Ghrelin (rat) |
Catalog No.GC11583
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Ghrelin (rat) is an endogenous brain-gut peptide secreted from rat stomach tissue, composed of 28 amino acids, and acts as an agonist of the growth hormone secretagogue receptor (GHS-R1a).
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Cas No.: 258338-12-4
Sample solution is provided at 25 µL, 10mM.
Ghrelin (rat) is an endogenous brain-gut peptide secreted from rat stomach tissue, composed of 28 amino acids, and acts as an agonist of the growth hormone secretagogue receptor (GHS-R1a). Ghrelin can promote pituitary growth hormone release by activating GHS-R1a and its downstream cAMP/Ca²⁺ signaling pathway, and act on hypothalamic NPY/AgRP neurons to stimulate food intake, regulate energy balance, gastrointestinal motility, and glucose metabolic homeostasis. Ghrelin can be used in research related to obesity, metabolic syndrome, cachexia, gastrointestinal and cardiovascular diseases[1-4].
In vitro, Ghrelin (0–30nM) was applied to rat C6 glioma cells and human U251 glioma cells for 5min to 24h. Ghrelin upregulated GHS-R expression, activated CaMKII, AMPK, and NF-κB signaling pathways, promoted IKKα/β, IκBα, and p65 Ser536 phosphorylation, enhanced NF-κB-DNA binding activity and κB transcriptional activity. Ghrelin increased glioma cell migration ability[5]. Ghrelin (0.01nM to 1μM) was applied to rat pancreatic islets and CRI-D2 cells for 24h. Ghrelin significantly downregulated KiSS-1 and KissR mRNA transcription, and inhibited insulin secretion from pancreatic islets and CRI-D2 cells[6].
In vivo, Ghrelin (300nmol/kg) combined with paclitaxel (2mg/kg) was intraperitoneally injected into wild-type C57BL/6J mice, Ghrelin-null mice, and growth hormone secretagogue receptor-null mice for 5 consecutive days. Ghrelin alleviated paclitaxel-induced mechanical and thermal hyperalgesia, prevented the loss of small unmyelinated intraepidermal nerve fibers, reduced plasma levels of 8-isoprostane, malondialdehyde, and nitric oxide, and upregulated the mRNA expression of mitochondrial antioxidant proteins UCP2, SOD2, and mitochondrial biogenesis regulator PGC-1α in dorsal root ganglia[7]. Ghrelin (3nmol/mouse; single injection) was administered via the third ventricle or intraperitoneally into male ddy mice, followed by tail clip and starvation stress interventions. Ghrelin induced anxiety-like behavior in the elevated plus maze test and upregulated hypothalamic CRH mRNA expression[8].
References:
[1] Kojima M, Hosoda H, Date Y, et al. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999 Dec 9;402(6762):656-60.
[2] Chung H, Choi J, Park S. Ghrelin protects adult rat hippocampal neural stem cells from excessive autophagy during oxygen-glucose deprivation. Endocr J. 2018 Jan 30;65(1):63-73.
[3] Kojima M, Kangawa K. Ghrelin: structure and function. Physiol Rev. 2005 Apr;85(2):495-522.
[4] Zhu K, Zhang ML, Liu ST, et al. Ghrelin Attenuates Retinal Neuronal Autophagy and Apoptosis in an Experimental Rat Glaucoma Model. Invest Ophthalmol Vis Sci. 2017 Dec 1;58(14):6113-6122.
[5] Chen JH, Huang SM, Chen CC, et al. Ghrelin induces cell migration through GHS-R, CaMKII, AMPK, and NF-κB signaling pathway in glioma cells. J Cell Biochem. 2011 Oct;112(10):2931-41.
[6] Sagheb MM, Azarpira N, Mokhtary M. The effect of ghrelin on Kiss-1 and KissR gene transcription and insulin secretion in rat islets of Langerhans and CRI-D2 cell line. Iran J Basic Med Sci. 2017 Jan;20(1):36-40.
[7] Ishii N, Tsubouchi H, Miura A, et al. Ghrelin alleviates paclitaxel-induced peripheral neuropathy by reducing oxidative stress and enhancing mitochondrial anti-oxidant functions in mice. Eur J Pharmacol. 2018 Jan 15;819:35-42.
