Effect of jatrorrhizine on delayed gastrointestinal transit in rat postoperative ileus.

OBJECTIVES: Postoperative ileus is major cause of postoperative complication and prolonged hospitalization. Jatrorrhizine, which is a protoberberine alkaloid isolated from the medicinal plants Berberis aristata and Coptis chinensis, has been found to increase contractility of gastric antral and ileum smooth muscles of rat gastrointestinal tract. We have investigated whether jatrorrhizine could offset gastrointestinal transit in rat with postoperative ileus. METHODS: Postoperative ileus was induced by laparotomy with intestinal manipulation under anaesthesia. Gastrointestinal transit was evaluated by measurement of gastric emptying, geometric centre and the migration of Evans blue. KEY FINDINGS: Postoperative ileus significantly delayed gastric emptying and intestinal transit. Jatrorrhizine dose-dependently (0.1, 0.3 and 1 mg/kg) offset delayed gastric emptying and intestinal transit (geometric centre and the migration of Evans blue) in postoperative ileus. Pretreatment of animals with atropine inhibited the action of jatrorrhizine on gastric emptying and intestinal transit, but pretreatment of animals with SB204070 did not influence the effect of jatrorrhizine on gastric emptying and intestinal transit in postoperative ileus. CONCLUSIONS: Jatrorrhizine offset postoperative ileus-induced delayed gastric emptying and intestinal transit in rats, an action mediated via the cholinergic pathway, but not involving activation of 5-HT(4) receptors.

Model and experimental studies for contact angles of surfactant solutions on rough and smooth hydrophobic surfaces.

Despite the practical need, no models exist to predict contact angles or wetting mode of surfactant solutions on rough hydrophobic or superhydrophobic surfaces. Using Gibbs' adsorption equation and a literature isotherm, a new model is constructed based on the Wenzel and Cassie equations. Experimental data for aqueous solutions of sodium dodecyl sulfate (SDS) contact angles on smooth Teflon surfaces are fit to estimate values for the adsorption coefficients in the model. Using these coefficients, model predictions for contact angles as a function of topological f (Cassie) and r (Wenzel) factors and SDS concentration are made for different intrinsic contact angles. The model is also used to design/tune surface responses. It is found that: (1) predictions compare favorably to data for SDS solutions on five superhydrophobic surfaces. Further, the model predictions can determine which wetting mode (Wenzel or Cassie) occurred in each experiment. The unpenetrated or partially penetrated Cassie mode was the most common, suggesting that surfactants inhibit the penetration of liquids into rough hydrophobic surfaces. (2) The Wenzel roughness factor, r, amplifies the effect of surfactant adsorption, leading to larger changes in contact angles and promoting total wetting. (3) The Cassie solid area fraction, f, attenuates the lowering of contact angles on rough surfaces. (4) The amplification/attenuation is understood to be due to increased/decreased solid-liquid contact-area.

The effects of jatrorrhizine on contractile responses of rat ileum.

This study was designed to evaluate the effect of jatrorrhizine on smooth muscle contractions isolated from rat ileum longitudinal muscles. Jatrorrhizine increased the amplitude of spontaneous contractions of ileum longitudinal muscles in concentration-dependent manner with an EC(50) of 30.0±8.4µM. Preincubation of ileum strips with atropine (1µM), 4-diphenyllacetoxy-N (2-chloriethyl)-piperidine (4-DAMP, 1µM) or darifenacin (1µM) significantly inhibited acetylcholine (0.1µM)- and jatrorrhizine (100µM)-induced ileum longitudinal muscle contractions, whereas they were not affected by AF-DX116 (1µM) or hexamethonium (100µM). Pretreatment with SB204070 (1µM) rather than 3-tropanyl-indole-3-carboxyleat (tropisetron, 1µM) significantly inhibited 5-HT (10µM)-induced ileum longitudinal muscle contractions. In contrast, jatrorrhizine-induced ileum longitudinal muscle contractions were not inhibited by tropisetron or SB204070. Furthermore, jatrorrhizine-induced ileum longitudinal muscle contractions were strongly inhibited by nifedipine (1µM), and also attenuated by removal of extracellular Ca(2+), U73122 (1µM), ruthenium red (50µM) or 2-aminoethoxydiphenylborate (2-APB, 10µM). Taken together, jatrorrhizine-elicited spontaneous contractions in rat ileum longitudinal muscles are mediated by activation of acetylcholine receptors, mostly the M(3) receptor. Ca(2+) influx through L-type Ca(2+) channel is significantly contributed to jatrorrhizine-elicited spontaneous contractions, and Ca(2+) release via IP(3) and ryanodine pathways are also involved.

