Abstract
This study investigated the effect of gut microbial sodium butyrate (NaB) on renal ischemia-reperfusion injury (IRI) and its mechanism using a rat model of renal IRI and a HK-2 cell model of hypoxia-reoxygenation (HR) injury. The activity of malondialdehyde, superoxide dismutase, glutathione peroxidase, and catalase in kidney tissues and HK-2 cells was detected. ELISA was performed to measure the concentrations of TNF-α, IL-1β, and IL-6 in serum and cell culture supernatant. TUNEL staining and flow cytometry were used to assess apoptosis in kidney tissues and HK-2 cells, respectively. UCSC and JASPAR predicted the binding sites between HES1 and PPARα promoter, followed by experimental verification of the binding. NaB pretreatment inhibited oxidative stress, inflammation, and apoptosis following renal IRI in vivo and in vitro. NaB suppressed the expression of HES1 and promoted that of PPARα. Overexpression of HES1 or knockdown of PPARα in HR-treated HK-2 cells inhibited the protective effects of NaB. HES1 repressed the expression of PPARα by binding PPARα promoter. In conclusion, NaB may alleviate renal IRI by promoting the transcription of PPARα via downregulation of HES1.
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