scholarly journals Novel protective effects of pulsed electromagnetic field ischemia/reperfusion injury rats

2016 ◽  
Vol 36 (6) ◽  
Author(s):  
Fenfen Ma ◽  
Wenwen Li ◽  
Xinghui Li ◽  
Ba Hieu Tran ◽  
Rinkiko Suguro ◽  
...  

Pulsed electromagnetic field (PEMF) treatment protected ischaemia/reperfusion (I/R) injury from apoptosis via B-cell lymphoma 2 (Bcl-2), Bax and nitric oxide (NO) releasing.

2018 ◽  
Vol 7 (2) ◽  
pp. 124-130 ◽  
Author(s):  
D. Coric ◽  
D. E. Bullard ◽  
V. V. Patel ◽  
J. T. Ryaby ◽  
B. L. Atkinson ◽  
...  

Objectives Pulsed electromagnetic field (PEMF) stimulation was evaluated after anterior cervical discectomy and fusion (ACDF) procedures in a randomized, controlled clinical study performed for United States Food and Drug Administration (FDA) approval. PEMF significantly increased fusion rates at six months, but 12-month fusion outcomes for subjects at elevated risk for pseudoarthrosis were not thoroughly reported. The objective of the current study was to evaluate the effect of PEMF treatment on subjects at increased risk for pseudoarthrosis after ACDF procedures. Methods Two evaluations were performed that compared fusion rates between PEMF stimulation and a historical control (160 subjects) from the FDA investigational device exemption (IDE) study: a post hoc (PH) analysis of high-risk subjects from the FDA study (PH PEMF); and a multicentre, open-label (OL) study consisting of 274 subjects treated with PEMF (OL PEMF). Fisher’s exact test and multivariate logistic regression was used to compare fusion rates between PEMF-treated subjects and historical controls. Results In separate comparisons of PH PEMF and OL PEMF groups to the historical control group, PEMF treatment significantly (p < 0.05, Fisher’s exact test) increased the fusion rate at six and 12 months for certain high-risk subjects who had at least one clinical risk factor of being elderly, a nicotine user, osteoporotic, or diabetic; and for those with at least one clinical risk factor and who received at least a two- or three-level arthrodesis. Conclusion Adjunctive PEMF treatment can be recommended for patients who are at high risk for pseudoarthrosis. Cite this article: D. Coric, D. E. Bullard, V. V. Patel, J. T. Ryaby, B. L. Atkinson, D. He, R. D. Guyer. Pulsed electromagnetic field stimulation may improve fusion rates in cervical arthrodesis in high-risk populations. Bone Joint Res 2018;7:124–130. DOI: 10.1302/2046-3758.72.BJR-2017-0221.R1.


2019 ◽  
Vol 8 (11) ◽  
pp. 2008 ◽  
Author(s):  
Patrick Ziegler ◽  
Andreas K. Nussler ◽  
Benjamin Wilbrand ◽  
Karsten Falldorf ◽  
Fabian Springer ◽  
...  

Extremely low-frequency pulsed electromagnetic field (ELF-PEMF) therapy is proposed to support bone healing after injuries and surgical procedures, being of special interest for elderly patients. This study aimed at investigating the effect of a specific ELF-PEMF, recently identified to support osteoblast function in vitro, on bone healing after high tibial osteotomy (HTO). Patients who underwent HTO were randomized to ELF-PEMF or placebo treatment, both applied by optically identical external devices 7 min per day for 30 days following surgery. Osseous consolidation was evaluated by post-surgical X-rays (7 and 14 weeks). Serum markers were quantified by ELISA. Data were compared by a two-sided t-test (α = 0.05). Device readouts showed excellent therapy compliance. Baseline parameters, including age, sex, body mass index, wedge height and blood cell count, were comparable between both groups. X-rays revealed faster osseous consolidation for ELF-PEMF compared to placebo treatment, which was significant in patients ≥50 years (∆mean = 0.68%/week; p = 0.003). Findings are supported by post-surgically increased bone-specific alkaline phosphatase serum levels following ELF-PEMF, compared to placebo (∆mean = 2.2 µg/L; p = 0.029) treatment. Adverse device effects were not reported. ELF-PEMF treatment showed a tendency to accelerate osseous consolidation after HTO. This effect was stronger and more significant for patients ≥50 years. This ELF-PEMF treatment might represent a promising adjunct to conventional therapy supporting osseous consolidation in elderly patients.


