Study summary · research use only
[D-Lys3]-GHRP-6 exhibits pro-autophagic effects on skeletal muscle
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study, the authors examined effects of [D-Lys3]-GHRP-6, regarded as a selective growth-hormone secretagogue receptor (GHSR) antagonist, on autophagic and apoptotic signalling in skeletal muscle (species not stated in the abstract). The abstract reports [D-Lys3]-GHRP-6 enhanced autophagic signalling, shown by increased beclin-1 and LC3 II-to-LC3 1 ratio in both normal and doxorubicin-injured muscle, and reduced doxorubicin-induced muscle apoptosis, with no histological abnormalities. It states the doxorubicin-induced increase in centronucleated fibres was not seen with [D-Lys3]-GHRP-6, and that co-treatment with a CXCR4 antagonist abolished the autophagy activation, suggesting the pro-autophagic effect might be mediated through CXCR4.
Abstract
[D-Lys3]-GHRP-6 is regarded as a highly selective growth-hormone secretagogue receptor (GHSR) antagonist and has been widely used to investigate the dependency of GHSR-1a signalling mediated by acylated ghrelin. However, [D-Lys3]-GHRP-6 has been reported to influence other cellular processes which are unrelated to GHSR-1a. This study aimed to examine the effects of [D-Lys3]-GHRP-6 on autophagic and apoptotic cellular signalling in skeletal muscle. [D-Lys3]-GHRP-6 enhanced the autophagic signalling demonstrated by the increases in protein abundances of beclin-1 and LC3 II-to-LC3 1 ratio in both normal muscle and doxorubicin-injured muscle. [D-Lys3]-GHRP-6 reduced the activation of muscle apoptosis induced by doxorubicin. No histological abnormalities were observed in the [D-Lys3]-GHRP-6-treated muscle. Intriguingly, the doxorubicin-induced increase in centronucleated muscle fibres was not observed in muscle treated with [D-Lys3]-GHRP-6, suggesting the myoprotective effects of [D-Lys3]-GHRP-6 against doxorubicin injury. The [D-Lys3]-GHRP-6-induced activation of autophagy was found to be abolished by the co-treatment of CXCR4 antagonist, suggesting that the pro-autophagic effects of [D-Lys3]-GHRP-6 might be mediated through CXCR4. In conclusion, [D-Lys3]-GHRP-6 exhibits pro-autophagic effects on skeletal muscle under both normal and doxorubicin-injured conditions.
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