Résumé
OBJECTIVE@#To investigate the mechanism of Radix Kansui (RK) stir-fried with vinegar (VRK) decreased hepatotoxicity in mice.@*METHODS@#According to a random number table, 40 mice were randomly divided into negative control group (0.5% carboxymethylcellulose sodium, 20 mL/kg), positive control group (0.1% mixture of carbon tetrachloride in soybean oil, 20 mL/kg), RK group (the ethyl acetate extracts of RK, 250 g crude drug/kg) and VRK group (the ethyl acetate extracts of VRK, 250 g crude drug/kg) with 10 mice per group. All mice were administered orally by gavage daily for 7 continuous days. The morphology of liver tissues was examined to assess the liver injury by a transmission electron microscope. Hepatocyte apoptosis in vivo was determined by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nickend labeling (TUNEL) assay. Immunohistochemical technique was adopted to detect the expression of particular antiapoptotic and proapoptotic proteins in the mitochondrial pathways, including B-cell lymphoma (Bcl-2) and caspase-3, as well as the expression of inflammatory mediators, including nuclear factor kappa B (NF- κ B) and intercellular adhesion molecule-1 (ICAM-1).@*RESULTS@#Liver injury and hepatocyte apoptosis were observed in RK mice, and the liver injury were significantly reduced in VRK-treated mice. In immunohistochemistry study, compared with the negative control group, RK inhibited dramatically the Bcl-2 protein expression and significantly increased the expression of caspase-3, NF- κ B and ICAM-1 (all P<0.01). Compared with the RK group, VRK group induced significant increase on Bcl-2 protein expression, and decreased the caspase-3, NF- κ B and ICAM-1 protein expression (P<0.05 or P<0.01).@*CONCLUSION@#The mechanism of reduced hepatotoxicity of VRK may be associated with the reduced inflammation, regulation of antiapoptotic and proapoptotic mediators in the mitochondrial pathway.
Résumé
Aim: To evaluate the effects of bioactive extracts from Fructus Jujubae in attenuating the inflammation induced by Radix Kansui. Methods: Exoteric splenic lymphocyte ( SPL) of mouse and peritoneal macrophage ( PMψ) of rat were used as cell model to evaluate the anti-inflammatory effects of fractions from Fructus Jujubae. MTT method was used to assay SPL proliferation, and Griess method was used in NO release of PMψ. Firstly, Radix Kansui fraction was applied to induce inflammatory effects of the cells, and then, the anti-inflammatory effects of five extracts of Fructus Jujubae were investigated to determine the active fractions in Fructus Jujubae, which probably contribute to the attenuation of Radix Kansui. The effects of Fructus Jujubae extract in interfering the gastrointestinal acute damages caused by the extract of Radix Kansui were observed according to the pathological sections of mice. Results: The extract RK-3 ( diterpenes) exhibited the most significant pro-inflammatory effect. The bioactive extracts B (micromolecule saccharides and amino acids), D(flavonoid glycosides), and E (triterpenes) of Fructus Jujubae could attenuate the action of RK-3. The effective extract of Fructus Jujubae protected stomach and duodenum of mouse from acute damages caused by the extract of Radix Kansui. Conclusion: Fraction RK-3 (diterpenes) of Radix Kansui had pro-inflammatory effects, and some extracts of Fructus Jujubae could attenuate this effect of Radix Kansui. The results helped to clarify that Fructus Jujubae attenuates the toxic effect of Radix Kansui in certain cases, and the bioactive extracts of Fructus Jujubae discovered in the experiments offer the basis for further research to the active components of Fructus Jujubae.