- Humanin is a polypeptide widely existing in animals and born in mitochondria. It is conserved in animals and has neuroprotective and cellular effects.
- Magic Humanin peptide
- It can protect and recover toxic damage
- Humanin mice were protected from toxicity and the phenotype of transgenic worms was replicated
Humanin is a polypeptide widely existing in animals and born in mitochondria. It is conserved in animals and has neuroprotective and cellular effects.
Recently, scientists have confirmed that human peptide can prolong life span and reduce the risk of age-related diseases such as Alzheimer’s disease, which is crucial for regulating the health and longevity of animals and humans. In many species, the level of Humanin peptide decreases with age.
Pinchas Cohen of the University of Southern California, USA, published a research paper entitled “the mitochondrial derived peptide human is a regulator of lifespan and healthspan” in aging, and revealed the magic of this mitochondrial polypeptide.
After discovering that the human peptide could prolong the life span of worms, the researchers examined whether the human hormone treatment started in middle age could prolong the life span of mice. Administration of HNG to these female mice did not prolong their lifespan, but improved metabolic parameters without changing food intake.
The team found that overexpression of Humanin in Caenorhabditis elegans could effectively prolong life span, depending on the DAF-16 / FOXO signaling pathway.
Humanin transgenic mice have many phenotypes that overlap with helminth phenotypes, and similar to exogenous Humanin treatment, their protective effect on toxic injury is enhanced.
Twice a week, the researchers treated middle-aged mice with a potent human peptide analogue, HNG, which improves metabolic health range parameters and reduces inflammatory markers.
In many species, human protein levels generally decrease with age. But the study shows that the aging model of naked mole rats can be ignored, and the levels of human in them are surprisingly stable. Naked mole rats have always been a long-lived species for aging research, with a life span of 30 years – 10 times longer than other rodents.
In addition, similar results were observed in the offspring of centenarians. They were more likely to become centenarians, and their circulating serum levels of Humanin polypeptide were much higher than those of age-matched control subjects. Later, the researchers also observed lower levels of human peptide in patients with human diseases such as Alzheimer’s disease and MELAS (mitochondrial encephalopathy, lactic acidosis and stroke like episodes).
All in all, these studies are the first to demonstrate that Humanin peptides are involved in improving health and prolonging life expectancy.
Magic Humanin peptide
Mitochondria are at the center of the aging theory because they are the main producers of energy and free radicals. They regulate apoptosis, and their dysfunction is the key to the physiological decline observed during aging. Similarly, mitochondrial dysfunction has been found in many age-related diseases, although this is a causal or simple correlation.
In addition, in addition to their roles in energy utilization and cell survival, mitochondrial gene changes can also increase the lifespan of several model organisms, and the lifespan of mitochondria is also related to lifespan.
Interestingly, although most of the proteins found in mitochondria are encoded by nuclear genomes, mitochondria have their own unique translation mechanisms and genomes, which were previously thought to encode only 13 proteins.
In the past decade, the number of identified mitochondrial derived peptides (MDP) and micropeptides has increased exponentially. Human peptide is the first member of this new mitochondrial derived signal peptide, which now includes mots-c and shlp1-6.
Humanin peptides were first found in screening for proteins that protect against Alzheimer’s disease (AD). Since its initial discovery, the role of Humanin polypeptides in the prevention of many other age-related diseases, such as atherosclerosis and stroke, has expanded and now has many beneficial effects.
In different aging mouse models, the circulating level of Humanin polypeptide is related to life span, and injection of human protein analogue hn-s14g every two weeks can delay the cognitive decline of mice. Another type of MDP, mots-c, has been shown to be associated with longevity in centenarians.
It can protect and recover toxic damage
Humanin peptides can resist many toxic injuries. For example, the researchers found that Humanin peptide treatment prevented lethal doses of heat shock in yeast (supplementary Figure 1). To test whether the Humanin polypeptide is enough to prolong its life span, they used the ubiquitous promoter (ife-1) and mosci Technology (knudra, Murray, UT) to generate transgenic worms that overexpress the human peptide.
After backcrossing the worms with wild-type / N2 worms for six times, they examined their lifespan and found that trans human peptides were sufficient to prolong the life span of the worms (Fig. 1a).
Using epistatic analysis, we found that the increase of lifespan depends on DAF-16 / FOXO gene, because overexpression of Humanin peptide does not increase the life span of DAF-16 (mu86) deficient strains (Fig. 1b). The interaction between Humanin peptide and insulin / IGF signaling pathway has been shown in mice previously, which indicates that this is the conservative mechanism of Humanin peptide. Phenotypic analysis of these transgenic worms also revealed a decrease in body size, body fat and reproductive capacity (Fig. 1c-1e).
Overexpression of Humanin is enough to prolong the life span of Caenorhabditis elegans. Compared with wild-type / N2 (average life span 17.7 days), HN overexpression significantly increased the life span of worms (average life span 19.0 days) (a). The increase of life span depends on DAF-16, because the longevity of DAF-16 (mu86) mutant did not increase after hybridization with Humanin TG strain (average life span was 15.5 days and 16.1 days, respectively) (P B).
Figure 1. Overexpression of human is sufficient to prolong the life span of C. elegans.
Humanin mice were protected from toxicity and the phenotype of transgenic worms was replicated
After the creation of the transgenic worm, the researchers developed transgenic mouse models using constructs containing CMV promoter driven human ORF to test the effects of long-term exposure to human peptides. Transgenic mice carrying human protein can survive and feed. In previous findings, circulating human protein levels in these mice increased by 16%.
To examine whether human hormonal therapy can increase the life span and healthy life span of mammalian models, the researchers obtained 18 month old female C57BL / 6N mice from nia and administered HNG (4mg / kg, IP) every two weeks, an effective human hormone analogue. Compared with the injection control, the body weight was significantly reduced until old age (Fig. 3a).
However, there was no significant difference in food intake between HNG treated mice and control mice during the same period (Fig. 3b), indicating that there may be metabolic effects in the treatment of diseases.
At 28 months of age, there was no significant difference in body weight, visceral fat was also decreased in HNG treated mice (Fig. 3C), and subcutaneous fat was not changed (Fig. 3e) (n = 5 / group). After 14 months of treatment, there was no significant difference in life span among the groups (Fig. 3f). However, parameters related to health span were improved in the HNG group, such as a significant decrease in IGF-I and a downward trend in leptin (Fig. 3G, 3H).
Figure 3. Middle aged Humanin treatment improved metabolic health in mice.
The level of Humanin was negatively correlated with disease and positively correlated with life expectancy
In many diseases, the copy number of mitochondrial DNA decreased, and the researchers found a correlation between the mtDNA copy number of peripheral blood mononuclear cells and the level of Humanin in neonatal cord blood samples (Figure 4a).
In addition, in cell lines with 3243 MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke like attack syndrome) mutations, the level of Humanin polypeptide was negatively correlated with the percentage of mitochondrial mutations (Fig. 4b), suggesting that human protein may be a marker of mitochondrial dysfunction with aging. Compared with the control group (n = 4), the level of Humanin polypeptide in CSF of patients with AD (n = 3) was significantly lower (Fig. 4C).
Figure 4. Human protein levels are associated with human mitochondrial health.
Figure 5. The level of human body hormone is related to life span.
Editor / prospective economist app information group
reference material: https://www.sciencedaily.com/releases/2020/06/200624151613.htm
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