ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY. The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law.
BPC-157 is a partial form of the protein known as body protection compound (BPC). BPC is a natural component within the body and has been found, in experiments on animals, to promote healing. BPC is not just active in intestinal repair and healing, but appears to produce similar effects in a number of tissues. Scientific studies based on animal test subjects has shown that its healing actions are at least partially linked to growth hormone (GH).
Dementia is a chronic and progressive brain disorder that affects a person’s cognitive abilities, including memory, thinking, behavior, and communication. It is a broad term used to describe a range of symptoms caused by a variety of underlying diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and others. Furthermore, Alzheimer’s disease is a type of dementia that is characterized by a gradual and irreversible decline in cognitive abilities, including memory, language, perception, and reasoning. It is the most common cause of dementia, accounting for 60-70% of all cases.According to the World Health Organization (WHO), there are an estimated 50 million people worldwide living with dementia, and this number is expected to triple by 2050. Dementia is more common in older adults, but it can also affect younger people, especially those with genetic predispositions or other risk factors. Alzheimer’s disease is responsible for 60-80% of these cases. In the United States alone, over 6 million people are living with Alzheimer’s disease, and this number is expected to rise to nearly 14 million by 2050.
The mechanism of action of thymosin-beta 4 is multifaceted and complex. This peptide is involved in many essential biological processes, including tissue repair, wound healing, and angiogenesis. In the context of neurocognitive disorders, thymosin-beta 4 has been shown to have several potential mechanisms of action that may help improve brain function and alleviate symptoms of diseases such as dementia and Alzheimer’s.
One of the primary ways in which thymosin-beta 4 may help with neurocognitive issues is by promoting the growth and regeneration of neurons in the brain. Studies have shown that thymosin-beta 4 can stimulate the formation of new neurons and support the survival of existing neurons, which can lead to improved cognitive function.
Thymosin-beta 4 has also been found to have anti-inflammatory and antioxidant properties, which may be beneficial in the context of neurocognitive disorders. Inflammation and oxidative stress are known to contribute to the development and progression of these diseases, and thymosin-beta 4 may help reduce their impact on the brain. Additionally, thymosin-beta 4 has been shown to improve the function of microglia, immune cells in the brain that play a critical role in maintaining brain health. Microglia help clear out damaged cells and debris, but they can also contribute to inflammation and damage in certain contexts. Thymosin-beta 4 appears to help regulate microglia function and reduce their harmful effects, which may be beneficial in the context of neurocognitive disorders.
The potential mechanisms of action of thymosin-beta 4 in the context of neurocognitive disorders are diverse and complex, but the evidence suggests that this peptide has the potential to improve brain function and alleviate symptoms of diseases such as dementia and Alzheimer’s. Please see the very exciting research examples below as to how this peptide could benefit those with the diseases.
NAD+ is the second most abundant cofactor in the human body. Anti-aging therapies are becoming more mainstream as aging is now more often being viewed as a disease. Now that this transition is happening, the ability for NAD+ to activate PARPS, Sirtuins, and help with immune dysregulation has been thoroughly investigated and NAD+ and its precursors have been highly popularized. The clinical importance of maintaining cellular NAD+ levels was established early in the last century with the finding that pellagra, a disease characterized by diarrhea, dermatitis, dementia and death, could be cured with foods containing the NAD+ precursor niacin.
Additionally, cellular concentrations of NAD+ have been shown to decrease under conditions of increased oxidative damage such as occur during aging Altered levels of NAD+ have been found to accompany several disorders associated with increased oxidative/free radical damage including diabetes, heart disease, age-related vascular dysfunction, ischemic brain injury, misfolded neuronal proteins, and Alzheimer’s dementia. Interventions targeted at restoring NAD+ has been shown in animal models to support healthy aging and improve metabolic function, and dementia.
In a review study, researchers discuss the recent data that document conserved roles for NAD+ in skeletal muscle development, regeneration, aging, and disease as well as interventions targeting skeletal muscle and affecting NAD+ that suggest promising therapeutic benefits. The researchers also highlight gaps in our knowledge and propose avenues of future investigation to better understand why and how NAD+ regulates skeletal muscle biology.