[8] Asakawa A, Inui A, Kaga T, et al. A role of ghrelin in neuroendocrine and behavioral responses to stress in mice. Neuroendocrinology. 2001 Sep;74(3):143-7.
| Cell experiment [1]: | |
Cell lines | C6 cells (rat brain glioma cell line), U251 cells (human brain glioma cell line) |
Preparation Method | C6 cells were maintained in F12 medium supplemented with 10% heat-inactivated fetal bovine serum (FBS), 100U/mL penicillin and 100μg/mL streptomycin at 37°C in a humidified 5% CO₂ incubator; U251 cells were cultured in DMEM with the same supplements under identical condition. Cells were treated with Ghrelin at indicated concentrations for 5min to 24h for subsequent assays. |
Reaction Conditions | 0-30nM; 5min-24h |
Applications | Ghrelin dose-dependently enhanced the migration of both C6 and U251 glioma cells without affecting cell viability at concentrations up to 30nM. Ghrelin upregulated GHS-R protein and mRNA expression, and its pro-migratory effect was abolished by the GHS-R antagonist D-Lys3-GHRP-6 or GHS-R1 siRNA. Ghrelin activated CaMKII (Thr286 phosphorylation) and AMPK (Thr172/Ser485 phosphorylation), and inhibition of CaMKII or AMPK suppressed Ghrelin-induced migration. Ghrelin further triggered IKKα/β phosphorylation, IκBα phosphorylation, p65 Ser536 phosphorylation, promoted p65/p50 nuclear accumulation, and increased NF-κB-DNA binding activity and κB-transcriptional activity to drive glioma cell migration, with NF-κB activation downstream of the CaMKII/AMPK signaling pathway. |
| Animal experiment [2]: | |
Animal models | 8-10-week-old male C57BL/6J wild-type (WT) mice, 8-week-old ghrelin-null mice, 8-week-old growth hormone secretagogue receptor (GHSR)-null mice |
Preparation Method | To establish paclitaxel-induced peripheral neuropathy model, mice were intraperitoneally administered paclitaxel (2mg/kg) once daily for 5 consecutive days (cumulative dose 10mg/kg). Concurrently, Ghrelin (300nmol/kg in 0.2ml PBS) or vehicle PBS was intraperitoneally injected into WT mice once daily for 5 consecutive days. Ghrelin-null and GHSR-null mice received paclitaxel (2mg/kg) plus PBS for 5 consecutive days. Behavioral tests were conducted on day 1 before administration and day 7, and all mice were euthanized on day 7 for subsequent histological analysis, oxidative and nitrosative stress detection, and quantitative real-time PCR. |
Dosage form | 300nmol/kg; i.p.; once daily for 5 consecutive days |
Applications | In WT mice, Ghrelin alleviated paclitaxel-induced mechanical and thermal hypersensitivity, and partially prevented the loss of small unmyelinated intraepidermal nerve fibers without affecting large myelinated sciatic nerve fibers. Ghrelin reduced plasma levels of 8-isoprostane, malondialdehyde and nitric oxide, and upregulated the mRNA expression of Ucp2, Pgc-1α and Sod2 in dorsal root ganglia. Both Ghrelin-null and GHSR-null mice developed more severe paclitaxel-induced nerve injuries than WT mice, confirming that the neuroprotective effect of Ghrelin against paclitaxel-induced peripheral neuropathy is mediated by the endogenous Ghrelin/GHSR signaling pathway. |
References: | |
| Cas No. | 258338-12-4 | SDF | |
| Chemical Name | (4S,5Z,7S,8Z,10S,11Z,13S,14Z,16S,17Z,19S,20Z,22S,23Z,25S,26Z,28S,29Z,31S)-28-((1H-imidazol-5-yl)methyl)-4-((Z)-(((S,Z)-1-(((S,Z)-6-amino-1-(((S)-6-amino-1-((S)-2-((S)-2-((1Z,3S,4Z,6S,7Z,9S,10Z,12S)-6-(4-aminobutyl)-12-((S)-2-((Z)-(((S)-1-carboxy-4-guanidi | ||
| Canonical SMILES | CCCCCCCC(OC[C@@](/N=C(O)/[C@](/N=C(O)/CN)([H])CO)([H])/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](C(N1CCC[C@@]1([H])/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/ | ||
| Formula | C147H245N45O42 | M.Wt | 3314.83 |
| Solubility | Soluble to 1 mg/ml in Water | Storage | Desiccate at -20°C |
| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 301.7 μL | 1.5084 mL | 3.0167 mL |
| 5 mM | 60.3 μL | 301.7 μL | 603.3 μL |
| 10 mM | 30.2 μL | 150.8 μL | 301.7 μL |
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- Purity: >98.00% Appearance: A solid
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Average Rating: 5 (Based on Reviews and 14 reference(s) in Google Scholar.)