[Current evaluation situation and research strategies on enhanced immune function of health food containing Chinese materia medica].

At present,the function evaluation of health food containing Chinese materia medica is in lack of theoretical support of Chinese medicine,which can't reflect the function characteristics,dose-effect relationship and mechanism of functional food. What' s more,the evaluation technology of health food containing Chinese materia medica is relatively lagging behind and has been abolished now,which seriously restricts the development of health food containing Chinese materia medica industry. The proportion of health food containing Chinese materia medica with enhancing immune function is the highest among approved products,which is up to 30.33%. By collecting,analyzing and digging the current evaluation situation of enhancing immune function of health food containing Chinese materia medica,this paper has shown that there is no difference between health food containing Chinese materia medica evaluation and other functional food evaluation. What's more,there is a lack of characteristics of traditional Chinese medicine(TCM). The technological means including evaluation of immune active substances is under-developed and the immune cell evaluation needs to be refined and improved urgently,restricting the development of health food containing Chinese materia medica industry. Therefore,the evaluation of the enhanced immune function of health food containing Chinese materia medica should be guided by health-preserving theory in TCM,and based on the identification of TCM constitution for its claim of health function. With TCM theory and modern scientific technological means,a new evaluation model for immune function enhancement of health food containing Chinese materia medica is put forward to distinguish it from other functional food and traditional medicines. Formulation of the evaluation technology and technical specifications suitable for health food containing Chinese materia medica can fundamentally ensure the healthy,orderly,fast and sustainable development of health food containing Chinese materia medica industry.

SOCS3 Is Upregulated and Targeted by miR30a-5p in Allergic Rhinitis.

BACKGROUND: Suppressor of cytokine signaling 1 (SOCS1) and SOCS3 play important roles in T helper cell differentiation, which is involved with the pathologic mechanisms of allergic rhinitis (AR). The aim of this study was to evaluate the expression of SOCS1 and SOCS3 in AR and find their regulatory microRNAs (miRNAs) to provide a basis for the treatment of AR. METHODS: The expression of SOCS1 and SOCS3 were analyzed by real-time PCR, immunohistochemistry, and Western blot. The correlative regulatory miRNAs were detected by real-time PCR. Luciferase assays and AR mouse model experiments were applied to identify correlative miRNAs that target SOCS3. RESULTS: SOCS1 and SOCS3 mRNA were upregulated in the nasal mucosa and peripheral blood mononuclear cells of AR compared with controls. The expression of SOCS3 protein was significantly increased in the nasal mucosa of AR. The immunohistochemical staining results showed that SOCS3 was similarly localized in the superficial epithelium, submucosal glands, and vascular endothelium in the nasal mucosa of AR subjects and controls. However, SOCS3 protein was especially localized in the inflammatory cells, such as eosinophils, monocytes, and lymphocytes. CONCLUSIONS: SOCS3 was targeted by miR30a- 5p in AR. Further study should be performed to identify the regulatory effect of miR30a-5p in AR, which may provide insights into a new therapeutic strategy.

Microarray gene analysis of Toll-like receptor signaling elements in chronic rhinosinusitis with nasal polyps.

OBJECTIVE: To identify the regulatory mechanisms of Toll-like receptor (TLR)-associated genes in chronic rhinosinusitis (CRS) with nasal polyps (NP) using gene microarray analyses. METHODS: We pooled: (1) NP biopsy specimens from 10 nonatopic CRS patients and (2) healthy mucosal tissue from 10 additional nonatopic healthy patients (controls). These pooled samples were evaluated by gene microarrays that included 125 genes for TLRs and associated signaling elements. To validate gene product expressions, 20 NP and 15 normal nasal turbinate tissues were evaluated for TLR-9 expression by immunohistochemical staining and Western blots using samples from gland cells, epithelial cells, and mononuclear cells cytologically identified by HE staining. RESULTS: In pooled NP samples compared to pooled controls, 4 genes were upregulated (≥ 2-fold higher expression) and 19 were downregulated (≤ 0.5-fold lower expression). TLR-9 was an upregulated gene in NP tissue. Compared to control tissue, there were significantly higher percentages of TLR-9 positively stained NP gland cells, epithelial cells, and mononuclear cells (p < 0.001). On Western blots, while both normal and NP tissues expressed TLR-9 protein, the expression was significantly more pronounced for NP tissue (p < 0.001). CONCLUSIONS: Inflammation associated with CRS may be due to dysregulated innate immune elements, particularly TLR-9 and its associated signal transduction elements, which may impact upon prolonged activation of adaptive immune responses in the sinonasal mucosa.

[Expression and distribution of Fas and Fas-L in the nasal polyps].

OBJECTIVES: To confirm the expression and distribution of Fas and Fas-L in the nasal polyps and to illustrate the role of the Fas/Fas-L system in the pathogenesis of human nasal polyps. METHODS: Investigating the transcripts of the Fas/Fas-L gene in 30 human nasal polyp tissues and 30 nasal turbinate mucosa specimens using reverse transcription-polymerase chain reaction. Localization of Fas/Fas-L was performed with immunohistochemistry. RESULTS: The transcripts of the Fas/Fas-L gene were detected at similar levels in both polyps and nasal mucosa. There was a significant overexpression of Fas-L protein on nasal polyps (epithelium: 25 +/- 21, glands: 19 +/- 14) compared to nasal mucosa (epithelium: 14 +/- 13, glands: 12 +/- 10), (t = 1.66, P < 0.01), while Fas was overexpressed on nasal mucosa (epithelium: 17 +/- 11, glands: 17 +/- 13) compared to nasal polyps (epithelium: 13 +/- 10, glands: 11 +/- 9), (t = 1.98, P < 0.01). Fas-L positive cells were localized on the epithelial layers of cystically dilated glands and the down-growing epithelium of nasal polyps. Fas positive cells were localized on the cilia of the epithelial of nasal mucosa and mainly on the infiltrative cells. CONCLUSION: Fas/Fas-L may play an important role on the pathogenesis of human nasal polyps, including cystic degeneration of submucosal glands, apoptosis and conferring of immune privilege to nasal polyp formation.