Acortatarin A inhibits high glucose-induced extracellular matrix production in mesangial cells

Immunoprecipitation
DOI: 10.3760/cma.j.issn.0366-6999.20122445 Publication Date: 2024-01-16T18:12:42Z
ABSTRACT
Background Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. Various treatment regimens and combinations therapies provide only partial renoprotection. Therefore new approaches are needed to retard progression DN. The aim present study was evaluate role a novel spiroalkaloid from Acorus tatarinowii named acortatarin A (AcorA) in inhibiting high glucose-induced extracellular matrix accumulation mesangial cells (MCs). Methods cytotoxity AcorA on MCs examined by 3-(4,5-dimethylthiazol-2-yl)-2.5-diphenyltetrazolium bromide (MTT) assay. expression fibronectin collagen IV real time PCR western blotting. p22 phox p47 detected blot. interaction between co-immunoprecipitation. phosphorylation immunoprecipitation. protein kinase C (PKC) α, PKCβ, phospholiase gamma (PLCγ1), p85 subunit PI3K determined Western Results significantly inhibited activation NADPH oxidase, ROS-generating enzyme, increasing enhancing . Preincubation with production dose-dependent manner. Moreover, attenuated glucose enhanced PKCα, PLCγ1, PI3K. Conclusion inhibits via blocking oxidase activation.
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