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Studies suggest that Chonluten is a peptide that may regulate gene expression. It is sometimes referred to as tripeptide T-34. Research has suggested that it may be predominantly active in the tissues of the lungs, with secondary action in the gastrointestinal tract (GI tract). Chonluten has been hypothesized to influence the gene expression that codes for anti-inflammatory and antioxidant ways, particularly in the lungs and the gastrointestinal tract, as well as in inflammation-induced proliferation.

Research suggests that Chonluten peptide is a geroprotective substance that may slow the process of age-related physiological decline. In addition, it may act as an anti-inflammatory agent in the lungs and modify the function of the mucosa in research models of chronic obstructive pulmonary disease (COPD).

Chonluten Peptide and Biological Regulation

Studies conducted on animals have proposed that the presence of a few different short di-, tri-, and tetrapeptides may enhance life span by around 40%. Scientists speculate these peptides may possibly do this by suppressing the formation of tumors spontaneously. It has been hypothesized that these tripeptides may impact gene expression and cellular processes such as apoptosis. This theory is supported by the fact that age-related biomarkers decrease at a certain pace throughout time.

The potential of short peptides to affect all elements of gene expression and epigenetic DNA methylation has been speculated in research investigations. As suggested by these studies, a single short peptide may modify hundreds of genes by edging the cytoplasmic (cell) and nuclear membranes and attaching to DNA at the promoter, suppressor, and other DNA control turfs using a simple docking mechanism. This can be accomplished by edging the nuclear membrane.

Chonluten Peptide and Gene Expression in the Lungs

Chonluten peptide has been proposed to stabilize the mucosa in the bronchi by modifying the expression of DNA. The mucosa of the bronchi serves as a barrier between the interior chambers of the circulatory system and other systems, as well as between the bronchi and the outside world. Alterations and damage to the mucosa, as well as the cardiovascular chambers, may be caused by a combination of inflammatory disorders, such as asthma or chronic obstructive pulmonary disease (COPD). These illnesses can also lead to alterations in mucus production and the structure of the extracellular matrix. 

The action mechanism of Chonluten has been hypothesized to be mediated by genes such as c-Fos, the gene for the health shock protein HSP70, SOD, COX-2, and TNF-alpha, as well as genes involved in the antioxidant system. There is a lot of interest in the anti-inflammatory potential that gene regulation may have, such as c-Fos. The c-Fos protein is a proto-oncogene that is activated in some neurons when they get depolarized. Because it is detectable using immunohistochemical methods, the production of this protein may serve as a marker for neuronal activity throughout the neuraxis in response to stimulus from the periphery. A powerful regulator of cell proliferation, survival, and differentiation, the c-Fos protein is activated in response to hypoxia and cellular injury. This activation causes the c-Fos protein to take on its regulatory role. The broad production of the protein may lead to the thickening of the bronchial mucosa and even the development of cancer, even though the local effect of the protein might promote angiogenesis and cell proliferation in the aftermath of damage. As a direct consequence, one of the pathophysiological changes that occur in COPD and asthma is a loss of control over the activity and expression of c-Fos.

Chonluten Peptide and the Gastrointestinal Tract

The potential of Chonluten (T-34) in the digestive system (also known as the GI tract) is speculated to be quite similar to that in the lungs. Because of the frequency of inflammatory disorders, including ulcerative colitis and Crohn's disease, research suggests that the peptide may decrease inflammation and vascular alterations in the GI tract. "The emergence of a gastric ulcer is linked with morphological and molecular alterations resulting from modulation of the production of antioxidant and anti-inflammatory proteins," write Khavinson and colleagues. By modulating the expression of the genes that code for these proteins, peptide T-34 is speculated to bring the production of these proteins back to a normal level. Despite this, research on Chonluten is still being conducted.

Please note that neither humans nor animals are meant to consume the substances discussed in this article. The only purpose research compounds are designed to serve is in the context of in-vitro or laboratory experimentation. The law expressly forbids any introduction of a bodily kind. Only licensed researchers and competent professionals are allowed to make purchases now. The only intention of the material provided in this article is to further the reader's education.


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[ii] Anisimov, V. N. “Evolution of concepts in gerontology and physiological mechanisms of aging.” Molekulyarnye i fiziologicheskie mekhanizmy stareniya (Molecular and Physiological Mechanisms of Aging) Nauka, St Petersburg vol 1, parts 1–3, 49–95, 269–378. 2008.

[iii] Khavinson VK, Lin’kova NS, Tarnovskaya SI. Short Peptides Regulate Gene Expression. Bull Exp Biol Med. 2016 Dec;162(2):288-292. doi: 10.1007/s10517-016-3596-7. Epub 2016 Dec 1. PMID: 27909961.

[iv] Khavinson VKh, Lin’kova NS, Dudkov AV, Polyakova VO, Kvetnoi IM. Peptidergic regulation of expression of genes encoding antioxidant and anti-inflammatory proteins. Bull Exp Biol Med. 2012 Mar;152(5):615-8. English, Russian. doi: 10.1007/s10517-012-1590-2. PMID: 22803148.

[v] Khavinson, V., Linkova, N., Dyatlova, A., Kuznik, B., & Umnov, R. (2020). Peptides: Prospects for Use in the Treatment of COVID-19. Molecules (Basel, Switzerland), 25(19), 4389. 

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