Marine Drugs ◽  
2019 ◽  
Vol 17 (6) ◽  
pp. 368 ◽  
Author(s):  
Ji Hye Park ◽  
Na-Kyung Lee ◽  
Hye Ji Lim ◽  
Sinthia Mazumder ◽  
Vinoth Kumar Rethineswaran ◽  
...  

Cardiac progenitor cells (CPCs) are resident stem cells present in a small portion of ischemic hearts and function in repairing the damaged heart tissue. Intense oxidative stress impairs cell metabolism thereby decreasing cell viability. Protecting CPCs from undergoing cellular apoptosis during oxidative stress is crucial in optimizing CPC-based therapy. Histochrome (sodium salt of echinochrome A—a common sea urchin pigment) is an antioxidant drug that has been clinically used as a pharmacologic agent for ischemia/reperfusion injury in Russia. However, the mechanistic effect of histochrome on CPCs has never been reported. We investigated the protective effect of histochrome pretreatment on human CPCs (hCPCs) against hydrogen peroxide (H2O2)-induced oxidative stress. Annexin V/7-aminoactinomycin D (7-AAD) assay revealed that histochrome-treated CPCs showed significant protective effects against H2O2-induced cell death. The anti-apoptotic proteins B-cell lymphoma 2 (Bcl-2) and Bcl-xL were significantly upregulated, whereas the pro-apoptotic proteins BCL2-associated X (Bax), H2O2-induced cleaved caspase-3, and the DNA damage marker, phosphorylated histone (γH2A.X) foci, were significantly downregulated upon histochrome treatment of hCPCs in vitro. Further, prolonged incubation with histochrome alleviated the replicative cellular senescence of hCPCs. In conclusion, we report the protective effect of histochrome against oxidative stress and present the use of a potent and bio-safe cell priming agent as a potential therapeutic strategy in patient-derived hCPCs to treat heart disease.


2015 ◽  
Vol 122 (5) ◽  
pp. 1239-1247 ◽  
Author(s):  
Denis E. Bragin ◽  
Gloria L. Statom ◽  
Sean Hagberg ◽  
Edwin M. Nemoto

OBJECT High-frequency pulsed electromagnetic field stimulation is an emerging noninvasive therapy being used clinically to facilitate bone and cutaneous wound healing. Although the mechanisms of action of pulsed electromagnetic fields (PEMF) are unknown, some studies suggest that its effects are mediated by increased nitric oxide (NO), a well-known vasodilator. The authors hypothesized that in the brain, PEMF increase NO, which induces vasodilation, enhances microvascular perfusion and tissue oxygenation, and may be a useful adjunct therapy in stroke and traumatic brain injury. To test this hypothesis, they studied the effect of PEMF on a healthy rat brain with and without NO synthase (NOS) inhibition. METHODS In vivo two-photon laser scanning microscopy (2PLSM) was used on the parietal cortex of rat brains to measure microvascular tone and red blood cell (RBC) flow velocity in microvessels with diameters ranging from 3 to 50 μm, which includes capillaries, arterioles, and venules. Tissue oxygenation (reduced nicotinamide adenine dinucleotide [NADH] fluorescence) was also measured before and for 3 hours after PEMF treatment using the FDA-cleared SofPulse device (Ivivi Health Sciences, LLC). To test NO involvement, the NOS inhibitor NG-nitro-l-arginine methyl ester (L-NAME) was intravenously injected (10 mg/kg). In a time control group, PEMF were not used. Doppler flux (0.8-mm probe diameter), brain and rectal temperatures, arterial blood pressure, blood gases, hematocrit, and electrolytes were monitored. RESULTS Pulsed electromagnetic field stimulation significantly dilated cerebral arterioles from a baseline average diameter of 26.4 ± 0.84 μm to 29.1 ± 0.91 μm (11 rats, p < 0.01). Increased blood volume flow through dilated arterioles enhanced capillary flow with an average increase in RBC flow velocity by 5.5% ± 1.3% (p < 0.01). Enhanced microvascular flow increased tissue oxygenation as reflected by a decrease in NADH autofluorescence to 94.7% ± 1.6% of baseline (p < 0.05). Nitric oxide synthase inhibition by L-NAME prevented PEMF-induced changes in arteriolar diameter, microvascular perfusion, and tissue oxygenation (7 rats). No changes in measured parameters were observed throughout the study in the untreated time controls (5 rats). CONCLUSIONS This is the first demonstration of the acute effects of PEMF on cerebral cortical microvascular perfusion and metabolism. Thirty minutes of PEMF treatment induced cerebral arteriolar dilation leading to an increase in microvascular blood flow and tissue oxygenation that persisted for at least 3 hours. The effects of PEMF were mediated by NO, as we have shown in NOS inhibition experiments. These results suggest that PEMF may be an effective treatment for patients after traumatic or ischemic brain injury. Studies on the effect of PEMF on the injured brain are in progress.


