Tissue & cell · 2026
Sevoflurane alleviates renal ischemia/reperfusion injury by upregulating miR-664-5p to activate the PI3K/AKT signaling axis.
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Wang Zhongsu, Ji Yuelong, Sulaiman Muhammad, Yuan Conghu, Chen Peijun
Аннотация
BACKGROUND: Sevoflurane treatment has been shown to effectively alleviate kidney ischemia-reperfusion injury, but the specific mechanism of its renal protective effects is still not entirely understood. This study aimed to uncover the potential mechanisms underlying the renoprotective effect of sevoflurane against ischemia-reperfusion injury.
METHODS: Serum creatinine (Scr), blood urea nitrogen (BUN), and urea levels in mice were biochemically determined. PAS staining was used to assess renal tissue injury. The expression levels of miR-664-5p and PTEN in tissue and cells were determined by qRT-PCR. Interactions between the two were confirmed by luciferase reporter gene assays, and protein levels of PTEN, PI3K, AKT, and mTOR were assessed via Western blotting.
RESULTS: Sevoflurane pretreatment upregulated the expression of miR-664-5p. Downregulation of miR-664-5p increased levels of Scr, BUN, and urea, exacerbated renal tissue damage and promoted cell apoptosis upon sevoflurane pretreatment. PTEN was identified as a target of miR-664-5p. MiR-664-5p activated the PI3K/AKT signaling pathway through PTEN.
CONCLUSION: This study confirmed the protective effect of sevoflurane pretreatment on renal ischemia-reperfusion injury and elucidated the regulatory mechanism of miR-664-5p/PTEN in renal injury.
METHODS: Serum creatinine (Scr), blood urea nitrogen (BUN), and urea levels in mice were biochemically determined. PAS staining was used to assess renal tissue injury. The expression levels of miR-664-5p and PTEN in tissue and cells were determined by qRT-PCR. Interactions between the two were confirmed by luciferase reporter gene assays, and protein levels of PTEN, PI3K, AKT, and mTOR were assessed via Western blotting.
RESULTS: Sevoflurane pretreatment upregulated the expression of miR-664-5p. Downregulation of miR-664-5p increased levels of Scr, BUN, and urea, exacerbated renal tissue damage and promoted cell apoptosis upon sevoflurane pretreatment. PTEN was identified as a target of miR-664-5p. MiR-664-5p activated the PI3K/AKT signaling pathway through PTEN.
CONCLUSION: This study confirmed the protective effect of sevoflurane pretreatment on renal ischemia-reperfusion injury and elucidated the regulatory mechanism of miR-664-5p/PTEN in renal injury.