Traditional Chinese formula, lubricating gut pill, stimulates cAMP-dependent CI(−) secretion across rat distal colonic mucosa.

AIM OF THE STUDY: Lubricating gut pill (LGP), a traditional Chinese formula, had been conformed to improve the loperamide-induced rat constipation by stimulation of Cl(-) secretion, but its mechanism has not been fully explored. Thus, the purpose of this study was to identify the action sites of LGP-stimulated Cl(-) secretion across rat distal colonic mucosa. MATERIALS AND METHODS: Rat distal colonic mucosa was mounted in Ussing chambers and short circuit current (I(SC)), apical Cl(-) current and basolateral K(+) current were recorded. Intracellular cyclic adenosine monophosphate (cAMP) content and protein kinase A (PKA) activity were determined with ELISA kit and the non-radioactive PepTag test, respectively. RESULTS: LGP at 800µg/ml elicited a sustained increase in Cl(-) secretory response, which was inhibited by CFTR(inh)172, a cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor. Permeabilizing apical membrane with nystatin revealed that LGP-stimulated basolateral K(+) current was significantly inhibited by KCNQ1 K(+) channel inhibitor chromanol 293B. LGP-stimulated I(SC) was markedly reduced by pretreatment with cis-N-[2-phenylcyclopentyl]-azacyclotridec-1-en-2amine (MDL-12,330A) and N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), but not with inhibitors of Ca(2+)-dependent signaling pathway. Treatment of tissue with LGP resulted in an increase in intracellular cAMP level and the activation in protein kinase A. The E-prostanoid(4) (EP)(4) receptor antagonist L-161,982 completely eliminated LGP-induced response. CONCLUSIONS: The results showed that LGP enhances Cl(-) and fluid secretion via prostanoid receptor signaling and also cAMP and protein kinase A pathway, subsequently triggering the activation of apical Cl(-) channels mostly CFTR and basolateral cAMP-dependent K(+) channel.

[The utility of trnH-psbA gene for phylogenetic analysis of Huperziaceae and plant barcoding].

OBJECTIVE: The purpose of study was to discover the phylogenetic relations and plant barcoding of 17 plants from Huperziaceae. METHODS: Phylogenetic tree of chloroplast trnH-psbA gene of 17 plants from Huperziaceae was constructed by software. RESULTS: It showed that Huperziaceae could be divided into two genera Huperzia and Phlegmariurus and bootstrap value reached 91%. CONCLUSIONS: Holub and Qing' taxonomy was supported and 17 species in Huperziaceae were monophyletic groups and it suggested that trnH-psbA could be used as a DNA barcode to identify plants.

Traditional Chinese formula, lubricating gut pill, improves loperamide-induced rat constipation involved in enhance of Cl- secretion across distal colonic epithelium.

AIM OF THE STUDY: Lubricating gut pill (LGP), a traditional Chinese formula, was widely used for the treatment of chronic constipation, especially in the elderly, in China. However, it is unclear whether LGP-induced laxative and/or lubricating effect is involved in water and electrolytes transport in distal colonic epithelium. MATERIALS AND METHODS: The present study was designed to evaluate the effect of LGP on Cl(-) secretion across rat distal colonic epithelium mounted in Ussing chambers, and on a rat constipation model induced by loperamide, respectively. RESULTS: Application of LGP in the apical side elicited a sustained increase in short circuit current (I(SC)) response in a concentration-dependent manner. Evidence that LGP-stimulated I(SC) was due to Cl(-) secretion is based on inhibition of current by (a) a Na(+)-K(+)-2Cl(-) cotransporter inhibitor bumetanide, (b) removal of Cl(-) ions in bath solution, and (c) the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel blocker DPC, suggesting that a apical cAMP-dependent Cl(-) channel was activated. LGP-stimulated I(SC) was also strongly inhibited by pretreatment with clotrimazole, indicating that the basolateral K(+) channel was also involved in maintaining this cAMP-dependent Cl(-) secretion. Pretreatment of tissues with indomethacin, but not atropine, tetrodotoxin or hexamethonium, inhibited LGP-induced response. In a rat constipation model, oral administration with LGP was significantly restored number of fecal pellets, water content and mucus secretion compared with loperamide-treated group alone. CONCLUSIONS: LGP enhances Cl(-) secretion that is mostly mediated through the release of cyclooxygenase metabolites, by which provided an osmotic force for the subsequent laxative action observed in the rat constipation model.

