extracellular amino acids, which may cause secondary, perifocal injuries of the cord. MP (30 mg/kg) was given intravenously 30 min before compression and hourly thereafter (15 mg/kg). Other rats with compression, given saline, served as controls. Samples from the extracellular fluid of one dorsal hom were collected by microdialysis and analyzed by HPLC. Microdialysis was performed for 1.5 h to establish basal levels. Samples were collected for 3 h after compression. MP-treated rats showed a reduction of dialysate lactic acid and arginine levels during the first 1-2 h after trauma. The mean dialysate levels of glutamate in MP-treated rats were lower than those of the controls, but the difference was not statistically significant. MP treatment did not influence dialysate levels of aspartate, glutamine, histidine, glycine, threonine, taurine, alanine, GABA, and tyrosine. Our study shows that MP has several effects, including reduced lactic acid formation, reduced levels of arginine (the substrate for nitric oxide production), and a trend toward decreased extracellular accumulation of the excitotoxic amino acid glutamate. We conclude that MP has the capacity to change the composition of the extracellular edema fluid after trauma to the spinal cord. These changes may counteract free radical formation and may be important mechanisms by which MP exerts its beneficial actions.

The influence of methylprednisolone on the energy metabolism of Ehrlich ascites tumour cells.

Using Ehrlich ascites tumour cells, the short-term effects of the therapeutic glucocorticoid Methylprednisolone (MP) on the cellular energy metabolism were studied. ATP-consuming processes involved in the rapid MP effects were identified indirectly from the effects of MP on cellular oxygen consumption related to the inhibition of respiration by selective inhibitors of Ca(2+)-ATPase and protein synthesis. The effects of MP on plasma membrane permeability for Ca2+ ions and phospholipid turnover were studied directly by using confocal laser scanning microscopy and tracerkinetic measurements, respectively. MP inhibited cellular oxygen consumption, suppressed the inhibitory effect of lanthanum but not that of cycloheximide on oxygen consumption, blocked the [Ca2+]i rise in response to calcium ionophore A 23187, and decreased phospholipid turnover. MP acted instantly in a dose-dependent manner. The observed effects of MP are discussed in relation to the hypothesis that the drug has direct membrane effect affecting plasma membrane permeability and function.

Effect of methylprednisolone on small bowel spleen and liver changes in a murine model of inflammatory bowel disease

The aim of this study was to evaluate the influence of methylprednisolone (1 mg/kg, i.p.) on inflammatory lesions in the small bowel, liver (pericholangitis) and spleen (lymphofollicular proliferation), in a model of inflammatory bowel disease induced by 2.4-dinitrofluorobenzene in previously sensitized BALB-c mice. As a parameter of corticosteroid anti-inflammatory and immunosuppressive action, we simultaneously investigated its effects on mononuclear cell accumulation within the ileal lamina propria and submucosa during the observed time period (1-30 days). We noted a significant decrease in accumulation of mononuclear cells within the lamina propria (P < 0.001). An effect on mononuclear cell infiltration within the ileal submucosa was also noted but was not statistically significant. In addition, pericholangitis in the liver and lymphofollicular proliferation in the spleen were not observed in the experimental group during treatment with methylprednisolone. The results of this study indicate that the previously described model of intestinal inflammation could be used in further research of present and new therapeutic modalities for inflammatory bowel disease.

Influence of methylprednisolone on the intracellular antimicrobial activity of erythromycin and clindamycin against Legionella pneumophila.

We have investigated the effect of methylprednisolone on the intracellular activity of erythromycin and clindamycin in vitro. An assay system was developed for the determination of intracellular activity of antibiotics against Legionella pneumophila using guinea pig resident alveolar macrophages. Erythromycin at a concentration of 0.625 mg/L (5 x MIC) and clindamycin at a concentration of 8 mg/L (MIC) inhibited the growth of a single strain of L. pneumophila in macrophages, whilst ceftizoxime at a concentration of 0.625 mg/L (5 x MIC) did not. Methylprednisolone at therapeutic concentrations did not affect the intracellular antibacterial activity of either erythromycin or clindamycin against L. pneumophila. We found no direct effect of methylprednisolone on the intracellular antibacterial activity of either erythromycin or clindamycin.

Characterization of Lymphocyte Subsets in Cynomolgus Monkeys Using Flow Cytometry. Influence of Methylprednisolone

The use of a nonrodent species is helpful to confirm results obtained in preclinical immunotoxicity assessment in rodents. As no specific reagents are available to study lymphocyte subsets in monkeys, the cross-staining properties of a panel of commercially available human monoclonal antibodies were studied in cynomolgus monkeys using a whole-blood technique for the separation of lymphocytes. The flow cytometry analysis showed that anti-leu-16 (B cells), anti-leu-5b (T cells), anti-leu-2a (suppressor/cytotoxic T cells), and OKT4 (helper/inducer T cells) gave homogeneous and reproducible results in contrast to anti-leu-12 (B cells), anti-leu-4 (T cells), OKT8 (suppressor/cytotoxic T cells), and anti-leu-3a (helper/inducer T cells). This technique allowed us to determine the lymphocyte subset profile in this species with a reversed ratio of helper/suppressor T cells as compared to humans. Finally, results obtained following a single intravenous injection of 4 mg/kg methylprednisolone confirmed the validity ...