1.Electroacupuncture accelerates recovery of muscle atrophy induced by hindlimb suspension in mouse skeletal muscle.
Sachiko IKEMUNE ; Mika OHTA ; Masanao MACHIDA ; Tohru TAKEMASA ; Yutaka TAKAOKA ; Toshikazu MIYAMOTO
Journal of the Japan Society of Acupuncture and Moxibustion 2010;60(4):707-715
[Objective]The influence of electroacupuncture (EA) stimulation on physical inactivity is not clear. This study aimed to investigate the effects of EA on the recovery of mouse soleus muscle atrophy induced by hindlimb suspension (HS).
[Methods]We used 8-week-old male ICR mice (n = 20). The mice were divided into 4 groups:the No treatment group (NT, n = 5), HS group (HS, n = 5), Control group (CT, n = 5), and Reloading-with-EA-stimulation group (EA, n = 5). HS mice were suspended for up to 14 days. CT and EA mice were reloaded for an additional 14 days after the HS for 14 days. The HS method used a modified version of an apparatus used in a previous study. EA mice received EA every other day immediately after reloading and were stimulated in the triceps surae muscle at 10 Hz for 30 min with a stainless steel needle. The weight, muscle fiber area size and number of macrophages in the soleus muscle were analyzed.
[Results]The number of skeletal muscle macrophages was increased significantly in EA mice compared with that in CT mice (P < 0.01). The soleus muscle weight and muscle fiber cross-sectional area were decreased in HS mice compared with NT mice (P < 0.01). However, the muscle weight of EA and CT mice increased significantly compared with that of HS mice (P < 0.01). In addition, the muscle weight of EA mice was significantly higher than that of CT mice (P < 0.01), without a significant difference in muscle fiber cross-sectional area between CT and EA mice.
[Conclusion]These results indicate that EA was effective in facilitating the recovery of skeletal muscle atrophy in mice. In addition, resolution of the skeletal muscle atrophy suggested the satellite cell activation by macrophages, because macrophages invaded the skeletal muscle after EA stimulation.
2.Allergy to carminic acid: in vitro evidence of involvement of protein-binding hapten
Mika OSUMI ; Masao YAMAGUCHI ; Naoya SUGIMOTO ; Maho SUZUKAWA ; Hidenori ARAI ; Hiroshi AKIYAMA ; Hiroyuki NAGASE ; Ken OHTA
Asia Pacific Allergy 2019;9(1):e2-
We previously described a rare case of anaphylaxis presumably induced by carminic acid in cochineal dye used as a food additive. In this study, highly pure carminic acid was added to an albumin-containing buffer at various concentrations, followed by serial dilution. Varying the mixing ratio of carminic acid and albumin affected the extent of histamine release from passively sensitized basophils. Similar basophil histamine release occurred with carminic acid-globulin solutions. These results provide experimental evidence indicating that basophil activation is dependent on hapten (carminic acid) and carrier (protein) interaction.
Anaphylaxis
;
Basophils
;
Carmine
;
Food Additives
;
Histamine Release
;
Hypersensitivity
;
In Vitro Techniques
3.Molecular Mechanisms of Inhibiting the Muscle Atrophy by Electroacupuncture
Sachiko IKEMUNE ; Mika OHTA ; Toshikazu MIYAMOTO ; Yutaka TAKAOKA
The Journal of The Japanese Society of Balneology, Climatology and Physical Medicine 2011;74(2):103-111
Electroacupuncture (EA) is an acupuncture technique that is stimulated by acupuncture needles with low-frequency microcurrent. The aim of this study is to elucidate the effect of EA and it's molecular mechanism on muscle atrophy by using an animal model: hindlimb-suspended (HS) mice in the disuse muscle atrophy model. To compare the effects of EA in HS mice and HS mice treated with EA (EA/HS), soleus muscle mass and soleus myofiber diameter were measured. We then used real-time quantitative RT-PCR to analyze the expression of myostatin and ubiquitin ligase genes in atrophic muscles of HS mice and in muscles of EA/HS mice. We found that EA/HS mice maintained a soleus muscle mass that was not significantly different from that of wild mice (WT), whereas HS mice had significantly reduced muscle mass. Also, the diameters of myofibers in EA/HS mice, which were not significantly different from wild values, were significantly larger than those in HS mice. Repeated EA treatment suppressed gene expression of myostatin and ubiquitin ligase genes in skeletal muscle of EA/HS mice but induced expression of these genes in HS mice. These findings suggest the molecular mechanism by EA: suppression of myostatin and ubiquitin ligase gene may be a key reaction of inhibiting the disuse muscle atrophy.