Transcutaneous carbon dioxide application with hydrogel prevents muscle atrophy in a rat sciatic nerve crush model

Nishimoto, Hanako; Inui, Atsuyuki; Ueha, Takeshi; Inoue, Miho; Akahane, Shiho; Harada, Risa; Mifune, Yutaka; Kokubu, Tatsuo; Nishida, Kotaro; Kuroda, Ryosuke; Sakai, Yoshitada

doi:10.1002/jor.23817

Cited by 11 publications

(13 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The weight of the gastrocnemius muscle at 4 weeks post-operation was compared between the nerve-crushed model (refer to the Methods section, Fig. 1 a, b), in which the sciatic nerve was crushed as described in a previous study 13 , and the control group, which had sham surgery wherein only a skin incision was made. The gastrocnemius muscle weight was significantly decreased on the affected side in the nerve-crushed group than on the unaffected side.…”

Section: Resultsmentioning

confidence: 99%

“…Muscle atrophy and fatty infiltration are known to cause chronic inflammation 8 , and we hypothesized that decrease of adiponectin expression is related to expression of inflammatory cytokines after the nerve injury. Therefore, in this study, we evaluated the expressions of adipokines on chronic inflammation using a rat sciatic nerve-crushed injury model 13 . In addition, few reports have shown the effect of adiponectin receptor agonist administration on muscle atrophy and fatty infiltration.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Influence of adiponectin and inflammatory cytokines in fatty degenerative atrophic muscle

Shinohara

Kataoka

Mifune

et al. 2022

Sci Rep

Self Cite

View full text Add to dashboard Cite

Tendon rupture and nerve injury cause fatty infiltration of the skeletal muscle, and the adipokines secreted from the infiltrated adipocytes are known to contribute to chronic inflammation. Therefore, in this study, we evaluated the effects of the adipokines on chronic inflammation using a rat sciatic nerve-crushed injury model. In vitro and in vivo experiments showed that the expression of adiponectin was decreased (0.3-fold) and the expression of Il6 (~ 3.8-fold) and Tnf (~ 6.2-fold) was increased in the nerve-crushed group compared to that in the control group. It was also observed that the administration of an adiponectin receptor agonist decreased the levels of Il6 (0.38-fold) and Tnf (0.28-fold) and improved cellular viability (~ 1.9-fold) in vitro. Additionally, in the fatty infiltrated skeletal muscle, low adiponectin levels were found to be associated with chronic inflammation. Therefore, the local administration of adiponectin receptor agonists would prevent chronic inflammation.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Influence of adiponectin and inflammatory cytokines in fatty degenerative atrophic muscle

Shinohara

Kataoka

Mifune

et al. 2022

Sci Rep

Self Cite

View full text Add to dashboard Cite

show abstract

“…The rat model of SNI was prepared by crush injury [23,24]. Under anesthesia with 1.5-2.0% isoflurane (Pfizer Japan Inc., Tokyo), the left sciatic nerve was exposed and was compressed for 90 sec with a pair of forceps at a site 10 mm proximal to the bifurcation.…”

Section: Sni Model and Drug Treatmentmentioning

confidence: 99%

Nano PGE1 Enhances Phosphorylation of ERK1/2 and Akt to Promote Recovery from Motor Dysfunction and Muscle Atrophy Induced by Sciatic Nerve Injury

Takenaga¹,

Ishihara²,

Niimi³

et al. 2019

Preprint

View full text Add to dashboard Cite

The effect of prostaglandin E1 (PGE1) encapsulated in nanoparticles (Nano PGE1) on motor dysfunction and muscle atrophy induced by sciatic nerve injury (SNI) was investigated in rats, and was compared with PGE1 encapsulated in lipid microspheres (Lipo PGE1) or PGE1 clathrated in cyclodextrin (PGE1-CD). The hind limb muscle weight ratio decreased until 2 weeks after SNI. All 3 PGE1 formulations significantly improved SNI-induced motor dysfunction. Nano PGE1 significantly promoted recovery from muscle atrophy at 2 and 3 weeks after SNI. Lipo PGE1 was also effective, but multiple doses were required. Compared with the SNI control group, the Nano PGE1 group showed upregulation of vascular endothelial growth factor (VEGF) and agrin expression in the injured sciatic nerve and atrophic muscles. Nano PGE1 accumulated prominently at the site of nerve injury and persisted for longer than Lipo PGE1 or PGE1-CD. Expression of all EP receptors was detected in the normal sciatic nerve, and EP2 expression increased after SNI. Finally, Nano PGE1 promoted ERK1/2 and Akt phosphorylation. These findings suggest that PGE1 released from nanoparticles accumulates at sites of nerve injury and increases VEGF production by augmenting ERK1/2 phosphorylation via EP receptor signaling, thus promoting tissue repair and regeneration.

show abstract

“…ripheral nerve injury 10) , and suppressed tumor progression 11) . Additionally, it generates muscle fiber types switching, induces peroxisome proliferator activated receptor gamma coactivator 1-alpha (PGC-1α), and increases mitochondria and angiogenesis in rat muscles 12) .…”

mentioning

confidence: 99%

Transcutaneous application of carbon dioxide improves contractures after immobilization of rat knee joint

et al. 2020

Self Cite

View full text Add to dashboard Cite

Joint contractures are a major complication following joint immobilization. However, no fully effective treatment has yet been found. Recently, carbon dioxide (CO2) therapy was developed and verified this therapeutic application in various disorders. We aimed to verify the efficacy of transcutaneous CO2 therapy for immobilization-induced joint contracture. Method: Twenty-two Wistar rats were randomly assigned to three groups: caged control, those untreated after joint immobilization, and those treated after joint immobilization. The rats were treated with CO2 for 20 min once a daily either during immobilization, (prevention) or during remobilization after immobilization (treatment). Knee extension motion was measured with a goniometer, and the muscular and articular factors responsible for contractures were calculated. We evaluated muscle fibrosis, fibrosis-related genes (collagen Type 1α1 and TGF-β1) in muscles, synovial intima's length, and fibrosis-related proteins (Type I collagen and TGF-β1) in the joint capsules. Results: CO2 therapy for prevention and treatment improved the knee extension motion. Muscular and articular factors decreased in rats of the treatment group. The muscular fibrosis of treated rats decreased in the treatment group. Although CO2 therapy did not repress the increased expression of collagen Type 1α1, the therapy decreased the expression of TGF-β1 in the treatment group. CO2 therapy for treatment improved the shortening of the synovial membrane after immobilization and decreased the immunolabeling of TGF-β1 in the joint capsules. Conclusions: CO2 therapy may prevent and treat contractures after joint immobilization, and appears to be more effective as a treatment strategy for the deterioration of contractures during remobilization.

show abstract

Transcutaneous carbon dioxide application with hydrogel prevents muscle atrophy in a rat sciatic nerve crush model

Abstract: Transcutaneous CO application has the therapeutic potential to accelerate the recovery of muscle atrophy in peripheral nerve injury. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:1653-1658, 2018.

Cited by 11 publications

References 31 publications

Influence of adiponectin and inflammatory cytokines in fatty degenerative atrophic muscle

Influence of adiponectin and inflammatory cytokines in fatty degenerative atrophic muscle

Nano PGE1 Enhances Phosphorylation of ERK1/2 and Akt to Promote Recovery from Motor Dysfunction and Muscle Atrophy Induced by Sciatic Nerve Injury

Transcutaneous application of carbon dioxide improves contractures after immobilization of rat knee joint

Contact Info

Product

Resources

About