“Pentadecapeptide BPC 157 antagonizes the incidence of a series of gastrointestinal lesions, it has a positive impact on the healing processes of various wounds, a proven angiogenic effect, protective effect on endothelium and it modulates synthesis of NO.” (1)”Apart from the effects on various gastrointestinal lesions, the potentially beneficial effect on pancreas, liver injuries, endothelium and heart damage, i.e. dysrhythmias following reoxygenation, and blood pressure, along with effect on experimental acute/chronic inflammation, wound and fracture (pseudoarthrosis) healing are described. It appears that these beneficial effects all together provide a particular network reflecting activity of a special peptidergic defence system.” (4)”In support of this concept, it appears that there are interactions of this pentadecapeptide with many important systems (namely, dopamine-, NO-, prostaglandin-, somatosensory neurone-systems), that could provide a basis for the observed protective effects. Moreover, since disturbance of these systems’ functions (i.e. dopamine-, NO-, somatosensory neuronal-system) which manifest either over-activity or as inhibition, may contribute to the multiple lesions in different organs. The reported evidence that this pentadecapeptide is able to counteract both their over-action, and their inhibition, may suggest this pentadecapeptide as a new, but most probably essential physiological defence system and that should be further investigated.” (4)
Osteoporosis is the most prevalent systemic skeletal system disease, leading to increased bone fragility and vulnerability to fractures. Due to the microarchitectural destruction in bone tissue, fracture healing in osteoporoti patients is often delayed and compromised compared with non‑osteoporotic individuals. Osteoporosis usually results from meno‑ pause, aging, metabolic diseases and drug therapies with the precise cellular and molecular mechanism remaining to be elucidated.
Recent studies have shown that four peptides (BPC-157, AOD 9604, MOTS-c, Peptide 11R‐VIVIT) have been proven to have healing effects for such disease in several types of model… High concentration and long-term stimulation of TGF-β1 induced osteogenic differentiation of bone marrow mesenchymal stem cells (MSCs) in vitr2. TGF-β pathway-related genes exert anti-osteoporosis effects by regulating the function of bone deposits and osteoclasts. TGF-β also affects the bone formation by promoting the proliferation and differentiation of osteoblasts, as well as the synthesis of extracellular matrix.
“Thymosin β4, a ubiquitous 4.9‐kDa polypeptide originally isolated from bovine thymus, is a potent mediator of cell migration and differentiation. It was identified as a gene up‐ regulated four‐ to sixfold during early endothelial cell tube formation and found to promote angiogenesis. It is present in wound fluid, and when added topically or given systemically, it promotes angiogenesis and wound healing. Thymosin β4 elicits cell migration through a specific interaction with actin. In angiogenesis and in wound healing, thymosin β4 acts by accelerating the migration of endothelial cells and keratinocytes and increasing the production of extracellular matrix‐degrading enzymes.”
“Thymosin β4 promotes hair growth in normal rats and mice. A specific subset of follicular keratinocytes in the mouse skin, which originates at the bulge region, expresses thymosin β4. The temporal and spatial distribution of these keratinocytes parallel the pattern reported for the stem cells and their daughter TA cells at the different stages of the hair cycle (9, 10). We isolated clonogenic keratinocytes from the bulge compartment of the rat vibrissa follicle, further characterized them as an immediate progeny of the stem cells, and found that these cells express high levels of thymosin β4 when cultured in vitro. We show that thymosin β4 promotes hair clonogenic keratinocyte cell migration, as well as secretion of the extracellular matrix‐degrading enzyme matrix metalloproteinase 2 (MMP‐2).””Thus, thymosin β4 accelerates hair growth, in part, due to its effect on critical events in the active phase of the hair follicle cycle, including promoting the migration of stem cells and their immediate progeny to the base of the follicle, differentiation, and extracellular matrix remodeling.”
“Taken together, our results suggest that in addition to its known angiogenic and wound healing effects, thymosin β4 is a naturally occurring modulator of hair growth that acts by stimulation of stem cell migration, protease production, and differentiation.”
“While studying wound healing in rat skin, we unexpectedly observed visually and at the histological level increased hair growth at the wound margins 7 days after topical treatment with thymosin β4 (unpublished observation). In this study, we have shaved the skin of healthy rats and applied thymosin β4 topically on one side of the shaved area and the control vehicle on the opposing lateral side of the same animal. After 7 days of treatment, we observed an increased number of anagen‐phase hair follicles in the skin areas treated with thymosin β4 (Fig. 1a and d). The number of anagen follicles was approximately twofold greater than in rats treated with vehicle alone. The increased number of hairs in anagen phase was retained with continued tri‐ weekly treatment over 30 days. Within 14 days of treatment cessation, the number of active hair follicles decreased to control levels. We next tested whether thymosin β4 would promote hair growth in 8‐wk‐old C57BL6 wild‐type mice. Animals used in this experiment have all of their hair follicles in the telogen stage as judged by their pink skin color. The mice were shaved and thymosin β4 was applied topically on the shaved area as described in Methods. Control animals were treated with vehicle alone. As shown in Fig. 1c and ƒ, thymosin β4‐treated (but not control) animals displayed quick hair regrowth. Histological examination confirmed the thymosin β4‐induced activation of the hair follicles (Fig. 1b and e).”
