The effect of cerebrolysin treatment on skeletal muscle healing in adult albino rat: a histological and immunohistochemical study

Abstract

Objective The aim of this study was to evaluate the role of Cerebrolysin in muscle healing in vivo. Materials and methods Twenty adult albino rats were used in this study. Both right and left gastrocnemius muscles of the albino rats were cut at 60% of their length from their distal insertion through 75% of their width and 50% of their thickness and then sutured with simple sutures using absorbable catgut sutures. The gastrocnemius muscles of all albino rats were injected directly in the lesion with 100 ng/ml/kg of cerebrolysin at 1, 3, and 5 days after laceration. The sham control muscles were subjected to the same treatment but were injected with the same volume of physiological normal saline. One week after the injury the animals were killed and the gastrocnemius muscles were removed and processed for paraffin sectioning and stained with hematoxylin and eosin, Bcl-2 (B-cell lymphoma 2), and P53 (tumor suppressor gene) immune peroxidase stains. Results There was a significant increase in the mean myonuclei/myofiber diameter ratio and the size of the regenerating myofibers as an index of muscle regeneration in the cerebrolysin-injected group compared with the control. It is anticipated that cerebrolysin is a potent stimulator of muscle regeneration in vivo. It has also been found that regenerating myofibers were located both in the deep and the superficial areas of the injured site of muscles only when treated with cerebrolysin, thereby demonstrating greater initial healing when the injured muscle is treated with cerebrolysin. Cerebrolysin retarded apoptosis in neutrophils, macrophages, and other inflammatory cells by activating the anti-apoptotic Bcl-2 (B-cell lymphoma 2) protein leading to accumulation of these inflammatory cells. Conclusion This study has shown that injections of cerebrolysin into an injured muscle improved muscle healing in vivo. Also, documents the occurrence of a protective Bcl-2 in inflammatory neutrophils and macrophages, which were expressed in cerebrolysin-treated muscles, leading to enhancement of the effect of these inflammatory cells. We have also found that Inflammatory cells play a role in satellite cell activation and proliferation but, the tumor suppressor gene p53, which is recognized as a central regulator of cell cycle and apoptosis, had no role in muscle regeneration in this in-vivo study.