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PKC and PKA involved in the protection of rhGLP-1 on glomeruli and tubules in diabetic rats.
Journal of Diabetes Investigation 2018 October 12
AIMS/INTRODUCTION: Blockade or reversal the progression of diabetic nephropathy is a clinical challenge. To study whether the recombinant human glucagon-like peptide-1 have an effect on alleviate urinary protein and urinary albumin levels in diabetic rats or not.
MATERIALS AND METHODS: STZ induced Diabetes Rats were treated with rhGLP-1, Insulin, and Saline. Using Immunostaining, H&E, EM and PAS staining to study the pathology of DN, and we performed qRT-PCR, Western blot and IHC to identify the differentially expressed proteins. The mechanism was studied via AGEs-induced tubular epithelial cells.
RESULTS: The recombinant human glucagon-like peptide-1 (rhGLP-1) inhibit PKC-β but increase PKA, which reduce oxidative stress in glomeruli and in cultured glomerular microvascular endothelial cells. In tubules, rhGLP-1 increase the expression of two key proteins relate to re-absorption, megalin, and cubilin, which was accompanied by downregulation of PKC-β and upregulation of PKA. On human proximal tubular epithelial cells, rhGLP-1 enhance the absorption of albumin, and this was blocked by a PKC activator or PKA inhibitor.
CONCLUSIONS: These findings suggest that rhGLP-1 can reverse diabetic nephropathy by protecting both glomeruli and tubules via inhibiting PKC and activating PKA. This article is protected by copyright. All rights reserved.
MATERIALS AND METHODS: STZ induced Diabetes Rats were treated with rhGLP-1, Insulin, and Saline. Using Immunostaining, H&E, EM and PAS staining to study the pathology of DN, and we performed qRT-PCR, Western blot and IHC to identify the differentially expressed proteins. The mechanism was studied via AGEs-induced tubular epithelial cells.
RESULTS: The recombinant human glucagon-like peptide-1 (rhGLP-1) inhibit PKC-β but increase PKA, which reduce oxidative stress in glomeruli and in cultured glomerular microvascular endothelial cells. In tubules, rhGLP-1 increase the expression of two key proteins relate to re-absorption, megalin, and cubilin, which was accompanied by downregulation of PKC-β and upregulation of PKA. On human proximal tubular epithelial cells, rhGLP-1 enhance the absorption of albumin, and this was blocked by a PKC activator or PKA inhibitor.
CONCLUSIONS: These findings suggest that rhGLP-1 can reverse diabetic nephropathy by protecting both glomeruli and tubules via inhibiting PKC and activating PKA. This article is protected by copyright. All rights reserved.
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