Actoeside mitigated the renal proximal tubule cells damage triggered by high glucose through miR-766/VCAM1/NF-κB signalling pathway

  • Arch Physiol Biochem. 2021 Aug 2;1-10. doi: 10.1080/13813455.2021.1920983.
Xiaodong Zhao  1 ,  Honglei Hu  1 ,  Kun Sun  2 ,  Wenlong Liang  1 ,  Zhenzhen Wang  1 ,  Xingqian Jin  1 ,  Shujuan Wang  1
Affiliations
  • 1. Department of Endocrinology, Zibo Central Hospital, Zibo City, PR China.
  • 2. Department of Nephropathy, Zibo Central Hospital, Zibo City, PR China.
PMID: 34338087 DOI: 10.1080/13813455.2021.1920983
Abstract

Context: Diabetic nephropathy (DN) triggered by diabetes mellitus is one of the primary causes of end-stage renal failure worldwide.

Objective: This study intends to explore the function and potential mechanism of actoeside on renal proximal tubule (HK-2) cells damage induced by high-glucose (HG).

Methods: The DN model was established in HK-2 cells with 30 mM HG treatment. The viability, Apoptosis and inflammation of HK-2 cells were analysed severally via CCK-8, flow cytomery and ELISA. The key factors related to NF-κB were detected by western blotting.

Results: Actoeside attenuated the HG-induced HK-2 cells damage. The differentially expression of miR-766 and VCAM1 in DN patients was reversed by actoeside. Moreover, the increased phosphorylation levels of p65 NF-κB/IκBα induced by HG were attenuated by actoeside.

Conclusions: Actoeside promoted the growth and repressed the Apoptosis and inflammation of HK-2 cells via miR-766/VCAM1/NF-κB signalling pathway, affording a promising idea for the treatment of DN.

Keywords
Actoeside; VCAM1; apoptosis; diabetic nephropathy; miR-766.
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