GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Antinociceptive Effect of Ghrelin in a Rat Model of Irritable Bowel Syndrome Involves TRPV1/Opioid Systems.
Mao. Yuqing Y; Li. Zhengyang Z; Chen. Kan K; Yu. Huafang H; Zhang. Shaoren S; Jiang. Miao M; Ma. Yuanhua Y; Liang. Chunli C; Liu. Hongyan H; Li. Huanqing H; Hua. Qian Q; Zhou. Hao H; Sun. Yonghong Y; Fan. Xiaoming X
Key Findings
- Ghrelin administration (10 µg/kg, s.c.) lowered visceral pain responses in an IBS‑like rat model.
- The pain‑relieving effect was linked to higher opioid receptor levels (MOR, KOR) and reduced TRPV1 expression in colon, DRG, and brain tissue.
- Blocking the ghrelin receptor with [D‑Lys3]-GHRP‑6 or opioid receptors with naloxone partially reversed ghrelin’s antinociceptive effect.
Practical Outcomes
- The study suggests that boosting ghrelin activity could help ease IBS‑related gut pain, but it’s an early animal finding. For biohackers, there’s no clear dosing guidance or evidence that GHRP‑6 (often used to raise growth hormone) will have the same effect in humans. Until human trials are done, it’s mainly a mechanistic insight rather than a ready‑to‑use protocol.
Summary
In rats that were stressed to mimic IBS, giving the hormone ghrelin reduced gut pain. The pain relief seemed to work because ghrelin boosted opioid receptors and lowered a pain‑related protein called TRPV1. When the researchers blocked ghrelin’s receptor or opioid receptors, the benefit went away, showing those pathways are important.
Abstract
Irritable bowel syndrome (IBS), defined as recurrent abdominal pain and changes in bowel habits, seriously affects quality of life and ability to work. Ghrelin is a brain-gut hormone, which has been reported to show antinociceptive effects in peripheral pain. We investigated the effect of ghrelin on visceral hypersensitivity and pain in a rat model of IBS. Maternal deprivation (MD) was used to provide a stress-induced model of IBS in Wistar rats. Colorectal distension (CRD) was used to detect visceral sensitivity, which was evaluated by abdominal withdrawal reflex (AWR) scores. Rats that were confirmed to have visceral hypersensitivity after MD were injected with ghrelin (10 µg/kg) subcutaneously twice a week from weeks 7 to 8. [D-Lys3]-GHRP-6 (100 nmol/L) and naloxone (100 nmol/L) were administered subcutaneously to block growth hormone secretagogue receptor 1α (GHS-R1α) and opioid receptors, respectively. Expression of transient receptor potential vanilloid type 1 (TRPV1) and µ and κ opioid receptors (MOR and KOR) in colon, dorsal root ganglion (DRG) and cerebral cortex tissues were detected by western blotting, quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemical analyses and immunofluorescence. Ghrelin treatment increased expression of opioid receptors and inhibited expression of TRPV1 in colon, dorsal root ganglion (DRG) and cerebral cortex. The antinociceptive effect of ghrelin in the rat model of IBS was partly blocked by both the ghrelin antagonist [D-Lys3]-GHRP-6 and the opioid receptor antagonist naloxone. The results indicate that ghrelin exerted an antinociceptive effect, which was mediated via TRPV1/opioid systems, in IBS-induced visceral hypersensitivity. Ghrelin might potentially be used as a new treatment for IBS.
Study Information
pubmed
2017
2017-09-20T00:00:00.000Z
10.1159/000480478
24
36