Effects and mechanism of Chinese medicine Jiawei Yupingfeng in a mouse model of allergic rhinitis / 中西医结合学报

OBJECTIVE@#Chinese medicine has the potential to modulate allergic rhinitis (AR). There have been studies investigating the treatment efficacy of Yupingfeng San, alone or in combination with other ingredients, in AR, though few have studied the potential mechanisms of these drugs. In the present study, we measured the effects of Jiawei Yupingfeng (JWYPF), a traditional Chinese medicine formula, on mice with ovalbumin-induced AR and explored its underlying mechanism of action.@*METHODS@#Forty BALB/c mice were randomly divided into normal control, allergy control and two treatment groups of ten mice each. In the normal control group, mice were sensitized and challenged with saline. The mice in the allergy control and treatment groups were sensitized and challenged with ovalbumin and aluminum hydroxide gel. The treatments of JWYPF and Nasonex were administered intranasally in the AR mice for one week. Several signs of allergic inflammation, such as nasal eosinophils and inflammatory cytokines, were measured to determine the underlying mechanisms.@*RESULTS@#Mice in the JWYPF and Nasonex groups had significantly lower AR symptom scores than those in the allergy control group (the mean differences between JWYPF and the allergy control, and Nasonex and the allergy control were -2.00 ± 0.35 and -2.40 ± 0.32). After treatment with JWYPF and Nasonex, the levels of ovalbumin-specific IgE and histamine were significantly reduced, as were the levels of interlukin-4 and transforming growth factor-β, while interferon-γ levels were increased (all P < 0.0001, vs. allergy control). These two treatments also significantly inhibited eosinophil and mast cell infiltration into the nasal cavity but were not statistically different from one-another.@*CONCLUSION@#JWYPF has a potential therapeutic effect on AR via adjusting the rebalance of T helper 1 and T helper 2.

Panax Notoginseng Saponin Attenuates Gastric Mucosal Epithelial Cell Injury Induced by Dual Antiplatelet Drugs through COX and PI3K/Akt/ VEGF-GSK-3β-RhoA Network Pathway / 中国结合医学杂志

OBJECTIVE@#To elucidate the underlying mechanism of Panax notoginseng saponin (PNS) on gastric epithelial cell injury and barrier dysfunction induced by dual antiplatelet (DA).@*METHODS@#Human gastric mucosal epithelial cell (GES-1) was cultured and divided into 4 groups: a control, a DA, a PNS+DA and a LY294002+PNS+DA group. GES-1 apoptosis was detected by flow cytometry, cell permeability were detected using Transwell, level of prostaglandins E2 (PGE2), 6-keto-prostaglandin F1α (6-keto-PGF1α) and vascular endothelial growth factor (VEGF) in supernatant were measured by enzyme linked immunosorbent assay (ELISA), expression of phosphatidylinositide 3-kinase (PI3K), phosphorylated-PI3K (p-PI3K), Akt, phosphorylated-Akt (p-Akt), cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), glycogen synthase kinase-3β (GSK-3β) and Ras homolog gene family member A (RhoA) were measured by Western-blot.@*RESULTS@#DA induced apoptosis and hyper-permeability in GES-1, reduced supernatant level of PGE2, 6-keto-PGF1α and VEGF (P<0.05). Addition of PNS reduced the apoptosis of GES-1 caused by DA, restored the concentration of PGE2, 6-keto-PGF1α and VEGF (P<0.05). In addition, PNS attenuated the alteration of COX-1 and COX-2 expression induced by DA, up-regulated p-PI3K/p-Akt, down-regulated RhoA and GSK-3β. LY294002 mitigated the effects of PNS on cell apoptosis, cell permeability, VEGF concentration, and expression of RhoA and GSK-3β significantly.@*CONCLUSIONS@#PNS attenuates the suppression on COX/PG pathway from DA, alleviates DA-induced GES-1 apoptosis and barrier dysfunction through PI3K/Akt/ VEGF-GSK-3β-RhoA network pathway.

Elicitation of mismatch negativity and its influence from stimuli deviant in the healthy youth / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To work out the elicitation plan, obtain the mismatch negativity (MMN) and get out the laboratory normal value as well as to study the influence to MMN from the deviation of auditory stimuli.</p><p><b>METHODS</b>Hearing test of the tone burst stimulation was performed on 21 healthy young volunteers according to oddball stimulation sequence. Each subject was performed two kinds of auditory stimuli including frequency deviant stimuli and intensity deviant stimuli, and of each one included three series of stimulation. MMN was gained by subtracting the ERP of deviant stimuli from the ERP of standard stimuli. The latency and amplitude of each MMN were recorded, and then the effect of the deviant extent for MMN was analyzed.</p><p><b>RESULTS</b>By this setup the MMN of normal young people was recorded and normal value of latency and amplitude of MMN were got. In the group of frequency deviant stimuli, the MMN latency [(155.81 +/- 29.08) ms], if the frequency was up to 2000 Hz, was shorter than that when the frequency deviance was 1000 Hz [(182.89 +/- 45.85) ms, (183.32 +/- 43.33) ms] (P = 0.033, 0.030); when the deviant extent were the same, the latency had no obvious difference if changing the frequency of the standard and deviant stimuli (P = 0.973); the MMN amplitude of three groups [(3.85 +/- 2.22) microV, (2.90 +/- 2.05) microV, (2.66 +/- 2.12) microV] had no obvious difference among them (P > 0.05). In the group of intensity deviant stimuli, the MMN latency [(157.04 +/- 34.87) ms], if the frequency was up to 20 dB, was shorter (P = 0.025, 0.017) than that when the intensity deviance was 10 dB [(184.46 +/- 38.05) ms, (186.24 +/- 42.36) ms]. When the deviant extent were the same, the latency had no obvious difference (P = 0.882) if changing the intensity of the standard and deviant stimuli but only group 4 and group 6 [(3.41 +/- 1.64) microV, (2.37 +/- 1.47) microV] were different in evidence (P = 0.031) while the others had no obvious difference (P = 0.524, 0.122).</p><p><b>CONCLUSIONS</b>MMN was only related to the difference between standard stimuli and deviant stimuli, but there was no relationship between MMN and the notice, which indicate that MMN could objectively reflect the capability of brain to detect the change of stimuli. MMN is the representation of brain high-level sensory function.</p>