Article Sidebar
Published:
Apr 14, 2024DOI:
10.4314/tjpr.v23i3.6Keywords:
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
A study on the mechanism of cordycepin in regulating autophagy and alleviating renal tubular interstitial fibrosis
Abstract
Purpose: To elucidate the role of cordycepin in modulating autophagy and mitigating renal tubular interstitial fibrosis in a rat model of unilateral ureteral obstruction (UUO).
Methods: Forty male Sprague-Dawley (SD) rats were assigned to four groups: control, sham, UUO and cordyceps-treated groups (10 rats per group). The UUO and cordyceps groups underwent surgery to induce unilateral ureteral obstruction. The cordyceps group received intravenous cordycepin (10 mg/kg) daily for 14 days, while the control and UUO groups received normal saline. Histopathological examination, assessment of fibrosis markers (α-SMA, collagen III) and autophagy markers (Atg5, LC3II/I) were conducted.
Results: The UUO group exhibited significant tubular damage and interstitial fibrosis, with elevated serum levels of pro-inflammatory and oxidative markers (p < 0.05). Cordycepin treatment attenuated these pathological changes, evidenced by reduced fibrosis, inflammation and oxidative stress. Enhanced autophagic activity was observed in the cordycepin group, suggesting a potential mechanism of its renoprotective effect.
Conclusion: Cordyceps is effective in inhibiting renal tubulointerstitial fibrosis, potentially through the activation of autophagy and reduction of inflammation and oxidative stress. Future studies should focus on unraveling the specific molecular mechanisms of cordycepin's action and assessing its applicability in CKD treatment.