2009 ◽  
Vol 20 (4) ◽  
pp. 423-428 ◽  
Author(s):  
PRJVC Boopalan ◽  
Samuel B Chittaranjan ◽  
Ramadass Balamurugan ◽  
NS Nandakumar ◽  
A Sabareeswaran ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247659
Author(s):  
Niladri S. Kar ◽  
Daniel Ferguson ◽  
Nianli Zhang ◽  
Erik I. Waldorff ◽  
James T. Ryaby ◽  
...  

Pulsed-electromagnetic-field (PEMF) treatment was found to enhance cellular differentiation of the mouse preosteoblast, MC3T3-E1, to a more osteoblastic phenotype. Differentiation genes such as Alp, BSPI, cFos, Ibsp, Osteocalcin, Pthr1 and Runx2 showed increased expression in response to PEMF stimulation. Detailed molecular mechanisms linking PEMF to the activation of these genes are limited. Two adenosine receptors known to be modulated in response to PEMF, Adora2A and Adora3, were functionally impaired by CRISPR-Cas9-mediated gene disruption, and the consequences of which were studied in the context of PEMF-mediated osteoblastic differentiation. Disruption of Adora2A resulted in a delay of Alp mRNA expression, but not alkaline phosphatase protein expression, which was similar to that found in wild type cells. However, Adora3 disruption resulted in significantly reduced responses at both the alkaline phosphatase mRNA and protein levels throughout the PEMF stimulation period. Defects observed in response to PEMF were mirrored using a chemically defined growth and differentiation-inducing media (DM). Moreover, in cells with Adora2A disruption, gene expression profiles showed a blunted response in cFos and Pthr1 to PEMF treatment; whereas cells with Adora3 disruption had mostly blunted responses in AlpI, BSPI, Ibsp, Osteocalcin and Sp7 gene activation. To demonstrate specificity for Adora3 function, the Adora3 open reading frame was inserted into the ROSA26 locus in Adora3 disrupted cells culminating in rescued PEMF responsiveness and thereby eliminating the possibility of off-target effects. These results lead us to propose that there are complementary and parallel positive roles for adenosine receptor A2A and A3 in PEMF-mediated osteoblast differentiation.


Cartilage ◽  
2021 ◽  
pp. 194760352110495
Author(s):  
Xiaotian Yang ◽  
Hua Guo ◽  
Wenwen Ye ◽  
Lin Yang ◽  
Chengqi He

Objective: To investigate the anti-inflammatory effects and mechanisms of pulsed electromagnetic field (PEMF) in the treatment of osteoarthritis (OA) in the destabilization of the medial meniscus (DMM) mice. Design: Ten-week-old male wild-type (WT), interleukin (IL)-6−/− and tumor necrosis factor (TNF)-α−/− mice undergoing DMM surgery were randomly divided into 2 groups ( n = 10 each): mice with PEMF exposure and mice with sham PEMF exposure. PEMF (75 Hz, 3.8 mT, 1 h/day) or sham PEMF was applied for 4 weeks. Pain behavior of mice, histological assessment of cartilage and synovium, micro-CT (computed tomography) analysis of bone, real-time polymerase chain reaction, and immunohistochemical staining of cartilage were performed. Results: After DMM surgery, PEMF had a beneficial effect on pain, cartilage degeneration, synovitis, and trabecular bone microarchitecture in WT mice; these protective effects were reduced in IL-6−/− and TNF-α−/− mice. In addition, PEMF downregulated IL-6 and TNF-α expression in cartilage. PEMF also ameliorated cartilage matrix, chondrocyte apoptosis, and autophagy, while deletion of IL-6 or TNF-α suppressed the effects. Conclusions: PEMF attenuates structural and functional progression of OA through inhibition of TNF-α and IL-6 signaling. The protective effects of PEMF on chondrocyte apoptosis and autophagy are regulated by TNF-α and IL-6 signaling.


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