Antibacterial peptides inhibit MC3T3-E1 cells apoptosis induced by TNF-α through p38 MAPK pathway.

BACKGROUND: Antimicrobial peptides (AMP), as a small molecular polypeptide with a broad antibacterial spectrum and high efficiency, have attracted more and more attention. Few pieces of research on the effect of the antimicrobial peptide on osteoblast under inflammatory conditions have so far been reported. The main aim of this work was to investigate the antiapoptosis effect of the antimicrobial peptide on MC3T3-E1 cells induced by TNF-α and its related mechanism. METHODS: Rat MC3T3-E1 cells were co-cultured with different concentrations of antibacterial peptide DP7 and TNF-α.MTS assay, cell scratch test, alkaline phosphatase activity, and alizarin red staining assay were used to determine osteoblast viability in this experiment. Annexin V-FITC/PI double staining cells and flow cytometry were used to analyze apoptosis and Western blot assay detection to show mitogen-activated protein kinase (MAPK) protein expression in rat MC3T3-E1 cells. Then, Realtime polymerase chain reaction (PCR) was used to examine the caspase-3 gene expression. Also, ELISA detection was used to clarify the anti-apoptotic effect of the p38 MAPK inhibitor, SB203580, on cells' apoptosis. RESULTS: Antimicrobial peptide could promote the proliferation, migration, and osteogenic ability of MC3T3-E1 cells induced by TNF-α, but inhibit cell apoptosis rate (P<0.05), and the effect was concentration-dependent. Western blot results showed after TNF-αtreatment, the expression of p-p38 MAPK in the MC3T3-E1 cells increased after TNF-α and antimicrobial peptide cotreatment, TNF-α induced p-p38 MAPK phosphorylation was inhibited, and the difference was statistically significant (P<0.05). Realtime PCR results showed that the gene expression of caspase-3 mRNA was up-regulated after TNF-α treatment, while their expression was down-regulated after cultured with TNF-α and antimicrobial peptide. Elisa's analysis showed that cell apoptosis increased after TNF-α treatment alone, and cell apoptosis was reduced to the normal levels when combined with antimicrobial peptide, and cell apoptosis induced by TNF-α was partially abolished when combined with SB203580. CONCLUSIONS: Antimicrobial peptide DP7 could inhibit MC3T3-E1 cells apoptosis induced by TNF-α, and the effect was concentration-dependent. The antiapoptosis activation of the antimicrobial peptide on MC3TE-E1 cells may be related to the inhibition of the p38 MAPK pathway.

The effectiveness of adjustable oral appliance for older adult patients with obstructive sleep apnea syndrome.

BACKGROUND: Oral appliance (OA) treatment for obstructive sleep apnea syndrome (OSAS) has attracted more and more attention due to its low price, comfort, portable and non-invasion. This study aimed to investigate the clinical effectiveness of adjustable oral appliance on older adult patients with OSAS. METHODS: Thirty older adult patients diagnosed with OSAS were chosen as the study participants and received an adjustable OA for 6 months. Then, the patients were subjected to a polysomnographic examination, Berlin Questionnaire (BQ) scale questionnaire, and cone beam computer tomography (CBCT) analytical measurement to evaluate their symptom improvement and the morphologic changes of the upper airway. RESULTS: After treatment with adjustable oral appliance for six months, the results showed that there was an improvement of different degrees in the subjective symptoms. Apnea hypopnea index (AHI) had decreased from (27.65±1.31) per hour to (6.74±0.75) per hour (P<0.05); the maximum apnea time (MAT) had decreased from 43.82±2.69 to 21.37±3.18 s (P<0.05); the average oxygen saturation (MSaO2) had increased from (89.24±7.27)% to (92.69±4.46)%; the lowest oxygen saturation (LSaO2) from (81.85±8.31)% to (86.93±4.45)%. Moreover, the CBCT scanning analysis showed that the minimal sagittal diameter, sectional area, and the volume of the palatopharynx, as well as the sagittal diameter and volume of the glossopharynx significantly increased. CONCLUSIONS: The adjustable OA had considerable clinical efficacy and comfort in older adult OSAS patients by enlarging the palatopharynx and glossopharynx.

