Calycosin Alleviates Lupus Nephritis by Activating the Nrf2/HO-1 Signaling Pathway

Lupus nephritis is a serious condition, for which treatments are limited; hence, there is a need for new cure approaches. The aim of this study was to evaluate the therapeutic effects of calycosin against lupus nephritis induced by lipopolysaccharide (LPS) in human renal cortex proximal convoluted tubule epithelial cells (HK-2). HK-2 cells were stimulated with 1 mu g/ml LPS to create a lupus nephritis cell model; the cells were pretreated with calycosin. Cell viability and apoptosis rate were determined using the cell counting kit-8 assay and flow cytometry, respectively. A caspase-3 activity detection kit was used to determine caspase-3 activity. Interleukin (IL)-6, IL-1 beta, and tumor necrosis factor alpha (TNF-alpha) levels were determined using enzyme-linked immunosorbent assay kits. Lactate dehydrogenase (LDH) level was determined using an LDH assay kit. Finally, western blotting and reverse transcription-quantitative polymerase chain reaction were performed to determine apoptosis-related protein levels and nuclear factor erythroid 2-related factor 2 ( Nrf2)/heme oxygenase-1 ( HO-1) signaling. Calycosin had no cytotoxic effects on HK-2 cells. Lipopolysaccharide stimulation significantly inhibited cell viability; increased the IL-6, IL-1 beta, and TNF-alpha levels; and elevated apoptosis rate, caspase3 activity, and LDH level in HK-2 cells. The protein level of cleaved caspase3 was also increased in LPS-treated HK-2 cells. In addition, the pattern of Nrf2/HO-1 signaling was disturbed by LPS. These effects were reversed by calycosin treatment. Calycosin could alleviate LPS-induced lupus nephritis and may thus be a novel agent for its treatment.