Sermorelin Tablet is an oral preparation with Sermorelin as its core ingredient. Sermorelin is an artificially synthesized 29 peptide with a chemical structure identical to the amino terminal 1-29 fragment of endogenous growth hormone releasing hormone (GHRH). Its molecular weight is 3357.88 and its chemical formula is C ₁₄₉ H ₂₄₆ N ₄₄ O ₄₂ S. As an analog of GHRH, Sermorelin stimulates the release of growth hormone (GH) from the anterior pituitary gland by mimicking the mechanism of natural hormones, thereby regulating growth, metabolism, and immune function. It activates the adenylate cyclase (AC) - cyclic adenosine monophosphate (cAMP) - protein kinase A (PKA) signaling pathway by binding to GHRH receptors on the surface of anterior pituitary cells, promoting GH gene transcription and GH granule release. This process is negatively regulated by somatostatin, forming a physiological circadian secretion pattern. Simultaneously, it indirectly regulates immune function through the GH-IGF-1 axis and may directly act on GHRH receptors on the surface of immune cells (such as macrophages and T lymphocytes) to enhance immune response. In addition, animal experiments have shown that Sermorelin can promote the survival of hippocampal neurons, improve cognitive function, and has potential therapeutic value for neurodegenerative diseases such as Alzheimer's disease.
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Sermorelin COA
Sermorelin Tablet on the Intestinal Nervous System and Vaginal Reflex
Sermorelin Tablet is an artificially synthesized growth hormone releasing hormone (GHRH) analogue, whose chemical structure is identical to the 1-29 fragments of endogenous human GHRH. As a core tool for diagnosing growth hormone deficiency, it exerts physiological effects by stimulating the pituitary gland to release growth hormone (GH). In recent years, studies have found that Sermorelin not only participates in neuroendocrine regulation, but also significantly affects the enteric nervous system (ENS) and vagus nerve reflex through a complex neural immune endocrine network.
The regulatory effect of Sermorelin Tablet on the intestinal nervous system
Structure and function of intestinal nervous system
The enteric nervous system (ENS) is known as the 'second brain', consisting of approximately 100 million neurons that form independent neural networks. ENS coordinates gastrointestinal function through the enteric myenteric plexus (which controls gastrointestinal movement) and submucosal plexus (which regulates secretion and absorption), and its activity is regulated by both the central nervous system (CNS) and local neurotransmitters such as serotonin and acetylcholine.
The Direct and Indirect Effects of Sermorelin on ENS
GH and IGF-1 can directly act on ENS neurons through the blood-brain barrier. Research has shown that GH can promote neuronal survival, synaptic formation, and neurotransmitter release, while IGF-1 inhibits neuronal apoptosis by activating the PI3K/Akt pathway. In animal models, GH deficiency leads to a decrease in the density of enteric plexus neurons and gastrointestinal motility disorders; After supplementing Sermorelin, the number of neurons recovered and the frequency of gastrointestinal peristalsis increased, indicating that the GH-IGF-1 axis has a direct protective effect on ENS.
Indirect effects: immune regulation and neuroinflammation control
Sermorelin regulates immune cell function through GH dependent pathways, indirectly affecting ENS. For example:
Macrophage activation: GH can enhance macrophage phagocytic function, reduce intestinal pathogen colonization, and lower local inflammatory response.
T cell differentiation: GH promotes CD4+T cell differentiation into Th1 type, enhances cellular immune response, and inhibits excessive activation of Th17 cells, reducing intestinal inflammatory damage.
Cytokine balance: GH downregulates the levels of pro-inflammatory factors such as TNF - α and IL-6, upregulates the expression of anti-inflammatory factors such as IL-10, and maintains intestinal immune homeostasis.
In the inflammatory bowel disease (IBD) model, Sermorelin can significantly reduce the area of intestinal mucosal ulcers, decrease myeloperoxidase (MPO) activity, and improve intestinal barrier function. Its mechanism is closely related to GH mediated immune regulation.
The regulatory effect of Sermorelin Tablet on vagus nerve reflex
Anatomical and physiological basis of vagus nerve reflex
The vagus nerve is the main branch of the parasympathetic nervous system, and its afferent fibers (80%) transmit peripheral inflammatory signals (such as IL-1 β, TNF - α) to the solitary tract nucleus (NTS), activate the hypothalamic pituitary adrenal axis (HPA axis), and release cortisol to suppress inflammation; The efferent fibers (20%) release acetylcholine (ACh) through the cholinergic anti-inflammatory pathway (CAP), which acts on the macrophage α 7 nicotinic acetylcholine receptor (α 7nAChR) and inhibits the release of pro-inflammatory factors such as TNF - α. In addition, the vagus nerve also regulates lymphocyte function through the splenic sympathetic nervous pathway, forming a multi-level anti-inflammatory network.
Sermorelin's bidirectional regulation of vagus reflex
Enhance vagus nerve conduction of incoming signals
Sermorelin Tablet upregulates neurotransmitter release from vagus nerve afferent fibers through GH dependent pathways. For example:
5-hydroxytryptamine (5-HT) synthesis: GH can promote the secretion of 5-HT by intestinal chromaffin cells, which acts as a vagus nerve signaling molecule to enhance NTS' perception of inflammatory signals.
