Coptisine, one of the main active components of Rhizoma Coptidis, possesses anti-inflammatory, antioxidant, anti-apoptosis and renoprotective effects. In this study, we investigated the protective effect of coptisine against hyperuricemia induced renal injury in vitro and in vivo, and determined the underlying mechanism. In the in vivo experiment, a mouse model of hyperuricemia induced acute renal injury was established using potassium oxonate (PO)/ hypoxanthine (HX), and in the in vitro experiment, HK-2 cells injury was induced by uric acid (UA). Results showed that coptisine treatment significantly attenuated the acute renal injury via reducing kidney weight and coefficient, UA, creatinine (CRE), blood urea nitrogen (BUN), and histological damages. Meanwhile, coptisine treatment significantly suppressed hyperuricemia induced oxidant stress, inflammatory injury and apoptosis through promoting superoxide dismutase (SOD) activity, restraining reactive oxygen species (ROS), malondialdehyde (MDA), tumor necrosis factor (TNF)-α, interleukin (IL)- 1β, IL-18 levels, down-regulating protein expressions of cleaved-caspase 3, apoptosis-inducing factor (AIF), cyto-CytC, cleaved poly ADP-ribose polymerase (PARP) and Bcl-2-associated X protein (Bax), and up-regulating protein expressions of Bcl-2 and p-Bad. Additionally, mitochondrial structure damage and ATP depletion in renal tissue and HK-2 cells were observably alleviated. Of note, coptisine treatment remarkably ameliorated hyperuricemia induced phosphatidylinositol 3-kinase (PI3K)/ protein kinase B (PKB/Akt) signaling pathway inhibition. When interference with Akt, the protective effect of coptisine against UA-induced injury in HK2 cells was reversed. All the results suggested that coptisine could protect against hyperuricemia induced renal inflammatory damage, oxidative stress and mitochondrial apoptosis via regulating PI3K/Akt signaling pathway.

Excessive alcohol consumption leads to serious liver injury, associating with oxidative stress and inflammatory response. Previous study has demonstrated that polydatin (PD) exerted antioxidant and anti‐inflammatory effects and attenuated ethanol‐induced liver damage, but the research remained insufficient. Hence, this experiment aimed to evaluate the hepatoprotective effect and potential mechanisms of PD on ethanol‐induced hepatotoxicity. Our results showed that PD pretreatment dramatically decreased the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) in the serum, suppressed the malonaldehyde (MDA) and triglyceride (TG) content and the production of reactive oxygen species (ROS), and enhanced the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), catalase (CAT), andalcohol dehydrogenase (ADH), and aldehyde dehydrogenase (ALDH), paralleled by an improvement of histopathology alterations. The protective effect of PD against oxidative stress was probably associated with downregulation of cytochrome P450 2E1 (CYP2E1) and upregulation of nuclear factor erythroid 2‐related factor 2 (Nrf2) and its target gene haem oxygenase‐1 (HO‐1). Moreover, PD inhibited the release of proinflammatory cytokines (TNF‐α, IL‐1β, and IL‐6) via downregulating toll‐like receptor 4 (TLR4) and nuclear factor kappa B (NF‐κB) p65. To conclude, PD pretreatment protects against ethanol‐induced liver injury via suppressing oxidative stress and inflammation.