Metabolomics and Lipidomics Study Unveils the Impact of Tauroursodeoxycholic Acid on Hyperlipidemic Mice.

Bear bile powder is an essential, traditional and valuable Chinese herbal medicine that clears heat, calms the liver, and improves eyesight. Early studies have shown that bear bile powder has lipid-lowering activity, but due to the scarcity of natural bear bile powder resources, it has yet to be used on a large scale. Researchers have found that tauroursodeoxycholic acid (TUDCA) is the primary characteristic bioactive substance of bear bile powder. This study aimed to investigate the therapeutic effect of TUDCA on high-fat diet (HFD)-induced hyperlipidemia. A hyperlipidemia model was established by feeding mice high-fat chow, following the intervention of different concentrations of TUDCA (25/50/100 mg/kg) orally, the hallmark biochemical indexes (total cholesterol (TC), total triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)), histopathological examination (hematoxylin-eosin (HE) staining and oil red O (ORO) staining), and metabolomic analysis of serum and liver. The results showed that TUDCA could downregulate total TC, TG, LDL-C, upregulate HDL-C, reduce fat deposition in hepatocytes, reverse hepatocyte steatosis, and exhibit prominent lipid-lowering activity. In addition, it may play a therapeutic role by regulating glycerophospholipid metabolism.

Neochamaejasmin B extracted from Stellera chamaejasme L. induces apoptosis through caspase-10-dependent way in insect neuronal cells.

To explore the toxicity mechanisms of neochamaejasmin B (NCB) extracted from Stellera chamaejasme L., we first evaluated its cytotoxicity in neuronal cells of Helicoverpa zea (AW1 cells). NCB inhibited cell growth and was cytotoxic to AW1 cells in a dose-dependent manner. Further, transmission electron microscopy (TEM) was used to analyze the microstructure, and typical apoptotic characteristics were observed in AW1 cells treated with NCB. Moreover, the NCB-induced apoptosis was dose dependent. Subsequently, we explored the mechanism of apoptosis. A decline in the mitochondrial membrane potential (MMP) was found. Also, the levels of Bax were increased with increases in drug concentration, but there was no statistical difference in Bcl-2 levels at different NCB doses. Caspase-3 and caspase-10 activity was increased. These findings confirmed that NCB induced apoptosis in AW1 cells through a caspase-10-dependent mechanism. The results provide the basic information needed for understanding the toxicity and mechanisms of action of NCB, which could potentially be used to develop NCB as a new insecticide.