Peptides > VIP


Research indicates that VIP (Vasoactive Intestinal Peptide) has the capacity to reduce inflammation throughout the body, with particular efficacy in addressing conditions like neurodegenerative diseases, pulmonary fibrosis, inflammatory bowel disease, and cardiac fibrosis. This peptide demonstrates notable effectiveness in multiple fibrotic pathways, offering potential therapeutic benefits for the common fibrosis-related processes that lead to significant morbidity and mortality.

Beyond its anti-fibrotic actions, which are believed to be mediated through its anti-inflammatory properties, VIP serves as a powerful regulator of the immune system and exhibits broad anti-inflammatory effects. Additionally, VIP has been shown to protect the central nervous system against insults and is actively studied for its potential in preserving cognitive function in the context of neurodegenerative diseases.

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1. What is VIP?


2. VIP Peptide Structure


3. VIP Research

What is VIP?

Vasoactive Intestinal Peptide (VIP), also known as vasoactive intestinal polypeptide or PHM27, is a short peptide hormone naturally produced in the gut, pancreas, and brain of most vertebrate animals, including humans. VIP exerts its effects by binding to class II G protein-coupled receptors, and its functions encompass a wide range of physiological processes:

  1. Glycogen Breakdown: VIP increases the breakdown of glycogen in the liver and muscles.
  2. Blood Pressure: It lowers blood pressure.
  3. GI Tract Relaxation: VIP induces relaxation of smooth muscle throughout the gastrointestinal (GI) tract.
  4. Cardiac Muscle Stimulation: VIP stimulates cardiac muscle, increasing both heart rate and the strength of contractions.
  5. GI Tract Secretion: It promotes the secretion of water in various areas of the GI tract.
  6. Vaginal Lubrication: VIP plays a role in vaginal lubrication.
  7. Prolactin Regulation: It regulates the release of prolactin.
  8. Cartilage Protection: VIP has protective effects on cartilage.
  9. Neuroprotection: It protects neurons against ischemia and oxidative stress.
  10. Autonomic Nerve Function: VIP influences autonomic nerve function.
  11. Circadian Rhythm: VIP helps synchronize the central nervous system, particularly neurons in the suprachiasmatic nucleus, with light cues to regulate circadian rhythm.

VIP has been a subject of extensive research due to its multifaceted roles in various physiological processes. One of its most significant findings is its ability to reduce inflammation and fibrosis in different organs, which has implications for potential therapeutic applications. The wide-ranging effects of VIP make it a molecule of great interest in scientific literature and research.


VIP Peptide Structure

Molecular Formula: C147H237N43O43S
Molecular Weight:
Human Gene:
 VIP; 6q25.2
PubChem CID: 44567960
CAS Number: 37221-79-7
Synonyms: VIP, PHM27, Vasoactive intestinal polypeptide

VIP Research

Alleviating Bowel Inflammation with VIP and Analogs

VIP, primarily produced by immune nerve fibers in blood vessels of the central and peripheral nervous systems and the heart, serves as a crucial player in regulating inflammation. Moreover, cells of the immune system directly produce VIP, which aids in promoting Th2-type responses. These responses have the potential to mitigate inflammation and dampen immune system activity. Researchers have extensively explored VIP and its analogs as potential mediators to combat inflammation in various conditions, including intestinal disease, heart disease, and neuroinflammatory disorders.

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The various roles of VIP in immunomodulation:

VIP in Inflammatory Bowel Diseases

VIP demonstrates effectiveness in alleviating inflammatory bowel diseases (IBDs) such as Crohn’s and ulcerative colitis. It plays a pivotal role in enhancing intestinal barrier homeostasis while curbing inflammation instigated by Th1 cell actions. This action even leads to the generation of T cells capable of producing the anti-inflammatory peptide interleukin-10. IBDs, characterized by Th1 inflammation, benefit from the improved intestinal barrier function provided by VIP, which helps mitigate the initial steps in the development of colitis and severe inflammatory bowel diseases.

VIP’s Impact on Lung Function

VIP exerts influence on lung function through various mechanisms. Firstly, it modulates pulmonary vascular remodeling in response to inflammation by suppressing NFAT, a peptide that activates T cells and augments inflammation. This modulation plays a critical role in preventing pulmonary fibrosis, a late-stage complication of various inflammatory conditions affecting the lungs. VIP also inhibits smooth muscle cell proliferation in pulmonary tissue, which often results from prolonged inflammation, particularly in bronchial asthma. Furthermore, VIP’s vasodilatory effects show promise in pulmonary vasculature, potentially enhancing lung function. Initial research suggests that VIP reduces blood pressure in the pulmonary artery, leading to increased cardiac output and better venous oxygen saturation.

VIP’s Role in Transplants

VIP offers potential solutions to the problem of organ transplant rejection. By affecting dendritic cells (DCs), key players in immune responses, VIP reduces their proliferation and activation. Notably, VIP tends to inhibit DCs attached to tolerogenic antigens, thus selectively suppressing immune responses that might lead to autoimmune reactions. This selective inhibition could revolutionize transplant anti-rejection treatments, offering a more targeted approach with fewer side effects.

VIP as a Neuroprotectant

VIP serves a threefold role in the central nervous system (CNS): neurotransmitter, neurotrophic/neurogenic factor, and anti-inflammatory/neuroprotectant. It plays a crucial part in maintaining the integrity of the blood-brain barrier, regulating substances entering the neurological tissue. VIP’s neuroprotective effects extend to conditions such as Alzheimer’s and Parkinson’s disease, where it reduces beta amyloid accumulation and balances immune responses. Additionally, VIP helps protect the developing brain from excitotoxic white matter damage and promotes neuron fatty acid myelination. Its neuroprotective effects are mediated through VPAC1 and VPAC2 receptors, resulting in increased secretion of neurotrophic factors like ADNP and BDNF, which safeguard synapses and astrocytes.

VIP in Preventing Cardiac Fibrosis

Cardiac fibrosis, a common end-stage outcome in various heart conditions, often leads to severe cardiac dysfunction and may require transplant. While most research has focused on slowing or preventing scar formation, recent studies in rats indicate that VIP not only slows fibrosis but can also reverse it. This effect appears to be associated with a significant reduction in angiotensinogen and angiotensin receptor type 1a expression. This discovery opens new possibilities for addressing cardiac fibrosis and preserving cardiac function.

Article Author

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.


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