- Tuesday, May 07, 2024
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Research results suggested that ARA 290 may potentially greatly decrease the frequency of micronuclei caused by cisplatin and the DNA damage parameters of the comet test. In addition, researchers suggest that ARA 290 appears to reduce levels of malondialdehyde and reactive oxygen species (ROS) and increase levels of antioxidant enzymes, lowering cisplatin-induced oxidative stress. Furthermore, ARA 290 presentations appeared to decrease cisplatin-induced renal inflammation as measured by lower levels of pro-inflammatory cytokines. On top of that, ARA 290 has been hypothesized to counteract cell death in response to cisplatin, which may improve cell damage.
Molecular analysis further suggested that compared to the cisplatin group, the ARA 290 + cisplatin group seemed to have considerably lower gene and protein levels of TNFα, IL1β, IL6, Caspase-3, and Bax, and significantly higher gene and protein levels of Bcl2. As speculated by these results, ARA 290 may potentially protect against cisplatin-induced nephrotoxicity. Findings imply it may do this primarily through its antioxidant, anti-inflammatory, and anti-apoptotic characteristics, and researchers suggest that ARA 290 could be a novel research compound for studies in the context of acute kidney injury. ARA 290, a nonhematopoietic peptide containing 11 amino acids generated from the three-dimensional structure of erythropoietin’s helix B, “arbitrates” tissue protection by specifically interacting with the innate repair receptor (IRR).
ARA 290 Peptide and Wounds
When damaged tissues create and release erythropoietin, it activates the innate repair receptor (IRR). Diabetic wound healing may possibly be improved by activating the IRR. The impact of the IRR agonist ARA 290 on the healing of dermal tissue was the subject of this investigation. The study aimed to assess the efficacy of an ARA 290-based topical substance in rats with diabetic incision wound models produced by streptozotocin.
The peptide was given every day up to the fourteenth day after wound induction. The quantity of collagen and protein content, biochemical parameters, antioxidant status, and pro-inflammatory cytokines were among the aspects studied in the restored tissue after wound closure was determined. The data speculated wound healing activities using molecular, immunofluorescent, biochemical, and microscopic approaches. Compared to the control group, the ARA 290 group seemed to have significantly improved wound closure rate, re-capitalization time, collagen quantity, and protein content. As blood glucose and lipid levels appeared to drop, there seemed to be a divergent pattern to the rise of serum insulin and HDL. Decreased inflammatory cytokine levels, decreased lipid peroxidation, and increased antioxidants corroborated the healing effect. The findings implied that ARA290-arbitrated IRR activation suggested promise as a potential adjuvant in the context of research in tissue damage through diabetes.
Groups III and IV were exposed to ARA 290 topically, and extensive wound healing was suggested beginning on day seven, compared to the control group and the diabetic rats (Group II). On day 14, the animals presented with 20% ARA 290 (Group IV) suggested the fastest rate of wound contraction compared to the other groups. The outcome was hypothesized to have a more pronounced impact in the animals given 20% ARA 290.
Throughout the 14-day trial, the wound contraction investigation purported that laboratory mice had almost identical patterns concerning the epithelialization period, total collagen, and total protein content. The research suggested that compared to normal control animals (group I), diabetic control rats (group I) took a little longer to reach full epithelialization compared to normal control animals (group II). In contrast to the diabetic control group (group II), animals presented with 10% and 20% ARA290 (groups III and IV, respectively) exhibited a faster rate of epithelialization. The collagen content appeared significantly lower in the diabetic control group (Group II) compared to the normal control group (Group I). In contrast, compared to diabetic control rats (Group II), animals given 10% and 20% ARA290 (Groups III and IV, respectively) suggested a significant increase in collagen content. The protein content examination indicated a significant reduction in the diabetic control animals (Group II) compared to the normal control group (Group I). Groups III and IV, which were diabetic animals given 10% and 20% ARA 290, respectively, seemed to have a higher protein content than group II, a control group of diabetic rats.
ARA 290 Peptide and the Cardiovascular System
In addition to potentially improving left ventricular function, inflammation in left ventricular tissue, and mitochondrial health, ARA 290 seemed to decrease a systemwide frailty score in old rats. Frailty is defined as impaired function in many organ systems, making an organism susceptible to negative health effects.
This research supports previous research suggesting that the frailty index, rather than chronological age, may best predict the age-related decline in LV structure and function. Therefore, researchers hypothesized that presentation with ARA 290 may increase health span over time based on examining 31 health-related characteristics. The potential of ARA 290 on body mass index was comparable. Rats given ARA290 appeared to reach their maximum weight later in life than those given saline. Beyond 80% of the maximum lifetime, ARA290 presentations seemed to result in greater peak body weight and a slower late-life decrease when expressed as a percentage of maximal lifespan in rats given with saline or ARA 290. These findings point to a possible connection between the potential of ARA 290 to reduce frailty and preserve healthspan in old rats and its potential to improve left ventricular systolic function, retain late-life body weight, and reduce systemic inflammation.
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References
[i] Ghassemi-Barghi, Nasrin, et al. “Mechanistic Approach for Protective Effect of ARA290, a Specific Ligand for the Erythropoietin/CD131 Heteroreceptor, against Cisplatin-Induced Nephrotoxicity, the Involvement of Apoptosis and Inflammation Pathways.” Inflammation, 10 Sept. 2022, https://doi.org/10.1007/s10753-022-01737-7.
[ii] Mashreghi, Moeen, et al. “An in Vivo Investigation on the Wound-Healing Activity of Specific Ligand for the Innate Repair Receptor, ARA290, Using a Diabetic Animal Mode.” Europe PMC, 2023, europepmc.org/article/ppr/ppr610510.
[iii] Winicki, Nolan M., et al. “A Small Erythropoietin Derived Non-Hematopoietic Peptide Reduces Cardiac Inflammation, Attenuates Age Associated Declines in Heart Function and Prolongs Healthspan.” Frontiers in Cardiovascular Medicine, vol. 9, 18 Jan. 2023, www.ncbi.nlm.nih.gov/pmc/articles/PMC9889362/, https://doi.org/10.3389/fcvm.2022.1096887.
