Objective To determine the content of monotropein in the different parts of Morinda officinalis and in its counterfeit species.Methods The method of HPLC was used with chromatographic conditions as follows:Kromasil C18(150 mm?4.6 mm,5 ?m) column,the mobile phase of methol-0.4 %phosphate solution(5:95→28.8:71.2,15 min),the velocity of flow being 1 mL/min,the detection wavelength at 231 nm and column temperature being 25 ℃.Results The content of monotropein in the leaves and radix of Morinda officinalis and Morinda parvifolis is the highest.Conclusion It is reasonable to replace the root of Morinda officinalis with the leaves of Morinda officinalis and Morinda parvifolis for the monotropein extraction.

Objective To study the chemical constituents of Ganoderma resinaceum. Methods Chemical constituents were isolated and purified by silica gel column, Sephadex LH-20, and ODS column chromatography. The structures were identified by means of physicochemical and spectral data. Results From the CHCl3 part of the fruiting bodies of this material, eight compounds were isolated. Their structures were determined to be ergosterol (1), β-sitosterol (2), ganoderic acid E (3), ganoderic acid G (4), ganoderic acid C2 (5), ganoderic acid B (6), ganoderic acid A (7), and lucidenic acid A (8). Conclusion All the compounds were obtained from this fungus for the first time.

To arouse students’autonomous study,a reform was carried out in experimen- tal teaching of preventive medicine. Taking exploratory experiment as a cut-in point,students were free to choose subjects,design blueprint,do spot research and compose papers etc.,which efficiently inspired students’learning interest and exploring spirit,cultivated their creative think-ing and researching ability.

OBJECTIVETo establish chromatographic fingerprints of triterpenoid compounds in ganoderma RP-HPLC for the quality control of ganoderma.

METHODHPLC fingerprints were established. The chromatographic conditions were as follows: the separation was performed on a Diamonsil C18 column (4.6 mm x 250 mm, 5 microm), using a gradient elution with acetonitrile-water containing 0.8% perchloric acid as the mobile phases. The flow rate was 0.9 mL x min(-1), the detection wavelength was 254 nm and the temperature of column was at ambient temperature. The common patterns of HPTLC and HPLC fingerprints were separately obtained through "Chromafinger" solution software, and quality assessments were analyzed by similarity.

RESULTThe HPLC fingerprint pattern of G. lucidum consists of 18 peaks, among them 6 peaks were identified by chemical reference substances.

CONCLUSIONThis study provided theory and experimental data in order to comprehensively evaluate the quality of ganoderma.

Chromatography, High Pressure Liquid ; methods ; Drugs, Chinese Herbal ; analysis ; Reishi ; chemistry ; Triterpenes ; analysis

Objective: To investigate the effects of 1, 25-dihydroxy vitamin D₃[1, 25(OH)₂D₃] on food allergy(FA) in mice and its mechanism. Methods: A total of 40 BALB/c mice were randomly divided into 5 groups, 8 in each group, including control group (group C) and FA model group (FA group), according to the dose of 1, 25(OH)₂D₃ intervention, the mice of the FA group were divided into FA₀ group (0), FA_l group [10 μg/(kg·d)], FA_m group [50 μg/(kg·d)] and FA_h group[100 μg/(kg·d)]. Egg albumin was used to establish a food allergy model, with different doses of 1, 25(OH)₂D₃ for gastric intervention, and the control group was replaced by 9 g/L saline.The serum levels of ovalbumin-immunoglobulin E(OVA-IgE), interleukin(IL)-9 and IL-17 of mice were measured by using enzyme linked immunosorbent assay after the last excitation, and HE staining and histopathological examination were carried out in the small intestine of mice. Results: Compared with group C, FA₀ group and FA_h group small intestinal mucosa in mice had different degrees of damage, partial peeling off, structure disorder, villi epithelial cell focal falls peeling off, necrosis, lamina propria edema, congestion, a large number of inflammatory cells infiltration, low but the FA_l group and FA_m group had light mucosa damage, intestinal epithelial basically intact, with integrity, no congestion, edema, and inflammatory cells infiltration to a lesser degree.The mean concentrations of serum IgE, IL-9 and IL-17 in different groups were statistically significant (F=40.770, 9.530, 5.624, all P<0.05). Compared with the FA₀ group [(41.87±3.19) ng/L], the OVA-IgE of the FA_l group [(22.71±4.77) ng/L] and the FA_m group [(16.34±2.81) ng/L] were significantly reduced (t=5.533, 11.835, all P<0.01), but there was no significant difference between the FA_h group [(36.29±6.52) ng/L] (t=1.673, P>0.05). Compared with the FA₀ group [(161.77±50.44) ng/L], the IL-9 levels of the FA_l group [(94.29±18.79) ng/L] and the FA_m group[(84.45±30.88) ng/L] were significantly lower (t=3.267, 3.366, all P<0.01), while that of the FA_h group [(36.29±6.52) ng/L] was not significantly lower (t=0.777, P>0.05). Compared with FA₀ group [(81.55±29.37) ng/L], IL-17 levels of FA_h group [(133.58±47.05) ng/L] was significantly increased (t=2.653, P<0.05), while IL-17 level of FA_l group [(79.41±25.15) ng/L] and FA_m group [(58.81±26.00) ng/L] were lower than that of FA₀ group [(81.55±29.37) ng/L], but the difference was not statistically significant (t=0.154, 1.640, all P>0.05). Conclusions Low, medium dose of 1, 25(OH)₂D₃ supplements can inhibit mice food allergies, but high doses of 1, 25(OH)₂D₃ improve performance in mice food allergies, and 1, 25(OH)₂D₃′s influence on the secretion of IL-9 is one that influences mechanism of food allergy.

Inhibitor of nuclear factor kappa-B kinase subunit beta (IKKβ) is one of important kinases in inflammation to phosphorylate inhibitor of nuclear factor kappa-B (IκBα) and then activate nuclear factor kappa-B (NF-κB). Inhibition of IKKβ has been a therapeutic strategy for inflammatory and autoimmune diseases. Here we report that IKKβ is constitutively activated in healthy donors and healthy Ikkβ ^C46A (cysteine 46 mutated to alanine) knock-in mice although they possess intensive IKKβ-IκBα-NF-κB signaling activation. These indicate that IKKβ activation probably plays homeostatic role instead of causing inflammation. Compared to Ikkβ ^WT littermates, lipopolysaccharides (LPS) could induce high mortality rate in Ikkβ ^C46A mice which is correlated to breaking the homeostasis by intensively activating p-IκBα-NF-κB signaling and inhibiting phosphorylation of 5' adenosine monophosphate-activated protein kinase (p-AMPK) expression. We then demonstrated that IKKβ kinase domain (KD) phosphorylates AMPKα1 via interacting with residues Thr183, Ser184, and Thr388, while IKKβ helix-loop-helix motifs is essential to phosphorylate IκBα according to the previous reports. Kinase assay further demonstrated that IKKβ simultaneously catalyzes phosphorylation of AMPK and IκBα to mediate homeostasis. Accordingly, activation of AMPK rather than inhibition of IKKβ could substantially rescue LPS-induced mortality in Ikkβ ^C46A mice by rebuilding the homeostasis. We conclude that IKKβ activates AMPK to restrict inflammation and IKKβ mediates homeostatic function in inflammation via competitively phosphorylating AMPK and IκBα.