β‑elemene attenuates IRI‑AKI by inhibiting inflammation and apoptosis via suppression of the TLR4/MyD88/NF‑κB/MAPK signal axis activation.

Ischemia‑reperfusion injury‑induced acute kidney injury (IRI‑AKI) involves inflammatory cell infiltration and increased apoptosis, although the potential association between these processes remains unclear. The aim of the present study was to assess the impact of β‑elemene treatment on the IRI‑AKI using both in vivo and in vitro models, reverse transcription‑quantitative PCR, western blot assays, hematoxylin and Eosin (H&E) staining, Immunohistochemical staining and TUNEL staining. β‑elemene significantly decreased morphological and pathological kidney inflammation in mice caused by IRI. Additionally, β‑elemene prevented the expression of inflammatory factors and apoptosis proteins dose‑dependently in IRI mice and rat renal proximal tubule NRK52E cells treated with H(2)O(2). Mechanistically, β‑elemene exerted its effects by inhibiting toll‑like receptor 4/myeloid differentiation primary response gene 88 (MyD88) signal activation and blocking NF‑κB/MAPK signal phosphorylation. Additionally, the increases in apoptosis and MAPK signal activation following hydrogen peroxide treatment were restored by MyD88 inhibition in NRK52E cells. The present study revealed that β‑elemene is a promising preclinical candidate for AKI.