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

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
• diabetic nephropathy
• miR-766
• VCAM1
• apoptosis

Disclosure statement

No potential conflict of interests was reported by the authors.

Data availability statement

The data that support the findings of this study are available from the corresponding author.