Phenolic and flavonoid compounds from the fruit shell of Camellia oleifera.

A new phenolic compound oleiphenol (1), and a new dihydrochalcone oleifechalcone (2) along with seven known compounds (3-9) were isolated from the fruit shell of Camellia oleifera Abel. The planar structures of compounds 1 and 2 were determined on the basis of extensive spectroscopic analyses (IR, UV, NMR, and HR-ESI-MS) and comparison with literature data. The absolute configurations of the new structures were determined by ECD calculations and chemical methods. In addition, compounds 1-9 underwent a series of pharmacological activity tests, including cytotoxic, anti-inflammatory, anti-RSV and antioxidant activities.

Metabolomic profiles illuminate the efficacy of Chinese herbal Da-Cheng-Qi decoction on acute pancreatitis in rats.

BACKGROUND AND OBJECTIVES: Chinese herbal drug Da-Cheng-Qi decoction (DCQD) has been widely used for decades to treat acute pancreatitis (AP). Previous trials are mostly designed to state the potential mechanisms of the therapeutic effects rather than to detect its whole effect on metabolism. This study aimed to investigate the efficacy of DCQD on metabolism in AP. METHODS: Twenty-two male adult Sprague-Dawley rats were randomized into three groups. AP was induced by retrograde ductal infusion of 3.5% sodium taurocholate solution in DCQD and AP group, while 0.9% saline solution was used in sham operation (SO) group. Blood samples were obtained 12 h after drug administration and a 600 MHz superconducting Nuclear Magnetic Resonance (NMR) spectrometer was used to detected plasma metabolites. Principal Components Analysis (PCA) and Partial Least Squares-Discriminant Analysis after Orthogonal Signal Correction (OSC-PLS-DA) were applied to analyze the Longitudinal Eddy-delay (LED) and Carr-Purcell-Meiboom-Gill (CPMG) spectra. RESULTS: Differences in concentrations of metabolites among the three groups were detected by OSC-PLS-DA of 1HNMR spectra (both LED and CPMG). Compared with SO group, DCQD group had higher levels of plasma glycerol, glutamic acid, low density lipoprotein (LDL), saturated fatty acid (FA) and lower levels of alanine and glutamine, while the metabolic changes were reversed in the AP group. CONCLUSIONS: Our results demonstrated that DCQD was capable of altering the changed concentrations of metabolites in rats with AP and 1HNMR-based metabolomic approach provided a new methodological cue for systematically investigating the efficacies and mechanisms of DCQD in treating AP.

1HNMR-based metabolomic profile of rats with experimental acute pancreatitis.

BACKGROUND: Acute pancreatitis (AP) is a common inflammatory disease of the pancreas accompanied by serious metabolic disturbances. Nevertheless, the specific metabolic process of this disease is still unclear. Characterization of the metabolome may help identify biomarkers for AP. To identify potential biomarkers, this study therefore investigated the 1H-nuclear magnetic resonance (NMR)-based metabolomic profile of AP. METHODS: Fourteen male adult Sprague-Dawley rats were randomized into two groups: the AP group, in which AP was induced by retrograde ductal infusion of 3.5% sodium taurocholate; and the sham operation group (SO), in which rats were infused with 0.9% saline. Blood samples were obtained 12 hours later and a 600 MHz superconducting NMR spectrometer was used to detect plasma metabolites. Principal components analysis (PCA) and partial least squares-discriminant analysis after orthogonal signal correction (OSC-PLS-DA) were used to analyze both longitudinal Eddy-delay (LED) and Carr-Purcell-Meiboom-Gill (CPMG) spectra. RESULTS: Differences in plasma metabolites between the two groups were detected by PCA and PLS-DA of 1HNMR spectra. Compared with the SO group, plasma levels of lactate (δ 1.3, 1.34, 4.1), valine (δ 0.98, 1.02), succinic acid (δ 2.38), 3-hydroxybutyric acid (3-HB, δ 1.18), high density lipoprotein (HDL, δ 0.8), and unsaturated fatty acid (UFA, δ 2.78, 5.3) were elevated in the AP group, while levels of glycerol (δ 3.58, 3.66), choline (δ 3.22), trimethylamine oxide (TMAO, δ 3.26), glucose (δ 3-4), glycine (δ 3.54), very low density lipoprotein (VLDL, δ 1.34) and phosphatidylcholine (Ptd, δ 2.78) were decreased. CONCLUSIONS: AP has a characteristic metabolic profile. Lactate, valine, succinic acid, 3-HB, HDL, UFA, glycerol, choline, TMAO, glucose, glycine, VLDL, and Ptd may be potential biomarkers of early stage AP.