[Inhibitory effect on activated renin-angiotensin system by astragaloside IV in rats with pressure-overload induced cardiac hypertrophy].

OBJECTIVE: To investigate the effect of astragaloside IV (As IV) on the activation of rennin-angiotensin system in rats with pressure-overload induced cardiac hypertrophy. METHOD: Left ventricle hypertrophy was induced by abdominal aorta banding between bilateral renal aortas for 12 weeks. Rats were given astragaloside IV 1.0 mg x kg(-1) and 3.3 mg x kg(-1) for 12 weeks, respectively. After treatment, the left ventricular mass index (LVMI)was calculated by morphometry methods. Plasma and cardiac tissue angiotensin II, and plasma aldosterone were measured by ELISA method. Gene expressions of ACE, AT1 and AT2 in cardiac tissue were detected by real time PCR. Protein expressions of AT1 and AT2 in cardiac tissue were detected by Western blot. RESULT: Compared with model rats, LVMI was decreased by astragaloside IV treatment. Biochemical results indicated that the contents of angiotensin II in plasma and cardiac tissue as well as aldosterone in plasma were all increased in abdominal aorta banding rats comparing with sham-operated rats, then, decreased by astragaloside IV treatment. Gene expressions of cardiac ACE was downregulated by astragaloside IV, however, gene and protein expressions of cardiac AT2 were upregulated by astragaloside IV. Both elevated gene and protein expressions of AT1 were not attenuated by astragaloside IV. CONCLUSION: Excessive activated rennin-angiotensin system in rats with pressure-overload induced cardiac hypertrophy is inhibited by astragaloside IV treatment.

[Effect of glaucocalyxin A on level of Th1/Th2 type cytokines in mice].

OBJECTIVE: To research the effect of glaucocalyxin A (GLA) on the level of Th1/Th2 type cytokines in mice. METHOD: By using flow cytometer with CBA software to detect Th1/Th2 type cytokines. RESULT: GLA had insighificant inhibitory effects on Th1 and Th2 cytokines (IL-2, IFN-gamma,TNF-alpha, IL-4 and IL-5) induced by ConA, in which more potential on cytokines from Th1 than those of from Th2 were displayed. However, GLA could produce inhibition on IL-2, IFN-gamma and TNF-alpha and acceleration on IL-4 and IL-5. CONCLUSION: Immunosuppressive effect of GLA is related to the influence the level of Th1/Th2 type cytokines.

[Study on screening immunocopetent position in Rabdosia amethystoieds (Benth.) Hara].

OBJECTIVE: To search for immunocompetent position in Rabdosia amethystoieds (Benth.) Hara. METHODS: Spleen cells of mice were stimulated by mitogen concannvalin A (ConA), and proliferation of lymphocytes were measured with tetrazolium salts (MTT) in vitro. With such immunopharmacological experiment, immunocompetent position of Rabdosia amethystoieds (Benth.) Hara directively were separated. RESULTS: FA and FC could promote proliferation, but FB and FD had stimulative and inhibitory effect respectively at different concentration. FB-1 and FB-2 had promotive effect but FB-3 and FB-4 had suppressive effect mainly. CONCLUSION: There are immunocomponents in Rabdosia amethystoieds (Benth.) Hara.

Effects of calycosin on the impairment of barrier function induced by hypoxia in human umbilical vein endothelial cells.

The purpose of the present study was to examine the effects of calycosin, an isoflavonoid isolated from Astragali Radix, on the impairment of barrier function induced by hypoxia in cultured human umbilical vein endothelial cells. Hypoxia induced an increase in endothelial cell monolayer permeability, indicating endothelial cell barrier impairment. Endothelial barrier dysfunction induced by hypoxia was accompanied by decreases in cytosolic ATP concentration and cAMP level, the development of actin stress fibers and intercellular gap formation, suggesting that the decreases in cytosolic ATP and cAMP levels and rearrangements of F-actin could be associated with an increase in permeability of endothelial monolayers. Application of calycosin inhibited the hypoxia-induced increase in endothelial permeability in a dose-dependent fashion, which is compatible with inhibition of lactate dehydrogenase release, decrease of the fall in ATP and cAMP contents, and improvement of F-actin rearrangements. These findings indicate that calycosin protected endothelial cells from hypoxia-induced barrier impairment by increasing intracellular energetic sources and promoting regeneration of the cAMP level, as well as improving cytoskeleton remodeling.