Nano-sized zeolites as modulators of thiacloprid toxicity on Chironomus riparius.

This study investigated whether zeolites of different size (Y30 (nano-sized) and H-Beta(OH)-III (forming large aggregates/agglomerates composed of 50 nm small primary particles)) exerted acute toxicity on larvae of the non-biting midge, Chironomus riparius, and whether such zeolites are able to modulate the toxicity of a common insecticide, thiacloprid, by means of adsorption of a dissolved toxicant. We conducted acute toxicity tests with fourth instar larvae of C. riparius. In these tests, larvae were exposed to zeolites or thiacloprid solely, or to mixtures of both compounds. The mixtures comprised 1.0 µg/L thiacloprid in addition to low (5.2 mg/L), medium (18.2 mg/L), and high (391.7 mg/L) zeolite concentrations, resulting in different adsorption rates of thiacloprid. As biological endpoints, changes in mortality rates and in behavior were monitored every 24 h over a total investigation period of 96 h. Furthermore, we conducted chemical analyses of thiacloprid in the medium and the larvae and located the zeolite particles within the larvae by LA-ICP-MS imaging techniques. Our results demonstrate that both types of zeolites did not exert acute toxicity when applied as single-substances, but led to reduced acute toxicity of thiacloprid when applied together with thiacloprid. These results are in line with the sorption properties of zeolites indicating reduced bioavailability of thiacloprid, although our data indicate that thiacloprid can desorb from zeolites to some extent. While freely dissolved (i.e., non-sorbed) fraction of thiacloprid was a good parameter to roughly estimate toxic effects, it did not correlate with measured internal thiacloprid concentrations. Moreover, it was shown that both zeolite types were ingested by the larvae, but no indication for cellular uptake of them was found.

Effects of sappanchalcone on the cytoprotection and anti-inflammation via heme oxygenase-1 in human pulp and periodontal ligament cells.

Sappanchalcone has been demonstrated to possess several biological effects. However, the molecular mechanism underlying these effects is not fully understood. In this study, we examined the effects of sappanchalcone on hydrogen peroxide (H(2)O(2))-induced cytotoxicity using human dental pulp (HDP) cells, and lipopolysaccharide (LPS)-induced inflammation using human periodontal ligament (HPDL) cells. Sappanchalone concentration proportionately increased heme oxygenase (HO)-1 protein expression and enzyme activity in both HDP and HPDL cells. It also protected HDP cells from H(2)O(2)-induced cytotoxicity and reactive oxygen species production. The cytoprotective effect of sappanchalcone was nullified by HO-1 inhibitor, Tin protoporphyrin (SnPP). Sappanchalcone is seen to inhibit LPS-stimulated nitric oxide (NO), prostaglandin E(2) (PGE(2)), interlukine-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interlukine-6 (IL-6) and interlukine-12 (IL-12) release in addition to inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in HPDL cells. SnPP, a specific inhibitor of HO-1, partly blocked sappanchalcone mediated suppression of inflammatory mediator production, in LPS-stimulated HPDL cells. HDP and HPDL cells treated with sappanchalcone exhibited the transient activation of c-Jun NH2-terminal kinase (JNK) and NF-E2-related factor-2 (Nrf2). The expression of HO-1 protein by sappanchalcone was significantly reduced by pretreatment with JNK inhibitor. In conclusion, induction of HO-1 is an important cytoprotective mechanism by which sappanchalcone protects HDP cells from H(2)O(2) and in addition it also exhibits anti-inflammatory effects in LPS-stimulated HPDL cells. Thus, sappanchalcone could potentially be a therapeutic approach for periodontal, pulpal and periapical inflammatory lesion.

The role of intestinal microflora on daidzein excretion in urine in humans treated with Chungpesagantang.

This study examined the relationship between the metabolism of the constituents of herbal medicines by human intestinal microflora and the level of metabolites excreted in the urine. This was performed by administering Chungpesagantang (CST) to volunteers and measuring their fecal metabolic activity CST to and urine excretion of daidzein, one of the metabolite of CST The metabolic activity of of CST dadizein was 54.8 +/- 16.7 mmol/h/g wet feces. When CST was administered orally to the subjects, the amount of daidzein excreted in the urine over 24 h was 103.7 +/- 55.8 mg, which accounted for 20.2% of the puerarin, daidzin and daidzein contained in CST. However, neither puerarin nor daidzin were excreted in the urine. The profile of daidzein excreted in the urine was found to be in proportion to that of the metabolic activity of the CST components. This suggests that the daidzein level excreted in the urine of the subjects administered CST is associated with the daidzein glycoside-hydrolyzing activity of the fecal microflora.

Control of IgE and selective T(H)1 and T(H)2 cytokines by PG102 isolated from Actinidia arguta.

BACKGROUND: Various allergic responses are thought to result from the unbalanced development of T(H)1 and T(H)2 pathways and, subsequently, the overproduction of IgE. Therefore the modulation of T(H)1 and T(H)2 responses is a rational strategy for the treatment of allergic diseases. OBJECTIVE: The present study was performed to investigate the immune-modulating activities of PG102 preparations from Actinidia arguta in ovalbumin-sensitized murine models. METHODS: Two preparations from A arguta, PG102T and PG102E, were chosen for animal experimentation on the basis of their ability to regulate the production of IgE in U266B1 cells. The changes in splenic levels of cytokines and plasma levels of immunoglobulin isotypes were examined. The effects of PG102 on subcellular composition (CD4(+)IL-4(+) or CD19(+)IgE(+) cells), IgE production in B cells, and selective transcription factors were analyzed. RESULTS: Oral administration of PG102T and PG102E significantly decreased the level of selective T(H)2 cytokines, whereas it increased the level of T(H)1 cytokines. The differential effects of PG102T and PG102E on T(H)1 and T(H)2 cytokines were accompanied by a decrease in the plasma levels of IgE and IgG1 and by an increase in the plasma level of IgG2a. The percentages of both IL-4-producing T cells and IgE-producing B cells were decreased. The concentration of IgE produced within B cells also appeared to be reduced. Finally, PG102T and PG102E downregulated the level of GATA-binding protein 3, while inducing that of T-box transcription factor and nuclear factor of activated T cells c2. CONCLUSION: PG102T and PG102E have great potential as orally active immune modulators for the therapy of various allergic diseases.