GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Rikkunshito, an herbal medicine, suppresses cisplatin-induced anorexia in rats via 5-HT2 receptor antagonism.
Takeda. Hiroshi H; Sadakane. Chiharu C; Hattori. Tomohisa T; Katsurada. Takehiko T; Ohkawara. Tatsuya T; Nagai. Koichi K; Asaka. Masahiro M
Key Findings
- Cisplatin and serotonin lower plasma acylated‑ghrelin and food intake via 5‑HT2B/2C receptors.
- Rikkunshito prevents the cisplatin‑induced drop in ghrelin and appetite, an effect blocked by a ghrelin antagonist.
- Flavonoids in Rikkunshito (e.g., heptamethoxyflavone, hesperidin, iso‑liquiritigenin) act as 5‑HT2B antagonists in vitro.
- Direct ghrelin administration restores food intake, confirming ghrelin’s central role.
Practical Outcomes
- For biohackers using GHRP‑6 to raise ghrelin, adding a 5‑HT2 antagonist or the herbal formula Rikkunshito could further support appetite and metabolic health, especially during stress or chemotherapy. The flavonoid components might be taken as a natural supplement to enhance ghrelin signaling without needing higher peptide doses.
Summary
The study shows that a Japanese herbal mix called Rikkunshito can stop chemotherapy‑induced loss of appetite by blocking certain serotonin receptors (5‑HT2B/2C), which in turn keeps the hunger hormone ghrelin high. This effect is similar to what GHRP‑6 does—raising ghrelin levels—so the herb might be a natural way to boost ghrelin and appetite, especially when the body’s own ghrelin is being suppressed.
Abstract
Chemotherapy with an anticancer agent generally causes gastrointestinal tract disorders such as vomiting and anorexia, but the mechanism remains unclear. Rikkunshito, a kampo preparation, is known to alleviate such adverse reactions. In this study, we attempted to clarify the mechanism. We investigated the decreases of plasma acylated-ghrelin level and food intake caused by cisplatin, serotonin (5-HT), 5-HT agonists, and vagotomy as well as the decrease-suppressing effects of rikkunshito and 5-HT antagonists. In addition, binding affinities of rikkunshito components were determined in receptor-binding assays using 5-HT2B and 5-HT2C receptors. Cisplatin, 5-HT, BW723C86 (5-HT2B-receptor agonist), and m-chlorophenylpiperazine HCl (5-HT2C agonist) markedly decreased plasma acylated-ghrelin levels, although 5-HT3 and 5-HT4 agonists had no effect. In contrast, 5-HT2B and 5-HT2C antagonists suppressed the cisplatin-induced decrease of plasma acylated-ghrelin level and food intake. Administration of rat ghrelin improved the cisplatin-induced decrease in food intake. Vagotomy decreased the plasma acylated-ghrelin level, which was decreased further by cisplatin. Rikkunshito suppressed such cisplatin-induced decreases of plasma acylated-ghrelin level and food intake. The suppressive effect of rikkunshito was blocked by a ghrelin antagonist. Components of rikkunshito, 3,3',4',5,6,7,8-heptamethoxyflavone, hesperidin, and iso-liquiritigenin showed a 5-HT2B-antagonistic effect in vitro, and oral administration of rikkunshito suppressed the cisplatin-induced decrease in the plasma acylated-ghrelin level. The cisplatin-induced decreases of the plasma acylated-ghrelin level and food intake are mediated by 5-HT2B/2C receptors and suppressed by flavonoids in rikkunshito.
Study Information
pubmed
2008
2008-02-29T00:00:00.000Z
10.1053/j.gastro.2008.02.078
302
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