The objective of this study is to investigate the preventive effect of phenolic-rich extracts from Chinese sumac (Rhus chinensis Mill.) fruits against nonalcoholic fatty liver disease (NAFLD) in rats induced by a high-fat diet and to clarify the underlying mechanisms. The results showed that the phenolic-rich extract remarkably improved some critical biochemical indexes, including TG, TC, MDA, ALT, AST, and endogenous antioxidant enzymes. The results of immunofluorescence and TUNEL assay showed that the extract obviously reduced the level of NF-κB in cell nuclei and suppressed hepatocyte apoptosis. Moreover, immunohistochemistry and western blot analyses further revealed that the phenolic-rich extract can improve NAFLD in high-fat diet induced rats by regulating several key proteins related to lipid metabolism, inflammation and apoptosis of hepatocytes, namely upregulating the expression levels of p-AMPK, PPAR-α, CPT1 and Bcl-2, and downregulating the levels of PPAR-γ, CYP2E1, p-P38, p-NF-κB, iNOS, COX-2, caspase-3D and Bax. These results indicate that the phenolic-rich extract from Chinese sumac fruits could prevent NAFLD in rats by regulating some critical proteins in several signalling pathways and may be provided as a new natural ingredient for developing functional foods and/or nutraceuticals to prevent NAFLD.
21 May 2018 in Journal of Thermal Analysis and Calorimetry
Objective: Storke is a leading cause of death and disability affecting million people worldwide, 80% of which is ischemic stroke (IS). Recently, traditional Chinese medicines (TCMs) have received great attentions in treating IS due to their low poisonous effects and high safety. Buyang Huanwu Decoction (BHD), a famous and classical Chinese prescription, has been used for treating stroke-induced disability for centuries. Yet, its underlying mechanism is still in fancy. Methods: We first constructed an IS model by middle cerebral artery occlusion (MCAO). Then, a metabonomics study on serum samples was performed using UHPLC-QTOF/MS, followed by multivariate data analysis including principal components analysis (PCA) and orthogonal partial least squares-discriminate analysis (OPLS-DA). Results: Metabolic profiling of PCA indicated metabolic perturbation caused by MCAO was regulated by BHD back to normal levels, which is in agreement with the neurobehavioral evaluations. In the OPLS-DA, 12 metabolites were screened as potential biomarkers involved in MCAO-induced IS. Three metabolic pathways were recognized as the most relevant pathways, involving one carbon pool by folate, sphingolipid metabolism and inositol phosphate metabolism. BHD significantly reversed the abnormality of 7 metabolites to normal levels. Conclusions: This is the first study to investigate the effect of BHD on IS at the metabolite level and to reveal the underlying mechanisms of BHD, which is complementary to neurobehavioral evaluation. In a broad sense, the current study brings novel and valuable insights to evaluate efficacy of TCMs, to interpret the action mechanisms, and to provide the theoretical basis for further research on the therapeutic mechanisms in clinical practice.
Two new monoterpenoid indole alkaloids, gelselegandines F (1) and G (2), were isolated from the aerial parts of Gelsemium elegans. Their structures were elucidated by means of spectroscopic techniques and quantum chemical calculations. The ECD calculations were conducted at the B3LYP/6-311G(d,p) level and NMR calculations were carried out using the Gauge-Including Atomic Orbitals (GIAO) method. Structurally, the two new compounds possessed rare, cage-like, monoterpenoid indole skeletons. All isolated compounds and the total alkaloids extract were tested for cytotoxicity against four different tumor cell lines. The total alkaloids extract of G. elegans exhibited significant antitumor activity with IC50 values ranging from 32.63 to 82.24 ug/mL. In order to discover anticancer leads from the active extraction, both new indole compounds (1–2) were then screened for cytotoxicity. Interestingly, compound 2 showed moderate cytotoxicity against K562 leukemia cells with an IC50 value of 57.02 uM.