Neuropeptide Y (NPY) expression: GH upregulates the expression of NPY in the vagus nerve ganglia. NPY indirectly enhances vagus nerve tension by inhibiting sympathetic nerve activity, forming a "sympathetic parasympathetic balance".
In animal experiments, the anti-inflammatory effect of the HPA axis was significantly reduced in mice treated with Sermorelin after vagotomy, suggesting that Sermorelin may optimize central anti-inflammatory response by enhancing vagus nerve afferent signals.
Activate cholinergic anti-inflammatory pathway (CAP)
Sermorelin indirectly enhances CAP activity through GH mediated immune regulation. For example:
Macrophage α 7nAChR expression: GH can upregulate the density of α 7nAChR on the surface of macrophages, enhancing the anti-inflammatory effect of ACh. In sepsis models, Sermorelin pretreatment significantly reduced serum TNF - α levels, and its effect was comparable to vagus nerve stimulation (VNS).
T cell acetylcholinesterase (AChE) activity: GH inhibits T cell AChE expression, reduces ACh degradation, and prolongs CAP action time. In the autoimmune encephalomyelitis model, Sermorelin combined with VNS can synergistically inhibit T cell infiltration and alleviate central nervous system inflammation.
Regulating the sympathetic nervous pathway of the spleen
Although there is controversy over the direct neural connection between the vagus nerve and the spleen, GH can indirectly affect spleen function through the following pathways:
Norepinephrine (NE) release: GH promotes the release of NE from splenic sympathetic nerve endings, acting on lymphocyte β 2 adrenergic receptors, inducing lymphocyte secretion of ACh, and forming a "sympathetic cholinergic" cascade reaction.
Lymphocyte migration: GH upregulates the expression of splenic chemokine receptors (such as CCR7), promotes lymphocyte migration to inflammatory sites, and enhances local immune surveillance function.
Clinical application and potential therapeutic value
Functional Gastrointestinal Diseases (FGIDs)
FGIDs (such as irritable bowel syndrome and functional dyspepsia) are closely related to ENS dysfunction and decreased vagal tone. Sermorelin improves symptoms through the following mechanisms:
Regulating gastrointestinal motility: GH can enhance the activity of enteric plexus neurons, promote gastrointestinal motility coordination, and alleviate symptoms such as bloating and constipation.
Reduce visceral hypersensitivity: GH suppresses excitability of spinal dorsal horn neurons, increases pain threshold, and reduces abdominal pain.
Improving emotional disorders: Patients with FGIDs often suffer from anxiety and depression. Sermorelin regulates brain gut axis function and alleviates psychological symptoms through GH mediated 5-HT synthesis.
Inflammatory bowel disease (IBD)
The onset of IBD (such as Crohn's disease and ulcerative colitis) is associated with immune imbalance and intestinal barrier dysfunction. Sermorelin exerts therapeutic effects through the following pathways:
Inhibition of inflammatory response: GH downregulates the levels of pro-inflammatory factors such as TNF - α and IL-17, upregulates the expression of anti-inflammatory factors such as IL-10, and alleviates intestinal mucosal damage.
Promoting intestinal mucosal repair: GH activates the IGF-1/Akt pathway, enhances intestinal epithelial cell proliferation and migration, and accelerates ulcer healing.
Regulating gut microbiota: GH can increase the abundance of probiotics (such as Bifidobacterium and Lactobacillus), inhibit pathogen colonization, and maintain microbiota balance.
Postoperative intestinal paralysis (POI)
POI is a common complication after abdominal surgery, associated with vagal nerve suppression and overactivation of inflammatory response. Sermorelin shortens POI duration through the following mechanism:
Enhance vagus nerve tension: GH upregulates 5-HT synthesis in vagus nerve afferent fibers, activates CAP, and inhibits the release of inflammatory factors.
Promote the recovery of gastrointestinal motility: GH directly acts on the enteric muscle plexus, enhances gastrointestinal peristalsis, and accelerates defecation.
Reducing complications: Sermorelin can lower the risk of POI related infections, shorten hospitalization time, and lower medical costs.
Security and Future Research Directions
Security Assessment
At present, clinical studies have shown that the adverse reactions of Sermorelin Tablet are mainly mild headache, injection site pain, and transient blood glucose fluctuations, with no reports of serious adverse events. Long term use requires monitoring the risk of acromegaly caused by excessive GH secretion, but low-dose periodic administration can effectively avoid this problem.
Future research directions
Mechanism deepening: Using single-cell sequencing technology to analyze the specific effects of Sermorelin on ENS neuronal subpopulations and clarify its molecular targets for regulating vagus reflex.
Combination therapy: Explore the synergistic effects of Sermorelin with VNS, probiotics, or immunomodulators to optimize treatment plans for FGIDs and IBD.
Individualized medication: Based on genetic polymorphism (such as GHRHr genotype), precise dosage is formulated to improve efficacy and reduce adverse reactions.
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