Tuftsin can powerfully balance and regulate the immune system. R
Tuftsin is naturally produced in the spleen. R
It was found by scientists Najjar and Nishioka in 1970 and named after Tufts University. R R
It can play an important role in:
Tuftsin shifts the immune response from an inflammatory response to an anti-inflammatory response. R
It does this by shifting T helper cells from Th1/TH17 turn into Th2/Treg (ie TNF-a -> IL-4, IL-10, TGFb1). R
Tuftsin (like ghrelin) can shift microglia into a M2 microglial anti-inflammatory response (as seen above). R R
Tuftsin signals through Nrp1 and TGFB pathways. R
Tuftsin competes with VEGF for binding to Nrp1. R R
Tuftsin regulates cyclic nucleotides and Cat+ concentration in the cell. R
Selank, a synthetic analogue of tuftsin, influences the concentration of monoamine neurotransmitters and induce metabolism of serotonin. R R R
Selank can decrease the expression of IL-6 and balance T helper cells's production of cytokines. R
Selank affects the activity of carboxypeptidase H and phenylmethylsulfonylfluoride-inhibited carboxypeptidase in rat nervous system tissue. R
Selank effects the XCL1–XCR1 axis, Il2rg gene expression and C3 gene expression. R
Selank is a nootropic, anxiolytic peptide based drug developed by the Institute of Molecular Genetics of the Russian Academy of Sciences. Selank is a somewhat mysterious peptide whose mechanism of action is not yet fully elucidated, despite the ample evidence collected so far that supports its unique clinical and preclinical efficacy. Selank is a heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro. It is a synthetic analogue of human tuftsin.
The benefits of Selank can be divided into the following categories:
Reinforcement of the body’s protective opioid system
Therapy of generalized anxiety and neurasthenia (ie. abnormal weakness)
Enhancement of learning and memory
Strengthens antiviral immune function
Protects against alcohol-induced memory impairment
Improves symptoms associated with alcohol withdrawal
Autoimmune disorders happen when the immune response is overactive and will not turn off. R
People who have their spleen removed have a higher chance of getting an autoimmune disorder. R
Tuftsin is able to shift the Th1 autoimmune response to a Th2 response, and thus turn off an autoimmune response. R
Multiple sclerosis (MS) is an autoimmune disease in which T cells, microglia and macrophages attack the myelin sheath that protects the nerve fibers in the brain and spinal cord. R
During multiple sclerosis, T cells become activated in the central nervous system (CNS) and attack the blood brain barrier (BBB). R
It generates an inflammatory cascade of cytokines and chemokines that cause demyelination of the CNS. R
Tuftsin activates microglia to promote a M2 anti-inflammatory response, allowing the regeneration of myelin. R R
Tuftsin is even more powerful in MS when combined with glutamate to generate neuronal-conditioned medium. R
Selank is commonly sold over the counter in Russia.
Selank, has shown in clinical trials to be useful against general anxiety disorder (GAD). R
Unlike benzodiazepines, it is not sedating and does not cause addiction or withdrawal. R
Although it can enhance the effects of benzodiazepines. R
It is anxiolytic like other opioids. R
On possible mechanism for selank's effect on anxiety is it's effects on the GABAergic system. R
In rats, tuftsin was able to reduce anxiety-phobic states significantly (by normalizing serotonin levels), without effecting weight. R R
In rats, selank in high doses (1000-2000 microg/kg), was able to counteract symptoms of depression. R
Selank was able to stimulate hibernating squirrels and induced a more exploratory-like behavior. R
Tuftsin can activate a M2 anti-inflammatory microglial response, increasing specific genes that help with neuroprotection. R
Selank has been shown to rapidly elevate brain derived neurotrophic factor (BDNF) in the hippocampus when taken intranasally (in rats). R
Also, selank can regulate ion homeostasis of the hippocampus (in rats). R
Tuftsin is also able to prevent damage from reactive oxygen species in the brain, helping protect against dopaminergic neuronal cell loss. This can possibly help Parkinson's disease. R
Tuftsin works on MAO-A, MAO-B, and acetylcholinesterase and activates dopamine metabolism. R
Activated microglia/macrophages are important contributors to brain injury after hemorrhagic strokes. R
If used soon after the onset of hemorrhage, tuftsin may improve injury volume, edema, and degenerating neurons, while improving the neurological functional outcome. R
In animals, tuftsin is able to protect against epileptic damage caused by high doses of penicillin. R
Tuftsin deficiency, either hereditary or following splenectomy, can result in an increased susceptibility to certain infections (H. influenza, pneumococci, meningococci and salmonella). R
Tuftsin initiates the production by phagocytes of superoxide and nitroxide radicals, which are necessary for killing phagocytized bacteria. R
Tuftsin can thoroughly destroy several microbes and viruses (not exclusive list):
Tuftsin stimulates macrophages from the liver spleen and lymph nodes and can mobilize other while blood cells to fight against cancer. R
In vitro, tuftsin can inhibit the growth of tumor cells. R
Tuftsin had anti-tumor properties in both mice and beagles, without causing toxicity to the animals. R R
In animal models, tuftsin has been shown to help:
Tuftsin-based, enediyne-energized, and EGFR-targeting fusion proteins exert highly antitumor efficacy with CD47 modulation (esp in EGFR- and CD47-overexpressing cancers). R
Sepsis is still the leading cause of death among critically ill patients in intensive care units. R
Survivors usually suffer from an impaired quality of life. R
There is a significant loss of immunocytes, including B/T lymphocytes, dendritic cells (DCs), gastrointestinal epithelial cells, even thymocytes from the beginning of sepsis as shown both in animal models and septic patients. R
In mice, a tuftsin-derived T-peptide was able to prevent immunosuppression and improve the survival rate. R
Tuftsin combined with phosphorylcholine (called TPC) was able to hamper lupus development in mice (by enhancing TGFB and IL-10, while inhibiting IFN-gamma and IL-17). R
TPC was also able to reduce proinflammatory cytokines and increased anti-inflammatory cytokine expression in early rheumatoid arthritis onset. R
Inflammatory bowel disease (IBD) is comprised of two major phenotypes, Crohn's disease (CD) and ulcerative colitis (UC). R
In mice, TPC was able to significantly prevent colitis symptoms (TNFa, IL-17 and IL-1b was supressed while IL-10 expression was increased). R
A vaccine conjugating tuftsin to infectious hepatitis vaccines (HE-ORF2 and HA-VP1), made it more effective. R
Also, conjugating tuftsin to four copies of M2e of influenza A enhanced the antigen-specific immune response. R
Linking tuftsin to envelope glycoproteins 41 (gp41) and 120 (gp120) of HIV enhanced the antigen-specific immune responses. R
Enhanced responses to the combined protein vaccine have been shown to be more effective intranasally, rather than intramuscular. R
Oligotuftsin derivatives can be considered as promising carriers for synthetic vaccines. R