Mogroside V alleviates diquat-induced renal tubular epithelial cell injury via the TUG1/miR-29-3p/SIRT1 axis

Mogroside V (MV), a major bioactive component isolated from Siraitia grosvenorii, exhibits diverse pharmacological properties, yet its protective role in toxin-induced renal injury remains incompletely defined. This study investigated the effects and underlying mechanisms of MV in diquat (DQ)-induced renal tubular epithelial cell (RTEC) injury. DQ-treated HK-2 cells were exposed to MV, and cell viability, Apoptosis, LDH release, and inflammatory cytokine production (IL-6, IL-1β, and TNF-α) were evaluated. Expression of lncRNA TUG1, miR-29-3p, and SIRT1 was analyzed by RT-qPCR and Western blotting. Functional roles were examined through TUG1 knockdown and miR-29-3p/SIRT1 modulation, while molecular interactions were validated using dual-luciferase reporter assay and RIP assay. DQ exposure markedly reduced cell viability and increased Apoptosis, LDH release, and inflammatory cytokine expression. MV treatment significantly attenuated these injury markers. Mechanistically, DQ suppressed TUG1 expression, whereas MV restored TUG1 in a dose-dependent manner. TUG1 knockdown diminished MV-mediated cytoprotection. Further analyses demonstrated that TUG1 acts as a competing endogenous RNA that sequesters miR-29-3p, thereby relieving repression of SIRT1. Overexpression of miR-29-3p or silencing of SIRT1 partially abrogated the protective effects of MV. Collectively, these findings indicate that MV alleviates DQ-induced RTEC injury through modulation of the lncRNA TUG1/miR-29-3p/SIRT1 axis, highlighting a potential therapeutic pathway for toxin-associated renal damage.

DQ; MV; SIRT1; lncRNA TUG1; miR-29-3p.