[Therapeutic effects of muscovite on ulcerative colitis in rats].

OBJECTIVE: To explore the efficacy of muscovite on iodoacetamide -induced ulcerative colitis in rats and elucidate its possible mechanism. METHODS: Ulcerative colitis was induced in female Sprague-Dawley (SD) rats by an intracolonic injection of iodoacetamide. A total of 48 rats were divided randomly(by the method of random digits table) into 6 groups: control group, model group, low-dose muscovite group (360 mg/kg), high-dose muscovite group (720 mg/kg), 5-aminosalicylie acid (5-ASA) group and muscovite plus 5-ASA group (combined treatment), and each group had 8 rats. The body weight, disease activity index (DAI), macroscopic damage and microscopic score of rats in each group were subsequently evaluated after dosing for 7 days. The protein levels of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8) and myeloperoxidase (MPO) activity were detected by enzyme-linked immunosorbent assay(ELISA) while the activity of nuclear facor(NF)-κB was determined by immunohistochemistry.One way ANOVA and rank-sum test were used. RESULTS: After doing, body weight macroscopic damage, microscopic score, TNF-α concentration, MPO and NF-κB activity of rats in each group were all significantly correlated with the dose of muscovite (r = 0.573, -0.647, -0.569, -0.681, -0.811, -0.842, all P < 0.05). High-dose muscovite group had no significant difference with 5-ASA group in body weightt, DAI, macroscopic damage, microscopic score, IL-8 concentration, TNF-α concentration, MPO and NF-κB activities((166 ± 5) vs (167 ± 5) g, 0.33 (0.00, 1.17) vs 0.17 (0.00, 0.83), 2.50 (2.00, 4.00) vs 3.00 (2.00, 3.00), 3.00 (2.00, 3.00) vs 2.50 (2.00, 3.00), (109 ± 17) vs (111 ± 15) pg/ml, (166 ± 38) vs (155 ± 45) pg/ml, (52 ± 6) vs (49 ± 4) U/g, 7.39 ± 0.42 vs 7.41 ± 0.34, all P > 0.05). The MPO and NF-κB activities of combined treatment group were lower than those of 5-ASA group((40 ± 4) vs (49 ± 4) U/g, 4.67 ± 0.72 vs 7.41 ± 0.34, all P < 0.05). However, other indices showed no significant difference with 5-ASA group (all P > 0.05). CONCLUSIONS: Rectal administration of muscovite ameliorates colonic inflammation of iodoacetamide-induced colitis. Its underlying mechanism is probably due to the regulation of inflammatory response. Muscovite may be a potential therapeutic agent for treatment of ulcerative colitis.

[Association of HAb18G with clinicopathologic features and prognosis in non-small cell carcinoma of lung].

OBJECTIVE: To study the association between HAb18G expression, tumor parameters, metastatic potential and prognosis in non-small cell lung carcinoma (NSCLC). METHODS: Immunohistochemical study for HAb18G protein using SP methods was carried out in 144 cases of NSCLC. Nineteen cases of benign lung lesions and 41 cases of normal lung tissue were used as controls. The intensity (positive unit/PU) of HAb18G expression was assessed quantitatively by image analysis software. The results were correlated with tumor parameters, metastatic potential and follow-up data. RESULTS: The intensity of HAb18G protein expression was significantly higher in NSCLC than that in controls (P = 0.000). In squamous cell carcinomas and adenocarcinomas, the expression of HAb18G protein in well-differentiated tumors was lower than that in moderately to poorly differentiated tumors (P = 0.001). Tumors of TNM stage IV had stronger expression than tumors of lower stages (P = 0.000). HAb18G PU was greater in tumors with lymph node metastasis than those without nodal metastasis (P = 0.045). The PU value of tumors with maximal diameter greater than 5 cm was higher than that of the smaller tumors (P = 0.000). It was also higher in male than in female patients (P = 0.046). There was no association between HAb18G protein expression and age of patients, history of smoking, tumor types and gross morphology (P > 0.05). The five-year survival rate in cases with low HAb18G protein expression was higher than that in cases with high expression (P = 0.006). Univariate analysis indicated that patients with high HAb18G protein expression carried a poor prognosis (P = 0.007). Multivariate analysis showed that expression of HAb18G protein was an independent prognostic factor in patients with NSCLC (P = 0.032, relative risk 3.962). CONCLUSIONS: HAb18G protein expression is associated with tumor progression and prognosis. It may represent a useful biomarker for prognostic evaluation.

Inhibition of miRNA-221 suppresses the airway inflammation in asthma.

This study investigated the expression of miRNA-221 in asthmatics in order to determine whether miRNA-221 plays a role in the development of asthma. Real-time PCR was used to detect the miRNA-221 in both asthmatic and control subjects. In addition, airway inflammation was evaluated by cell counting and tissue biopsy in the OVA-induced murine asthma model. miRNA-221 was differentially expressed in asthmatics and control subjects, and miRNA-221 blockade resulted in a reduction of airway inflammation in the OVA-induced murine asthma model. We conclude that miRNA-221 participates in the pathogenesis of asthma and that inhibition of miRNA-221 suppresses airway inflammation in asthmatics.

Involvement of mitochondrial pathway in NCTD-induced cytotoxicity in human hepG2 cells.

BACKGROUND: Norcantharidin, the demethylated analog of cantharidin derived from a traditional Chinese medicine, Mylabris, has been used in the treatment of anti-cancer effects. However, the detailed mechanisms underlying this process are generally unclear. The aim of this study was to investigate the mechanism of NCTD-induced apoptosis in HepG2 cells. METHODS: The cytotoxicity was measured by MTT assay for cellular viability and by flow cytometry. The mitochondrial membrane potential and reactive oxygen species production was evaluated by flow cytometry analysis. The role of caspase activities were assayed using caspase apoptosis detection kit . Western blot analysis was used to evaluate the level of Cyto-C, Bcl-2, Bax, Bid, caspase 3, -9, -8 and PARP expression RESULTS: After treatment with NCTD, a decrease in the viability of HepG2 cells and increase in apoptosis were observed. NCTD-induced apoptosis was accompanied by an increase in ROS production, loss of mitochondrial membrane potential and release of cytochrome c(cyto-c) from the mitochondria to the cytosol and down-regulation of anti-apoptotic protein Bcl-2 levels with concurrent up-regulation in pro-apoptotic protein Bax levels. However, another pro-apoptotic molecule, Bid, showed no change in such same treatment. NCTD-increased activity of caspase 9,caspase 3 and the subsequent cleavage caspase substrate PARP were also observed. The expression levels of pro-caspase-8 were not changed after NCTD treatment. CONCLUSION: These results indicate that NCTD induced cytotoxicity in HepG2 cells by apoptosis, which is mediated through ROS generation and mitochondrial pathway.