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VIP or vasoactive intestinal peptide is a short peptide hormone containing 28 amino acids, naturally found in both central and peripheral nervous systems.Β ResearchersΒ believe this peptide’s wide distribution indicates its diverse potential as a neurotransmitter, immune regulator, vasodilator, and secretagogue.
It is believed that VIP binds three types of G protein-coupled receptors: PAC1, VPAC1, and VPAC2. Before binding with these receptors, a key regulatory enzyme might be activated, potentially causing biological activity.
The main difference between these three peptides is their location. Clinical trials indicate that VPAC1 is mainly found in brain and peripheral areas, such as immune cells, intestine, lungs, and liver, while VPAC2 is located in the central nervous system and other peripheral areas, such as reproductive and gastrointestinal tract, skeletal muscles, kidney, heart, and pancreas. Finally, PAC1 is predominant in the adrenal region and brain.
Clinical trials have indicated that VIP, which immune cells seem to produce, shows various potential immunological actions to keep the immune system stable. A couple of studies showed that VIP has anti-inflammatory potential in innate and adaptive immunity.
When it comes to innate immunity, VIP has been inhibiting responses of inflammatory Th1-type cells and might promote Th2-type cell responses. VIP peptide might decrease inflammation and boost intestinal immunity because of its potential to minimize Th1-type inflammatory cell actions.
One study has explored the potential connection between inflammation and VIP within the context of NEC or necrotizing enterocolitis, primarily using rodents. VIP, praised for its anti-inflammatory properties, may manage intestinal epithelial barrier integrity and homeostasis.
All of this may indicate thatΒ VIP peptideΒ may have a role in moderating inflammatory responses. Moreover, clinical trials suggest that VIP might preserve tight junction integrity.
The blood-spinal and blood-brain barriers are two crucial parts of the nervous system, protecting the central nervous system’s tissue cells and blood vessels. The blood-brain barrier seems to filter everything, from oxygen to nutrition factors, which might affect immunity when they enter these neurological vessels. The compromised blood-brain barrier may cause severe psychological effects.
Based on some research, VIP peptide may show some neuroprotective potential, which might maintain the blood-brain barrier. This peptide is potentially involved in several functions, such as immune modulation, vasodilation, and neurotransmission.
By activating AC or adenylate cyclase, VIP peptide may play a crucial role in cAMP or cyclic adenosine monophosphate production. This substance regulatesΒ immune response, including those regulatory T cells.
When these functions are disrupted due to autoimmune reactions against VIP or its receptors, it might potentially lead to enhanced permeability of BSB and BBB, also known as βleakiness,β which might further alleviate autoimmune responses.
Cardiac fibrosis is believed to be highly linked to angiotensinogen-converting enzymes and angiotensinogen receptors, both leading to vascular inflammation. Some clinical trials concluded that VIP peptide could promote the reduction of these angiotensinogen expressions.
As a result, VIP might help with cardiac fibrosis and reverse heart muscle scarring. These findings are based on the VIP level in the body. Lover doses are linked with higher fibrosis and are almost undetectable in the end-stage of cardiomyopathy.
To investigate this link further,Β scientists experimentedΒ with VIP, which was administered to mice on a high-salt diet. They recorded changes in myocardial VIP levels, expression of pro-fibrotic mediators, and level of fibrosis through histomorphometry.
Findings indicate that mice might have higher myocardial VIP levels than controls while having significantly lower fibrosis metrics. However, VIP infusion doesnβt impact all pro-fibrotic mediators. Therefore, a significant reduction in Agt or angiotensinogen and type 1a mRNA expressions was recorded, indicating a possible downregulation of the renin-angiotensin system, a crucial component in fibrotic processes.
Moreover, while this peptide seems to affect some pro-fibrotic mediators, it did not seem to alter others, such as NFΞΊB, CTGF, TNFΞ±, and TGFΞ², indicating that anti-fibrotic properties of this peptide may be selective or mediated via alternative processes.
Clinical trials have indicated that behavior responses in animals may activateΒ VIP neurons. Activating the VIP neurons in the hypothalamus region may also cause the secretion of prolactin hormones, which is believed to trigger behaviors such as aggression, pair bonding, gregariousness, and affiliation.
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