RESUMO
Objective To detect the immunoregulation and clinical effect ofYupingfeng capsule combined with Seretide on patients with cough variant asthma (CVA).Methods CVA Patients were randomly divided into the Seretide control group (n=54) andYupingfeng capsule combined with Seretide group (n=54). Seretide group received inhaled Seretide. Combined traditional Chinese medicine group received Seretide and Yuping Feng capsule. Two groups were treated for 12 weeks. The IL-17, IL-10 and IL-6 expression was detected by ELISA analysis. The clinic effect rate and adverse events were compared.Results After treatment, compared with the Seretide group, the expression of IL-17 (18.72 ± 4.26 ng/mlvs. 26.17 ± 5.58 ng/ml;t=2.462,P<0.05) and IL-6 (21.58 ± 4.12 ng/mlvs. 30.66 ± 6.27 ng/ml;t=2.523,P<0.05) were significantly lower in combined traditional Chinese medicine group than that in Seretide group; and IL-10 (15.56 ± 2.74 ng/mlvs. 12.25 ± 2.81 ng/ml;t=2.244, P<0.05) was significantly higher in combined traditional Chinese medicine group. The daytime (1.12 ± 0.26 vs.1.42 ± 0.33,t=2.283) and night time cough score (1.24 ± 0.28vs. 1.52 ± 0.37,t=2.291) in combined traditional Chinese medicine group was significantly lower than that in Seretide group (P<0.05). The clinic effect rate (92.6%vs. 77.8%,χ2=2.438) in combined traditional Chinese medicine group was significantly higher than that in Seretide group (P=0.037).ConclusionYupingfengcapsule combined with Seretide can decrease IL-17 expression and increase IL-10 expression to inhibit inflammatory reaction in CVA patients, and showed significantly higher clinical effect rates.
RESUMO
Bismuth oxide bromide, BiOBr, was used to catalyze the degradation of microcystin-LR (MC-LR) in water at neutral pH under visible light. During the investigation, twelve intermediates from MC-LR decomposition were identified by LC-MS. In addition to attacking MC-LR at the typically susceptible sites (i.e., the conjugated double bond of the Adda chain and terminal unsaturated bond of the Mdha chain), the BiOBr photocatalyst has the remarkable ability to decarboxylate the free acid groups on d-glutamic acid (Glu) and methyl-d-aspartic acid (MeAsp). This reactivity has not been previously observed with TiO2 photocatalysis or with other MC-LR treatments in which decarboxylation does not occur until the MC-LR ring has been cleaved or mineralized to CO2. Some expected intermediate products were detected with oxygen-18 labeling by using H2(18)O as the solvent to confirm that the decarboxylation process is mediated by BiOBr. Results from characterizing the intermediates as well as oxygen-18 labeling studies indicates that oxidative decarboxylation of MC-LR by BiOBr photocatalysis is not always initiated by hydroxyl radical attack (and/or interaction with a hole followed by hydrolysis) proposed mechanism in TiO2 photocatalysis, whereas likely caused by a direct interaction between photoinduced hole of BiOBr and free carboxyl groups of MC-LR. This unusual decarboxylation behavior seems to be associated with the particular valence band and conduction band state of BiOBr photocatalyst. Also under BiOBr catalysis, a very stable guanidine group of l-arginine (l-Arg) that is nonreactive with TiO2 photocatalysis is converted to an amino group and subsequently oxidized to a nitro group during the decomposition of MC-LR. This reaction sequence is also related to decarboxylation because the guanidine conversion requires a completely or partially decarboxylated precursor. Our results indicate that BiOBr, a photocatalyst that selectively destroys sites crucial to MC-LR toxicity, shows great promise as a means of effectively treating drinking water.
