Camellia oil inhibits oxidative stress and inflammatory response to ameliorate LPS-induced acute kidney injury via downregulation of TLR4-mediated activation of the NF-κB/AP-1/IRF3 and NLRP3 pathways

Camellia oil, used as both a traditional Chinese medicine and a nutritious food, is an excellent candidate for arresting acute kidney injury (AKI) in sepsis. The present study aimed to provide further evidence for the clinical application of camellia oil to prevent AKI by further delineating the involvement of the TLR4 signaling cascades in its effects. Firstly, significant physiological indices were examined to assess the model and the intervention efficacy of camellia oil. The effect of camellia oil on the NLRP3 pathway and three key transcription factors of the TLR4 signaling cascades, NF-kappa B, AP-1 and IRF3, were also investigated in LPS-induced AKI rats using the multiplex biometric immunoassay. Furthermore, gas chromatography-mass spectrometry (GC-MS) was used to analyze the composition of camellia oil, and molecular docking was employed to evaluate the interaction between the most abundant component of camellia oil and the TLR4-MD-2 complex. The integrated results demonstrate that camellia oil had a protective effect on AKI by inhibiting TLR4 signaling. Oleic acid was found to be the most abundant component of camellia oil, which was able to bind to the TLR4-MD-2 complex and inhibit the TLR4 signaling cascades. This was likely the material basis for the protective effect of camellia oil. These data provide a further pharmacological basis for the clinical application of camellia oil to prevent AKI and help to understand the herbal function and homology of medicine and food.