D lys3 ghrp 6

Manufactured by Phoenix Pharmaceuticals

Sourced in United States

[D-Lys3]-GHRP-6 is a synthetic peptide that is a Growth Hormone Releasing Peptide (GHRP) analog. It is used in research settings to stimulate the release of growth hormone from the pituitary gland.

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Lab products found in correlation

5 protocols using d lys3 ghrp 6

Ghrelin, GHSR1a, and Leptin Interactions

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Recombinant human ghrelin and the GHSR1a antagonist; D-Lys-3-growth hormone-releasing peptide 6 (D-Lys-3-GHRP-6) were obtained from Phoenix Pharmaceuticals. Lipopolysaccharide (LPS) was purchased from Sigma-Aldrich. Recombinant human leptin was purchased from R&D Systems. The HNEpCs were obtained from PromoCell (C-12620).

Choi Y.S., Na H.G., Bae C.H., Song S.Y, & Kim Y.D. (2022). Ghrelin Downregulates Lipopolysaccharide/ Leptin-Induced MUC5AC Expression in Human Nasal Epithelial Cells. Clinical and Experimental Otorhinolaryngology, 16(1), 49-58.

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Signaling Pathways in Bovine Mammary Cells

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Human AG (Ser3-Decanoyl), Human UAG (Ser3-Des-Octanoyl), and [D-Lys3]-GHRP-6 were obtained from Phoenix Pharmaceuticals, Inc. (Belmont, CA, USA). Antibodies to P-ERK 1/2 (Thr202/Tyr204), ERK1/2 (Thr202/Tyr204), AKT(Ser473), and P-AKT (Ser473) were purchased from Cell Signaling Technology Inc. Antibodies to AG, GHSR1a, and CSN2 were purchased from Abcam. Bovine insulin, prolactin, hydrocortisone, phosphatase inhibitor cocktail 2, protease inhibitor cocktail, and DAPI were obtained from Sigma. The antibodies for goat anti-rabbit IgG-HRP, rabbit anti-cytokeratin 18 (CK-18), and rabbit anti-β-tubulin (1–19) were purchased from Santa Cruz Biotechnology. The selective inhibitors of NF449 (Gαs), pertussis toxin (PTX, Gαi), and U0126 (ERK 1/2) were obtained from TOCRIS (Ellisville, MO, USA). The selective inhibitor of YM-254890 (Gq11) was provided by Astellas Pharma Inc. (Tokyo, Japan). The selective inhibitor of MK2206 (AKT) was from Selleckchem (Houston, DE, USA).

Li S., Liu J., Lv Q., Zhang C., Xu S., Yang D., Huang B., Zeng Y., Gao Y, & Wang W. (2016). AG and UAG induce β-casein expression via activation of ERK1/2 and AKT pathways. Journal of Molecular Endocrinology, 56(3), 213-225.

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Rikkunshito Composition and Preparation

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Rikkunshito, powdered extract consisting of Atractylodis lanceae rhizoma (4 g, 18.6%), Ginseng radix (4 g, 18.6%), Pinelliae tuber (4 g, 18.6%), Hoelen (4 g, 18.6%), Zizyphi fructus (2 g, 9.3%), Aurantii nobilis pericarpium (2 g, 9.3%), Glycyrrhizae radix (1 g, 4.7%), and Zingiberis rhizoma (0.5 g, 2.3%) (Tsumura & Co., Tokyo, Japan) was suspended in water. l-dopa (l-3,4-dihydroxyphenylalanine methyl ester hydrochloride) and s-(−)-carbidopa (CD) were dissolved in vehicle composed of 10% dimethyl sulfoxide, 5% Tween-80 and 85% saline, all from Sigma-Aldrich. [d-Lys³]-GHRP-6 (Phoenix Pharmaceuticals, CA, USA) was dissolved in sterile saline.

Wang L., Mogami S., Karasawa H., Yamada C., Yakabi S., Yakabi K., Hattori T, & Taché Y. (2014). Preventive effect of rikkunshito on gastric motor function inhibited by l-dopa in rats. Peptides, 55, 136-144.

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Modulating p38 MAPK, JNK, and TNF-α in CRBI

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Immediately after CRBI, selective p38 MAPK blocker SB203580 (Sigma-Aldrich, USA, diluted in PBS) and JNK blocker SP600125 (Sigma-Aldrich, USA, diluted in polyethylene glycol) were administered subcutaneously, separately or jointly, each at 15 mg∙kg⁻¹∙d⁻¹ dose, for 7 days. [D-Lys3]-GHRP-6 (Phoenix Pharmaceuticals, Inc., Burlingame, CA, diluted in PBS), a specific blocker of GHS-R1a, was injected subcutaneously (5 mg∙kg⁻¹∙d⁻¹) at 6 h before each ghrelin infusion (200 nmol∙kg⁻¹∙d⁻¹), every day for 7 days. Polyclonal anti-rat TNF-α antibody (Janssen Pharmaceutica, Belgium, diluted in PBS) was i.p. administered (10 mg∙kg⁻¹∙d⁻¹, for 7 days). Four days after CRBI (or the initial inhibitor administration), rat peritoneal macrophages from each group (n = 3–5/group) were isolated for protein extraction, and serum samples (n = 5–7/group) were collected for TNF-α determination.

Liu C., Huang J., Li H., Yang Z., Zeng Y., Liu J., Hao Y, & Li R. (2016). Ghrelin accelerates wound healing through GHS-R1a-mediated MAPK-NF-κB/GR signaling pathways in combined radiation and burn injury in rats. Scientific Reports, 6, 27499.

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Ghrelin Modulates Gastric Distension

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In anesthetized rats, a first set of graded GD was performed. Fifteen minutes later, atropine (1 mg/kg) was injected intravenously (i.v.) to prevent acylated ghrelin stimulation of gastric motility that would have jeopardized isobaric distension of the stomach. Five minutes after atropine injection, acylated ghrelin (30 µg/kg; Phoenix Pharmaceuticals, Burlingame, CA) or saline was injected i.v. (n = 10/group). A second series of GD was started 5 min later. In one experiment, [D-Lys³]-GHRP-6 (Phoenix Pharmaceuticals, Burlingame, CA), a Ghrelin receptor antagonist, was injected (0.3 mg/kg i.v.) 10 min before acylated ghrelin injection (n = 8). The dose of peptides were selected accordingly to our previous report as the maximal effective dose to accelerate gastric emptying^{3 (link)} (Fig. 6).

Meleine M., Mounien L., Atmani K., Ouelaa W., Bôle-Feysot C., Guérin C., Depoortere I, & Gourcerol G. (2020). Ghrelin inhibits autonomic response to gastric distension in rats by acting on vagal pathway. Scientific Reports, 10, 9986.

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