Pyrintegrin (10 mg/kg; intraperitoneal injection; once; C57BL/6J mice) treatment protects mice from LPS-induced podocyte foot process effacement and proteinuria. Analysis of the murine glomeruli shows that LPS administration reduces the levels of active β1 integrin in the podocytes, which is prevented by cotreatment with Pyrintegrin.
In rats, Pyrintegrin reduces peak proteinuria caused by puromycin aminonucleoside-induced nephropathy.
Pyrintegrin induces postnatal adipose tissue formation in vivo of transplanted adipose stem/progenitor cells (ASCs) and recruited endogenous cells. In vivo, Pyrintegrin-treated human adipose stem/progenitor cells (ASCs) in 3D-bioprinted scaffolds, when transplanted in the dorsum of athymic mice, yielded ectopically formed adipose tissue that expressed human PPARγ. Remarkably, Pyrintegrin-adsorbed collagen gel implanted in the inguinal fat pad promoted adipogenesis formed by host endogenous cells, suggesting its ability to induce in situ adipogenesis without the need for cell transplantation.
Medlife has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model: |
Female wild type C57BL/6J mice (10-week-old) injected with LPS |
Dosage: |
10 mg/kg |
Administration: |
Intraperitoneal injection; once |
Result: |
Provided a significant protection for these animals from LPS-induced proteinuria and foot processe (FP) effacement.
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