TB-500 also known as Thymosin Beta 4 is a naturally occurring peptide. It is found in high concentrations in blood platelets, wound fluid and other tissues in the body. TB-500 is not a growth factor; rather, it is a major actin regulating peptide. TB-500 (Thymosin Beta 4) has been found to play an important role in protection, regeneration and remodeling of injured or damaged tissues. The gene for TB-500 (Thymosin Beta 4) has also been found to be one of the first to be upregulated after a wound occurs.
BPC-157 and TB-500 are both potent healing peptides with vast amounts of research investigating their properties and potential uses. Both are also synthetic derivatives of naturally occurring proteins that have been modified to enhance their already abundant features. Both peptides have been shown to improve immune function, enhance healing throughout the body, and even thwart the ravages of age in some ways. Still, BPC-157 vs TB-500 is a valid comparison as these two peptides are not the same and do not share all of the same functions. Below is a look at why someone might choose BPC-157 over TB-500 or vice versa.
Both TB-500 and BPC-157 have been shown to accelerate wound healing and tissue repair. BPC-157, a derivative of body protection compound (BPC), has a dose-dependent effect on the growth and migration of fibroblasts, the cells responsible for extracellular matrix repair[1]. TB-500, a derivative of thymosin beta-4 (Tβ-4) has a similar effect that it produces by manipulating actin filaments. Actin is a protein that plays central roles in cell reproduction and migration. Research shows that TB-500 can increase the rate of fibroblast growth and migration as well as boost health and migration of cells of the immune system.
BPC-157 is a partial sequence of body protection compound (BPC) found in human gastric juice. It is mostly used in research to accelerate healing of a variety of wounds including tendon-to-bone healing and healing of damaged ligaments. This peptide acts systematically in the digestive tract to combat leaky gut, IBS, gastrointestinal cramps, and Crohn’s disease. In addition, BPC-157 can protect and prevent ulcers, and it can be used to protect the liver from toxic damage from alcohol, antibiotics, etc. This peptide has also been promising in promoting the healing of traumatic brain injury (TBI) according to research.
JNK family participates in the apoptosis pathway, also known as programmed cell death.[4] The apoptosis mechanism is used to eliminate cells that are damaged in anyway. This mechanism is suitable for healthy people because it helps avoid developing cancer and other disorders.[1] On the other hand, apoptosis is detrimental in neurodegenerative diseases that share the abnormal accumulation of misfolded proteins, contributing to dementia, cognitive loss, memory loss, behavioral problems, and sleep problems, among others, through neuronal cell loss.[3,5,7] In addition, the JNK family also participates in pathways related to regulation, plasticity, development of the Central Nervous System (CNS), inflammation, and autophagy.[9] The well-functioning of all these processes is vital. Recent studies suggested that an imbalance of the JNK family members can accelerate the progression of both AD and PD pathologies. One of the hallmarks of AD is the aggregation of amyloid beta (Aβ) in the extracellular area.[7] The overexpression of Aβ triggers the activation of JNK-3, which also participates in the formation of Aβ42, a toxic species that affects the neuron’s cell function when it accumulates.[7] It is unclear whether the neurodegenerative disorder or the JNK imbalance comes first. However, they both have a direct relationship where PD and AD patients show high levels of JNK in the brain (postmortem), and irregular levels of the JNK family accelerate the progression of both disorders (see Fig. 2). [5,9] JNK imbalance could also lead to increased inflammation responses, low plasticity, and a flaw in autophagy performance, among other related adverse effects. An increase in apoptosis in PD and AD patients causes a decrease in neurons in the brain, affecting cognitive, behavioral, and memory performance.[8] JNK also decreases the α-syn accumulation in PD models, contributing to neuroprotection.[10] JNK pathway influence positively many vital processes of the body unless an imbalance occurs. [2,8] JNK has been the target for treating several diseases like cancer, strokes, PD, AD, Huntington’s disease, and other neurodegenerative disorders, showing promising results. More investigations need to be done to comprehend better how the correct levels of JNK can help combat important hallmarks of degenerative illnesses to eventually prevent or revert the progression of related diseases like PD and AD. In general, the benefits of inhibiting JNKs for treating neurodegenerative disorders are:
Improving autophagy for the elimination of misfolded proteins (Aβ (AD), tau protein (AD), and α-syn (PD)
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