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Can viral replication be reduced with MOTS-c and FOXO4-DRI by killing zombie (senescent) cells?

By Nemo 2 months ago

Senescent cells increase replication of a DNA virus in vitro.

“A significant increase in viral replication efficiency was detected by replicative senescence during IFV and VZV infection. ... As one of possible mechanisms for the increase in viral replication in senescent cells, a reduction in interferon (IFN) response after viral infection may account for it.” (2)

The concentration of this DNA virus in senescent cells is 300% more infected than non-senescent cells.

300% increase of viral infection in senescent cells

"Similarly, Andrew et al. showed that by increasing SASP phenotype, MOTS-c could make senescent cells more easily detected and then cleaned by the immune system, thus protecting normal cells."

How does Thymosin Alpha 1 improve anti-viral immune responses?

By Nemo 2 months ago

Antigen, Antibody, and Lymphocytic White Blood Cell Recruitment.

“Importantly, Ta1 acts without overstimulation of cytokine production and is generally well tolerated; it has an excellent safety profile and does not appear to induce the side effects and toxicities commonly associated with agents in this class such as interferon alpha and interleukin-2.” (1)

“Clinical trials using Ta1 in the treatment of patients with immunodeficiency or cancer indicate that this agent is nontoxic, enhances immune responsiveness and augments specific lymphocyte functions, including lymphoproliferative responses to mitogens, maturation of T-cells, antibody production, and T-cell-mediated cytotoxicity” (5)

• Increased Natural Killer (NK) activity

• A shift of T helper (Th or CD4) cells to the Th1 cell subset

• Increased expression of Th1 type cytokines such as Interleukin (IL) 2, and Interferon (IFN)-alpha

• Increased levels of Cytotoxic T (Tc1 or CD8) cells

Thymalin boosts immune system while mitigating fever and excess cell death induced by cytokine storms.

By Nemo 3 months ago

Immune Paralysis Following "cytokine storm" may be reversed by Thymalin.

"Uncontrolled development of the initial [cytokine storm] stage inevitably leads to immune imbalance, which increases the probability of secondary infections, such as pneumonia, and activation of latent herpes virus (including cytomegalovirus) infections." (2)

"Over the last decade, preclinical and clinical studies have definitively shown that sepsis leads not only to hyperinflammation, but also impaired immunity, including dysfunction of the adaptive immune system. Certain investigators and clinical practitioners believe that the main cause of the failure of sepsis therapy involves the development of severe immunodeficiency..." (2)

“Administration of Thymalin to old mice led to an increase of the titer of FTS in the blood, the restoration of disturbed circannual rhythm, the number of CD4+ cells in the bone marrow, and the concentration of corticosterone in the blood.” (4) “Both natural and synthetic pharmaceuticals activated T-cell differentiation, T-cell recognition of peptide-MHC complexes, induced the changes in intracellular composition of cyclic nucleotides and cytokine [interleukin (IL-2), interferon (IFN)] excretion of blood lymphocytes.” (3)

"Adequate zinc is essential for T-cell division, maturation, and differentiation. Zinc itself is a cofactor for thymulin, a best known zinc-dependent thymic hormone crucial for T-cell formation and maturation which exists in two forms, a zinc-bound active one, and a zinc-free inactive form. What’s more, zinc may also prevent the programmed death (apoptosis) of precursor T-cell populations and mature CD4+T cells through various enzymatic mechanisms and through chronic production of glucocorticoids. Thymulin and thymopentin restore antibody avidity in aged or thymectomized animals, enhance antibody production in aging mice... Additionally, thymulin reduces induced hyperalgesia in rats and mice.” (7)


Thymulin: An Emerging Anti-Inflammatory Molecule

MOTS-c Vascular Calcification and Insulin Resensitization

By Nemo 3 months ago

AMPK Activation Targets Vascular Calcification and Metabolic Homeostasis

"Recently, MOTS-c, a novel bioactive mitochondrial-derived peptide, has been demonstrated to activate the AMPK pathway to promote metabolic homeostasis... Our findings provide evidence that MOTS-c may act as an inhibitor of VC [Vascular Calcification] by activating the AMPK signaling pathway and suppressing the expression of the AT-1 and ET-B receptors." (1)

