Lonicerin alleviates LPS-evoked inflammation and apoptosis in HK2 cells

Background: Sepsis-induced acute kidney injury (AKI) is one of the most common complications of sepsis, characterized by extensive renal inflammation and progressive tissue damage, and poses a serious threat to human health. Lonicerin, a flavonoid glycoside derived from Lonicera japonica Thunb., is reported to exert beneficial effects in various inflammatory diseases. However, its potential regulatory role in sepsis-induced AKI has not been elucidated completely. Objective: To investigate the regulatory impacts of lonicerin in sepsis-induced AKI. Material and Methods: The cell viability was evaluated through CCK-8 assay. The LDH levels were examined through the LDH assay kit. The mRNA expression levels were analyzed through RT-qPCR. The levels of TNF-α, IL-6, and IL-1β were determined through ELISA. The ROS levels were detected through the DCF staining. Apoptosis rates were determined by flow cytometry. Protein expression levels were analyzed by western blot. Results: In this study, we demonstrated that lonicerin enhanced the viability of HK2 cells following lipopolysaccharide (LPS) stimulation. LPS significantly increased the inflammatory response, whereas this effect was attenuated after treatment with lonicerin. Furthermore, lonicerin effectively suppressed LPS-induced oxidative stress. In addition, although LPS stimulation promoted apoptosis in HK2 cells, this pro-apoptotic effect was largely counteracted by administration of lonicerin. Mechanistically, we found that activation of the nuclear factor kappa-B signaling pathway by LPS was inhibited in the presence of lonicerin. Conclusion: our findings provide that lonicerin can mitigate LPS-induced inflammation, oxidative stress, and apoptosis in HK2 cells. These results suggest that lonicerin may represent a promising therapeutic candidate for treating sepsis-induced AKI.