Meta-analysis of the relationship between the Metholenetetrahydrofolate reductase C677T genetic polymorphism, folate intake and esophageal cancer.

OBJECTIVE: To evaluate the effect of the methylenetetrahydrofolate reductase C677T genetic polymorphism (MTHFR C677T) and folate intake on the risk of esophageal cancer. METHODS: A total of 17 studies (3,277 cases and 4,661 controls) regarding MTHFR C677T and 6 studies (1,817 cases and 7,678 controls) regarding folate intake published between 2001 and 2011 were identified through researching MEDLINE, EMBASE and the Chinese Biomedical Database. The data of the last search was February 2011. A meta-analysis was performed to obtain summary estimated odd ratios and 95% confidence intervals of folate intake and MTHFR C677T for esophageal cancer. RESULTS: A significant association was seen between MTHFR 677 CT [adjusted OR (95% CI)=1.55(1.28-1.88)] and TT [crude OR (95% CI)=1.63(1.24-2.15)] genotypes and esophageal cancer. Folate intake was seen to have a preventive effect on esophageal cancer [OR (95% CI)=0.60(0.50-0.70)]. Non-drinkers with MTHFR 677 CT and TT showed light esophageal cancer risk, and higher esophageal cancer risk was found among smokers. Also, the MTHFR 677 CT and TT genotypes were associated with light esophageal cancer risk in non-drinkers and a higher risk in drinkers. The meta-regression analysis showed the effect of MTHFR 677 CT and TT increased with the level of alcohol and tobacco consumption. The MTHFR 677 TT genotype showed a decreased risk of esophageal cancer in the high folate intake group. CONCLUSION: MTHFR 677CT/TT increase the risk of esophageal cancer, and the effects are greatly modified by alcohol, tobacco and folate intake. Folate intake was seen to have a preventive effect on developing esophageal cancer.

Antiapoptotic mechanisms of Chinese medicine formula, Guan-Xin-Er-Hao, in the rat ischemic heart.

Considerable evidence indicates that apoptosis plays a critical role in acute myocardial infarction. We have previously shown that Guan-Xin-Er-Hao (GXEH), a Chinese medicine formula, attenuates postischemia myocardial apoptosis. The present study was designed to determine the mechanisms by which GXEH exerts its antiapoptotic effect. Adult male Sprague-Dawley rats were randomized to receive vehicle or GXEH (5 or 15 g/kg) orally 30 min before ischemia and subjected to myocardial ischemia of 3 h (apoptosis peak) or 24 h (necrosis peak) for determination of infarct size. Compared with rats receiving vehicle, those rats treated with GXEH (15 g/kg) showed significantly reduced infarct size, the reduced myocardial apoptosis, as judged by the decreases in TUNEL-positive staining (22.40 +/- 5.68% vs. 40.31 +/- 10.58%, p < 0.01), and the decrease in the degree of caspase-3 activation (82.97 +/- 10.54 vs. 159.95 +/- 9.16 mumol cleaved acetyl-Asp-Glu-Val-Asp-p-nitroanilide/mg protein, p < 0.01). Treatment with GXEH (15 g/kg) significantly reduced the release of mitochondrial cytochrome c, a primary mediator of apoptosis, the degree of caspase-9 activation, and the Bax/Bcl-2 ratio. Caspase-9 cleaves and activates caspase-3. Bax promotes apoptosis, while Bcl-2 inhibits apoptosis. Thus, the antiapoptotic mechanisms of GXEH may involve the mitochondrial cytochrome c-mediated caspase-3 activation in cardiomyocytes after acute myocardial infarction. Taken together, GXEH tilted the balance between Bax and Bcl-2 toward an antiapoptotic state, decreased mitochondrial cytochrome c release, reduced caspase-9 activation, and attenuated subsequent caspase-3 activation and postischemic myocardial apoptosis in rats. GXEH may be used as a promising agent for future treatment of cardiovascular diseases.