Aim: Inflammation and apoptosis are main pathological processes that lead to the development of hyperuricemic nephropathy (HN). This study aims to explore whether baicalin (BA) and baicalein (BAI) can relieve the damage through PI3K/AKT/NF-κB signal pathway and provide more reliable and precise evidence for the treatment of HN.Methods: HN mice were induced by yeast extract with potassium oxonate (PO), and HK-2 cells were induced by monosodium urate (MSU). Molecular docking, western blot, q-PCR, and other methods were used to explore the changes of various indicators in HN mice and HK-2 cells.Results: Molecular docking results showed that BA and BAI had good binding ability with PI3K, AKT, p65 and IκBα. BA and BAI significantly ameliorated the levels of renal function, decreased the p-PI3K, p-AKT and p-p65 expression, down-regulated the BAX/BCL2 and CASP3, and blunted the mRNA levels of tumour necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-18 in both renal tissue of HN mice and HK-2 cells induced by MSU. BA and BAI also decreased the oxidative stress level of MSU-induced HK-2 cells.Conclusion: BA and BAI were confirmed to attenuate HN through alleviating renal inflammatory and apoptosis in cells and tissues by inhibiting PI3K/AKT/NF-κB pathway. BA and BAI were expected to be developed as new anti-HN drugs.
Background: NLRP3 inflammasome activation results in liver inflammation and injury. Curcumin, a polyphenol from Curcumin longa, exhibits anti-inflammatory properties. The effects and anti-inflammatory mechanisms of curcumin were explored on acute liver injury induced by LPS/D-GalN.Methods and Results: An in vitro acute liver injury model was established on L-02 cells by treatment with10 μg/mL lipopolysaccharide (LPS); An in vivo model was established on SD rats by intraperitoneal injection of 0.02 mg/kg LPS and 500 mg/kg D-galactosamine (D-GalN). Biochemical index detection, histopathology, Western blotting, and qPCR were used to explore the effects and anti-inflammatory mechanisms of curcumin on acute liver injury induced by LPS/D-GalN in vitro and in vivo. Our results showed that curcumin significantly reduced the damage of L-02 cells induced by LPS, reduced the levels of transminase, inhibited oxidative stress induced by LPS in rats, and alleviated liver pathological injury. These effects accompanied by the downregulation of the expression of TLR4, NF-кB, and pyrotosis related proteins NLRP3 and caspase 1.Conclusions: Curcumin ameliorated acute liver injury induced by LPS and D-GalN in L-02 cells and SD rats by inhibiting TLR4/NF-кB/NLRP3 pathway.
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