Introduction: Many treatment modalities are used for muscle tissue recovery. Photobiomodulation is a modality that can be employed to improve the quality of tissue repair. The use of fractal dimension (FD) is an innovative methodology in the quantitative evaluation of treatment efficacy. Objective: Use FD as a quantitative analysis method to evaluate the effect of photobiomodulation of 904 nanometers (nm) in the initial phase of the muscle regeneration process. Method: Thirty male Wistar rats were divided into three groups: Control Group (CG), Injured and Untreated Group (IUT), and Injured and Treated Group (IT). Muscle injury was induced by cryoinjury in the central region of the anterior tibial (AT) belly of the left posterior limb. This was performed by an iron rod that was previously immersed in liquid nitrogen. Applications started 24 hours after the injury and occurred daily for five days. They were performed at two points in the lesion area. The rats were euthanized on the seventh day. The AT muscles were removed and frozen in liquid nitrogen. Then, the histological sections were stained using the Hematoxylin-Eosin (HE) technique and submitted to FD analysis performed by the box-counting method using ImageJ software. The Kolmogorov-Smirnov test was used for data normality, and the Kruskall-Wallis test and Dunn's post-test were used for group comparison (p<0.05%). Results: Differences between IT and IUT groups were statistically significant, and it was possible to observe the reduction of fractability with p=0.0034. Conclusion: FD is a useful tool for the analysis of skeletal muscle disorganization in the initial phase of regeneration and confirms the potentially beneficial effects of photobiomodulation to this process.
To gain insight on the impact of preventive exercise during pulmonary arterial hypertension (PAH), we evaluated the gene expression of myosins and gene-encoding proteins associated with the extracellular matrix remodeling of right hypertrophied ventricles. We used 32 male Wistar rats, separated in four groups: Sedentary Control (S, n = 8); Control with Training (T, n = 8); Sedentary with Pulmonary Arterial Hypertension (SPAH, n = 8); and Pulmonary Arterial Hypertension with Training (TPAH, n = 8). All rats underwent a two-week adaptation period; T and TPAH group rats then proceeded to an eight-week training period on a treadmill. At the beginning of the 11th week, S and T groups received an intraperitoneal injection of saline, and SPAH and TPAH groups received an injection of monocrotaline (60 mg/kg). Rats in the T and TPAH groups then continued with the training protocol until the 13th week. We assessed exercise capacity, echocardiography analysis, Fulton’s index, cross-sectional areas of cardiomyocytes, collagen content and types, and fractal dimension (FD). Transcript abundance of myosins and extracellular matrix genes were estimated through reverse transcription-quantitative PCR (RT-qPCR). When compared to the SPAH group, the TPAH group showed increases in functional capacity and pulmonary artery acceleration time/pulmonary ejection time ratio and decreases in Fulton’s index and cross-sectional areas of myocyte cells. However, preventive exercise did not induce alterations in col1a1 and myh7 gene expression. Our findings demonstrate that preventive exercise improved functional capacity, reduced cardiac hypertrophy, and attenuated PH development without interfering in mRNA-encoding myosin and collagen expression during PAH.
To gain insight on the impact of preventive exercise during pulmonary arterial hypertension (PAH), we evaluated the gene expression of myosins and gene-encoding proteins associated with the extracellular matrix remodeling of right hypertrophied ventricles. We used 32 male Wistar rats, separated in four groups: Sedentary Control (S; n=8); Control with Training (T; n=8); Sedentary with Pulmonary Arterial Hypertension (SPAH; n=8); and Pulmonary Arterial Hypertension with Training (TPAH; n=8). The rats trained for thirteen weeks on a treadmill. They had two weeks of adaptation training. The PAH was induced by application of monocrotaline 60 mg/kg. Consequential right ventricular dysfunction was observed after the 10th week of training. Rats in the control group received saline application. At the end of the 13th week, echocardiography analysis confirmed cardiac dysfunction. Collagen content and organization was assessed through picrosirius red staining and fractal dimension (FD) analysis, respectively. Transcript abundance was estimated through reverse transcription-quantitative PCR (RT-qPCR). Cardiac dysfunction was confirmed by the reduction in maximum pulmonary artery velocity and pulmonary artery acceleration time. Through histomorphometric assessment, we found no differences in the interstitial collagen FD between groups. Regarding gene expression, myh7 gene expression was upregulated in the TPAH group. However, this did not occur with the S group. PAH also increased the mRNA abundance of col1a1 in the SPAH and TPAH groups. Moreover, the TPAH group showed a higher abundance of this gene when compared to the S group. With these findings, we concluded that preventive exercise had a positive impact on compensated hypertrophy during pulmonary hypertension. This can be explained in part by the modulation of the extracellular matrix and myosin gene expression in trained rats.
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