Simvastatin Induces Avian Muscle Protein Degradation through Muscle Atrophy Signaling

Abstract

Many studies on poultry have been conducted in the poultry industry to improve their important economic traits, such as egg production, meat quality, and carcass yield. Environmental changes affect the poultry's economic traits, including muscle growth. The purpose of this study is to investigate the mechanisms by which simvastatin causes muscle injury in quail muscle cells. Following treatment with various doses of simvastatin, LD50 in the quail myoblast cells was determined using a cell viability test; cell death was caused by apoptosis and/or necrosis. Thereafter, the expression patterns of the atrophy marker genes were examined via quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The results showed that the transcriptional levels of the muscle atrophy marker genes (Atrogin-1, TRIM63) and the upstream genes in their signaling cascade were increased by simvastatin treatment. This indicated that simvastatin induced myogenic cell death and muscle injury via protein degradation through muscle atrophy signaling. Further studies should focus on identifying the mechanism by which simvastatin induces the protein degradation signaling pathway in quail muscle..