Studies of Chonluten in Protein Synthesis and Inflammation Reduction

Chonluten, also known as tripeptide T-34, is a gene expression peptide. According to research, it is most active in the lung tissues, with secondary activity in the gastrointestinal tract (GI tract)^[1]. Chonluten regulates gene expression that encodes antioxidant and anti-inflammatory pathways, specifically in the lungs and GI tract, and in inflammation-induced proliferation.

Chonluten peptide is a geroprotective agent that can slow and prevent aging. It is also an anti-inflammatory agent in the lungs, modulating mucosal function in chronic obstructive pulmonary disease (COPD).

Tripeptides in Bioregulatory Processes

Several small di-, tri-, and tetrapeptides have been shown in animal studies to increase life span by about 40%^[2]. These peptides accomplish this by inhibiting the spontaneous development of tumors. When combined with the rate at which age-related biomarkers decline, scientists believe these tripeptides may control gene expression and cellular processes such as apoptosis.

Clinical studies have shown short peptides to control all aspects of gene expression and epigenetic DNA methylation^[3]. These findings indicate that a single short peptide can modulate dozens of genes by edging the cytoplasmic (cell) and nuclear membranes to bind to DNA at the promoter, suppressor, and other DNA control turfs using a simple docking method. 

How Chonluten Peptide Regulates Gene Expression in the Lungs

Chonluten peptide modifies DNA expression to stabilize mucosa in the bronchi. The mucosa of the bronchi acts as a barrier between the outside world, the cardiovascular system’s inner chambers, and the rest of the body. Different inflammatory conditions, such as asthma or chronic obstructive pulmonary disease (COPD), can alter and damage the mucosa and cardiovascular chambers, resulting in changes in mucus secretion and extracellular matrix structure. Smoker’s cough is an example of an inflammatory condition that can cause chronic mucosal lining irritation and subsequent chronic cough, phlegm secretion, lung cancer, and other symptoms.

Chonluten’s mechanism of action is mediated by genes such as c-Fos, the health shock protein gene HSP70, SOD, COX-2, TNF-alpha, and antioxidant system genes. These anti-inflammatory effects of gene regulation, such as c-Fos, are of interest. The c-Fos protein is a proto-oncogene activated by depolarization in some neurons. Because it can be identified using immunohistochemical techniques, its expression can be a marker for neuronal activity throughout the neuraxis due to peripheral stimulation. The c-Fos protein, activated in response to hypoxia and cellular damage, is a potent regulator of cell proliferation, survival, and differentiation. Given that the protein’s local impact can benefit angiogenesis and cell proliferation following injury, widespread protein expression can cause bronchial mucosa thickening and even cancer development. As a result, one of the pathophysiological changes in COPD and asthma is the ability to control c-Fos activities and expression. 

The Functions of Chonluten Peptide in the Gastrointestinal Tract

Chonluten’s effects on the gastrointestinal tract (GI tract) are nearly identical to those in the lungs. According to research, the peptide can reduce inflammation and vascular changes in the GI tract due to the prevalence of inflammatory diseases such as ulcerative colitis and Crohn’s disease^[4]. According to Khavinson et al. “The development of gastric ulcer is associated with morphological and molecular changes resulting from modulation of the synthesis of antioxidant and anti-inflammatory proteins. Peptide T-34 normalizes the synthesis of these proteins by regulating the expression of the corresponding genes.” Despite this, chonluten research is ongoing. 

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References

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2. 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.
3. 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.
4. 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.
5. 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. https://doi.org/10.3390/molecules25194389