Objectives: Astaxanthin (ATX) is a strong antioxidant drug. This study aimed to investigate the effects of ATX on podocytes in diabetic nephropathy and the underlying renal protective mechanism of ATX, which leads to pathological crosstalk with mesangial cells.Methods: In this study, diabetic rats treated with ATX exhibited reduced 24-h urinary protein excretion and decreased blood glucose and lipid levels compared to vehicle-treated rats. Glomerular mesangial matrix expansion and renal tubular epithelial cell injury were also attenuated in ATX-treated diabetic rats compared to control rats.Results: ATX treatment markedly reduced the α-SMA and collagen IV levels in the kidneys of diabetic rats. Additionally, ATX downregulated autophagy levels. In vitro, compared with normal glucose, high glucose inhibited LC3-II expression and increased p62 expression, whereas ATX treatment reversed these changes. ATX treatment also inhibited α-SMA and collagen IV expression in cultured podocytes. Secreted factors (vascular endothelial growth factor B and transforming growth factor-β) generated by high glucose-induced podocytes downregulated autophagy in human mesangial cells (HMCs); however, this downregulation was upregulated when podocytes were treated with ATX.Conclusions: The current study revealed that ATX attenuates diabetes-induced kidney injury likely through the upregulation of autophagic activity in podocytes and its antifibrotic effects. Crosstalk between podocytes and HMCs can cause renal injury in diabetes, but ATX treatment reversed this phenomenon.

2024-12-31·Redox Report

Astaxanthin prevents bone loss in osteoporotic rats with palmitic acid through suppressing oxidative stress

Article

作者: Wu, Xing-Jing ; Tao, Zhou-Shan ; Shen, Cai-Liang ; Yang, Min

OBJECTIVESThe study aimed to assess the role of Astaxanthin (ATX) in palmitic acid(PA) -induced bone loss in Ovariectomized(OVX) rats.METHODSIn the OVX rat model, we observed that PA affects bone metabolism and accelerates bone loss. Additionally, treatment with ATX was able to suppress the deleterious effects of PA and a simultaneous decrease in serum MDA levels and an increase in SOD was observed.RESULTSIn addition, rats treated with ATX were observed to have significantly increased bone mass and elevated activity of SIRT1 and SOD2 in bone tissue. When MC3T3-E1 and RAW264.7 cells induced osteoblast and osteoclast differentiation, the ATX intervention was able to significantly restore the restriction of osteogenic differentiation and the up-regulation of osteoclast differentiation with PA therapy. Furthermore, we confirm that PA damage to cells is caused by increased oxidative stress, and that ATX can target and modulate the activity of SIRT1 to regulate the levels of oxidative stress in cells.CONCLUSIONSummarizing, ATX may inhibit PA-induced bone loss through its antioxidant properties via the SIRT1 signaling pathway.

2024-12-01·Molecular Biology Reports

“Combination treatments of imatinib with astaxanthin and crocin efficiently ameliorate antioxidant status, inflammation and cell death progression in imatinib-resistant chronic myeloid leukemia cells”

Article

作者: Rahimi, Atefeh ; Najafzadeh, Mahsa ; Golestani, Amin ; Sayadi, Mahtab ; Sajjadi, Seyed Mehdi

BACKGROUNDImatinib resistance remains a major obstacle in the treatment of chronic myelogenous leukemia (CML). Crocin (CRC) and astaxanthin (ATX) are phytochemicals with anti-cancer properties.AIMSThis study aimed to explore the effects of combination treatment of Imatinib with CRC and ATX on Imatinib-resistant K562 (IR-K562) cells.METHODS AND RESULTSAfter the establishment of IR-K562 cells, growth inhibitory activity was determined by the MTT assay. To test the regeneration potential, a colony formation assay was performed. Cell cycle analyses were examined by flow cytometry. Cell injury was evaluated by lactate dehydrogenase (LDH) leakage. Real-time PCR was applied to assess the expression of IL6, TNF-α, STAT3, BAD, CASP3, TP53, and Bcl-2 genes. Caspase-3 activity was determined by a colorimetric assay. Antioxidant activity was measured using a diphenylpicrylhydrazyl (DPPH) assay. After 48 h of treatment, ATX (IC₅₀ = 30µM) and CRC (IC₅₀ = 190µM) significantly inhibited cell proliferation and colony formation ability, induced G1 cell cycle arrest and cell injury, upregulated the expression of apoptosis-associated genes, and downregulated the expression of anti-apoptotic and inflammatory genes. The combination of IM with ATX and/or CRC synergistically reduced cell viability (combination index [CI] < 1).CONCLUSIONOur data suggest that IM shows better therapeutic efficacy at lower doses when combined with ATX and/or CRC.

项与 ATX-UV1 相关的新闻（医药）

2024-05-21

·BioSpace

Alloy Therapeutics Announces Platform License Agreement with Lilly

BOSTON--(BUSINESS WIRE)-- Alloy Therapeutics, a biotechnology ecosystem company dedicated to democratizing access to biologics drug discovery platforms and services, announced today a licensing agreement for its murine platforms for fully human antibody discovery with Eli Lilly and Company. The non-exclusive license provides Lilly access to the ATX-Gx™ and ATX-CLC™ mouse platforms and broad rights to use the Alloy platforms for antibody drug discovery and development under this multi-year collaboration. Launched in 2019, the Alloy ATX-Gx platform has rapidly become the industry standard fully human transgenic mouse platform to enable therapeutic discovery programs utilized by over 170 partners. Alloy is dedicated to reinvesting its revenue into innovation and has continuously expanded its murine platforms, adding new strains such as ATX-GL™ with the full human lambda repertoire as well as ATX-GKH™ hyperimmune strain for increased generation of antigen-specific B-cells and enhanced IgG class switching. In 2023 Alloy launched the ATX-CLC platform expressing common light chain antibodies with full heavy chain diversity to enable efficient, modular bispecific discovery. Access to Alloy’s platforms extends to Lilly’s Catalyze360™ program, a comprehensive platform designed to enable drug discovery and development for biotech partners, including opportunities for capital investment, world-class lab space, and exceptional R&D capabilities and expertise. Under the arrangement, biotech companies that work with Lilly Catalyze360 will have the opportunity for Alloy antibody discovery platforms to be deployed to rapidly progress partnered discovery campaigns and accelerate medicines to the clinic for patients. “Lilly is a great collaboration partner, and we are excited to further enable the company’s broader R&D ecosystem with access to Alloy’s best-in-class technologies for discovering superior fully human antibodies and bispecifics against even the most challenging targets,” said Heather Schwoebel, CBO of Antibodies and Strategic Collaborations at Alloy. “This collaboration represents just one example of the many ways Alloy is flexible in enabling our partners with a breadth of discovery solutions to support their objectives and improve patient lives.” About Alloy Therapeutics Alloy Therapeutics is a biotechnology ecosystem company empowering the global scientific community to make better medicines together. Through a community of partners across academia, biotech, and the largest biopharma, Alloy democratizes access to pre-competitive tools, technologies, services, and company creation capabilities that are foundational for discovering and developing therapeutic biologics across six modalities: antibodies, TCRs, genetic medicines, peptides, cell therapies, and drug delivery. Partners may access all current and future technologies through a discovery service relationship or for a flat fee through Alloy’s Innovation Subscriptions offering. As a reflection of Alloy’s relentless commitment to the scientific community, Alloy reinvests 100% of its revenue in innovation and access to innovation. Join the Alloy Therapeutics community by visiting alloytx.com and following Alloy on LinkedIn.

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