Effect of regulating platelet function on systemic inflammatory response and pul-monary oxygenation function in rats during extracorporeal circulation / 中国免疫学杂志

Objective:To investigate the effect of regulating platelet function on systemic inflammatory response and pulmonary oxygenation function in rats during extracorporeal circulation(ECC).Methods:The rats participating in the ECC model were randomly divided into ECC supplemented platelet group (group MH),ECC supplemented plasma group (group MP),and continuous pump Tirofiban+ECC supplemented platelet group (group TMH),with 8 rats in each group.Rats of the three groups lasted two hours with ECC,observed for two hours after operation.Enzyme linked immunosorbent assay (ELISA) was used to detect inflammatory factors in the plasma and bronchoalveolar lavage fluid of rats in the three groups.The oxygenation index and lung tissue water content were meas-ured.The number of circulating endothelial quantity was measured by flow cytometry,and pathological changes of lung tissue in rats were observed by hematoxylin eosin staining.The effects of regulating platelet function on the levels of systemic inflammatory response, the degree of vascular endothelial damage,the edema degree of lung tissue and pulmonary oxygenation function of ECC rats were analyzed.Results:There was no significant difference in platelet count between group MH and group MP after two hours with ECC(P>0.05),the group TMH was significantly higher than that in group MH and group MP (P<0.05).After two hours with ECC,the oxygenation indexes of the three groups were lower than that at the beginning of ECC(P<0.05).There was no significant difference in lung tissue water content between the three groups(P>0.05);the level of neutrophil elastase(NE) in bronchoalveolar lavage fluid of rats in group MH was lower than that in group TMH(P<0.05),the level of NE in plasma of group TMH was lower than that in group MP (P<0.05).At the end of ECC,there were no statistically significant differences in circulating endothelial quantity of the three groups (P>0.05).Pathological examination of lung tissue showed that the lung interstitium of group MH was thinner than that of other groups,and inflammatory cell infiltration was less.Conclusion:At the early stage of ECC,supplement fresh platelets after platelet sharp decrease can significantly reduce the inflammatory response in the circulation.The protective effect may be related to platelets adhere to the endothelium associated with ECC related inflammatory reactions,and decrease the neutrophils and endothelial tissue adhesion.It is suggested that certain number of platelets with normal adhesion and aggregation function in ECC may reduce inflammatory response and lung injury after operative,and improve prognosis.

CYP1A1 polymorphism interactions with smoking status in oral cancer risk: evidence from epidemiological studies.

The cytochrome CYP1A1 gene has been implicated in the etiology of oral cancer. However, the results have been inconsistent. In this study, a meta-analysis was performed to clarify the associations of polymorphisms in CYP1A1 gene with oral cancer risk. Published literatures from PubMed, MEDLINE, EMBASE, and China National Knowledge infrastructure (CNKI) databases were retrieved. A total of 12 studies were included in this meta-analysis. We found that significant positive associations between CYP1A1*2A polymorphism and oral cancer risk in recessive model (CC vs. TC + TT, OR = 1.93), dominant model (CC + TC vs. TT, OR = 1.33), and additive model (CC vs. TT, OR = 1.97). In subgroup analysis based on the ethnicity of study population, significant associations were found in all three genetic models for Asians (recessive OR = 2.29, 95% CI = .42-3.71; dominant OR = 1.54, 95% CI = 1.03-2.31; additive OR 2.39, 95% CI = 1.47-3.88) but not non-Asians. For the smoking stratification, the result indicated a significant association between CYP1A1*2A polymorphism and oral cancer among the smoking subjects (OR = 1.83, 95% CI = 1.47-2.26). This meta-analysis indicated a marked association of CYP1A1*2A polymorphisms with oral cancer risk, particularly among Asians, whereas there were significant interactions between the polymorphisms and cigarette smoking on oral cancer risk.