Article Sidebar
Published:
Feb 16, 2022DOI:
10.4314/tjpr.v20i8.1Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Rehmannioside A protects against high glucose-induced apoptosis and oxidative stress of renal tubular epithelial cells by inhibiting the MAPK pathway
Abstract
Purpose: To investigate the effects and mechanism of rehmannioside A (ReA) on diabetic nephropathy (DN) progression.
Methods: Various concentrations of glucose and ReA were added to HK2 cells, and cell viability was analyzed using the 3-(4,5)-dimethylthiahiazo(-2)-3,5 diphenytetrazoliumromide (MTT) assay. Cell apoptosis, caspase 3 activity, and expression levels of BAX, Bcl-2, and cleaved poly (ADP-ribose) polymerase were evaluated to assess the effect of ReA on cell apoptosis. The effect of ReA on oxidative stress was also evaluated by assessing superoxide dismutase, catalase, and malondialdehyde levels. Lactate dehydrogenase release and reactive oxygen species levels were also measured. Finally, activation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase 1/2 was determined by immunoblot technique.
Results: ReA significantly enhanced the survival of HK2 cells induced with high glucose (HG). In addition, ReA suppressed apoptosis and inhibited oxidative stress of HK2 cells induced with HG (p < 0.05). ReA protected against HG-induced apoptosis and oxidative stress of renal tubular epithelial cells by inhibiting the MAPK pathway (p < 0.05).
Conclusion: ReA is a potential as a therapeutic agent for DN; however, in vivo and clinical investigations are required to validate this assertion.
