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Ä«Å×°í¸® Hypothalamic Hormone
CAT.NO
PRODUCT [D-Lys3]-GHRP-6
Size
Price

Product name: [D-Lys3]-GHRP-6

Synonyms:
d-Lys-GHRP-6,

Sequence: His-(D-Trp)-(D-Lys)-Trp-(D-Phe)-Lys-NH2

Purity: 95% by HPLC

Counter ion: Trifluoacetate

Format: Lyophilized powder

Description: [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.



Usage: For Scientific Research Use Only, Not for Human Use.

 

Reference:

Molecular and Cellular Endocrinology, Volume 401, 5 February 2015, Pages 155-164.

Molecular and Cellular Endocrinology, Volume 343, Issues 1–2, 22 August 2011, Pages 55-62.

Cell Calcium, Volume 46, Issue 3, September 2009, Pages 197-208.

Neuropeptides, Volume 41, Issue 1, February 2007, Pages 45-49.

Peptides, Volume 38, Issue 2, December 2012, Pages 248-254.

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