Preventive effect and possible mechanisms of ultrashort wave diathermy on myogenic contracture in a rabbit model

Abstract

The purpose of this study was to determine the preventive effect of ultrashort wave diathermy on immobilization-induced myogenic contracture and to explore its underlying mechanisms. Forty-two rabbits were randomly assigned into control (Group C), immobilization (Group I, which was further divided into one week, Group I-1; two weeks, Group I-2; and four weeks, Group I-4, subgroups by the length of immobilization) and ultrashort wave prevention (Group U, which was further divided into one week, Group U-1; two weeks, Group U-2; and four weeks, Group U-4, by time of treatment) groups. Intervention effects were assessed by evaluating rectus femoris cross-sectional area (CSA), knee range of motion, and the protein levels for myogenic differentiation (MyoD) and muscle atrophy F-box (MAFbx-1) in the rectus femoris. Compared with those of Group C, in Groups I and U, total contracture, myogenic contracture, MyoD and MAFbx-1 levels were significantly elevated, and CSA was significantly smaller (p < 0.05). Compared with those of Group I at each time point, MyoD levels were significantly elevated, MAFbx-1 levels were significantly lower, CSA was significantly larger, and myogenic contracture was significantly alleviated in Group U (p < 0.05). In the early stages of contracture, ultrashort wave diathermy reduces muscle atrophy and delays the process of myogenic contracture during joint immobilization; the mechanism of this may be explained as increased expression of MyoD triggered by suppression of the MAFbx-1-mediated ubiquitin-proteasome pathway.

Keywords: MAFbx-1; MyoD; Prevention; muscle atrophy; myogenic contracture; ultrashort wave diathermy.

Figure 1.

Ultrashort wave diathermy could light the neon lamp encased in plaster.

Figure 2.

(A) A rabbit model of knee extension contracture. (B) The rabbits in Group U received ultrashort wave diathermy treatment.

Figure 3.

Mechanical arthrometer used to measure knee (A) flexion angle before myotomy and (B) flexion angle after myotomy.

Figure 4.

(A) Total contracture and (B) myogenic contracture of knee in each group. ^ap < 0.05 vs. Group C, ^bp < 0.05 vs. Group I-1, ^cp < 0.05 vs. Group I-2, ^a’p < 0.05 vs. Group I-0, ^b’p < 0.05 vs. Group U-1, ^c’p < 0.05 vs. Group U-2, ***p < 0.001, **p < 0.01 and ^nsp = 0.115.

Figure 5.

(A) Hematoxylin and eosin staining (400× magnification; 100 µm scale bar) of rectus femoris specimens from group C, group I and group U. (B) Rectus femoris cross-sectional area (CSA); ^ap < 0.05 vs. Group C, ^bp < 0.05 vs. Group I-1, ^cp < 0.05 vs. Group I-2, ^a’p < 0.05 vs. Group I-0, ^b’p < 0.05 vs. Group U-1, ^c'p < 0.05 vs. Group U-2 and *p < 0.05.

Figure 6.

Protein levels of myogenic differentiation (MyoD) and muscle atrophy F-box (MAFbx-1) relative to glyceraldehyde 3-phosphate dehydrogenase (GAPDH). (A) Photographs of MyoD, MAFbx-1 and GAPDH protein-band intensities. (B) MyoD protein levels relative to GAPDH. (C) MAFbx-1 protein levels relative to GAPDH. ^ap < 0.05 vs. Group C(I-0), ^bp < 0.05 vs. Group I-1, ^cp < 0.05 vs. Group I-2, ^a’p < 0.05 vs. Group I-0, ^b’p < 0.05 vs. Group U-1, ^c’p < 0.05 vs. Group U-2, ***p < 0.001, **p < 0.01 and *p < 0.05.