"Angiotensin II type 1 (AT-1) and endothelin B (ET-B) have been found to be involved in the AMPK pathway by binding to the AT-1 and ET-B receptors, respectively. A decreased level of the AT-1 receptor plays roles in reducing oxidative stress and preventing the development of myocardial contractile dysfunction, while a high level of the AT-1 receptor induces myocardial fibrosis and cardiac dysfunction. AT-1 can induce the relocation and suppression of the AMPK pathway via the AT-1 receptor in the development of diabetic proteinuria. After treatment with metformin, AMPK signaling is activated and AT-1 levels are decreased in the kidney. In epithelial ovarian carcinoma, ET-1 plays a role in epithelial-mesenchymal transition. A decrease in ET-1 receptor activation is beneficial in attenuating biventricular remodeling, and the overexpression of ET-1 causes sustained blood pressure elevation and vascular and renal injury. The activation of the AMPK pathway can also upregulate the ET-B receptor to inhibit autophagy in vascular smooth muscle cells under high glucose conditions." (1)

"Previous reports have shown that MOTS-c can amplify glucose uptake, inhibit the folate cycle and de novo purine biosynthesis following metabolic stress, and regulate nuclear gene expression in an AMPK-dependent manner. MOTS-c treatment dramatically reduced the number of disordered elastic fibers and significantly improved vascular wall structure (Fig. 2c). Moreover, MOTS-c also significantly reduced VDN [Vitamin D3 plus Nicotine] induced calcium phosphate salt deposition in the calcified aortas, as detected by alizarin red S staining and von Kossa staining... Our results showed that MOTS-c reverses VDN-induced AMPK downregulation. In mice with hypoxia-induced pulmonary hypertension, the activation of the AMPK pathway can effectively improve right ventricular systolic pressure and right ventricular hypertrophy due to treatment with liraglutide." (1)

Read More Posted in: MOTS-c

Potential Synergy of MOTS-c or Humanin with Senolytics

By Nemo 3 months ago

FOXO4-DRI senescent cell remover is potentiated by SASP factors

"SASP factors as IL-6 may be the cause for the observed loss in renal function, and we wondered how FOXO4-DRI would function under such high SASP conditions. In vitro experiments showed FOXO4-DRI to be more potent against senescent cells in which SASP wastransiently boosted by recombinant IL1a/b or lipopolysaccharide (LPS), whereas an IL1 receptor antagonist or the general anti-inflammatory drug cortisol reduced its potency (Figures 6H and 6I). Thus, FOXO4-DRI actually is most effective against senescent cells expressing high levels of SASP and could as such be particularly effective against loss of renal function. Excitingly, while not substantially influencing total body nor kidney weight (Figure S6G), FOXO4-DRI treatment normalized the percentage of tubular cells lacking LMNB1 (Figure 6G), the tubular IL-6 elevation (Figure 6J), and the elevations in plasma urea levels (Figure 6K)." (4)

GHK affects the Gene Expression of COPD, Damaged Protein Clearing, and Nervous System

By Nemo 3 months ago
"GHK (glycyl-l-histidyl-l-lysine) is a human copper-binding peptide with biological actions that appear to counter aging-associated diseases and conditions. GHK, which declines with age, has health promoting effects on many tissues such as chondrocytes, liver cells and human fibroblasts, improves wound healing and tissue regeneration (skin, hair follicles, stomach and intestinal linings, boney tissue), increases collagen, decorin, angiogenesis, and nerve outgrowth, possesses anti-oxidant, anti-inflammatory, anti-pain and anti-anxiety effects, increases cellular stemness and the secretion of trophic factors by mesenchymal stem cells. Studies using the Broad Institute Connectivity Map show that GHK peptide modulates expression of multiple genes, resetting pathological gene expression patterns back to health."
Read More Posted in: GHK-Cu