Fabrication of MIL-101(Cr)/silver nanocomposites as SERS substrate for sensitive determination of malachite green and crystal violet in tilapia.

Nanocomposites with multiple functions have attracted much attention in designing novel SERS substrates. In this report, the enrichment ability of MIL-101(Cr) and the local surface plasma resonance (LSPR) of silver nanoparticles are combined to fabricate a SERS substrate denoted as MIL-101-MA@Ag, which can simultaneously produce high-density and uniformly distributed hot spots. Moreover, the enrichment ability of MIL-101(Cr) can further improve the sensitivity by concentrating and transferring the analytes in the vicinity of hot spots. Under optimal conditions, MIL-101-MA@Ag showed good SERS activity for malachite green (MG) and crystal violet (CV), with detection limits as low as 9.5×10-11 M and 9.2×10-12 M at 1616 cm-1, respectively. The prepared substrate has been successfully applied to detect MG and CV in tilapia, the recovery rate of fish tissue extract was 86.4~102%, and the relative standard deviation (RSD) was 8.9~15%. The results demonstrate that MOF-based nanocomposites are expected to be useful SERS substrates and have a universal applicability for the detection of other hazardous molecules.

Metabolomics of Fuzi-Gancao in CCl4 induced acute liver injury and its regulatory effect on bile acid profile in rats.

BACKGROUND: Fuzi (Radix aconiti lateralis)-Gancao (Radix glycyrrhizae) is one of the most classical drug pairs of traditional Chinese medicine. In clinical practice, decoctions containing Fuzi-Gancao (F-G) are often used in the treatment of liver diseases such as hepatitis and liver failure. AIM: To investigate the metabolomics of F-G in CCl4 induced acute liver injury in rats and its regulatory effect on the bile acid profile. METHODS: The pharmacodynamic effect of F-G on CCl4 induced acute liver injury in rats was evaluated, and an ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method for the simultaneous determination of 92 metabolites from multiple pathways was established to explore the protective metabolic mechanism of F-G in serum on the liver. RESULTS: Twenty-four differential metabolites were identified in serum samples. The primary bile acid biosynthetic metabolic pathway was the major common pathway in the model group and F-G group. Subsequently, a UPLC-MS/MS method for simultaneous determination of 11 bile acids, including cholic acid, ursodeoxycholic acid, glycochenodeoxycholic acid, glycochenodeoxycholic acid, taurocholic acid, glycocholic acid, chenodeoxycholic acid, deoxycholic acid, taurochenodeoxycholic acid, taurocholic acid, and glycinic acid, was established to analyze the regulatory mechanism of F-G in serum. F-G decreased the contents of these 11 bile acids in serum in a dose-dependent manner compared with those in the model control group. CONCLUSION: F-G could protect hepatocytes by promoting the binding of free bile acids to glycine and taurine, and reducing the accumulation of free bile acids in the liver. F-G could also regulate the compensatory degree of taurine, decreasing the content of taurine-conjugated bile acids to protect hepatocytes.