Aim To investigate the apoptosis of lung cancer cells A549 induced by quercetin and the regulation of survivin and Bcl-2 on A549 cells induced by quercetin.Methods MTT,fluorescence stain,flow cytometric analysis and immunocytochemistry stain were carried out.Results Quercetin had a significant inhibition on growth and proliferation of A549 cell in a concentration-and time-dependent manner.Evidence was provided that apoptosis occurred in A549 cells treated with quercetin using fluorescence microscopy.Quercetin arrested A549 cells at the G0/G1 phase by FCM analyses.Expression of survivin and Bcl-2 protein were decreased,and activity of caspase-3 were enhanced.Conclusion Quercetin could induce apoptosis of A549 cells.The arrested cell cycle and the down-regulation of survivin and Bcl-2 protein could activate caspase-3 resulting in cells apoptosis,which may contribute to the apoptosis mechanisms.The down-regulated survivin and Bcl-2 may play an important role in A549 cells apoptosis induced by quercetin.

Objective To assess the prediction value of Pmax and Pd on idiopathic paroxysmal atrial fibrillation(IPAF) and the possible mechanism of amiodrone preventing the recurrence of IPAF.Methods Pmax and Pd were measured in 60 patients with IPAF and 60 healthy control subjects by 12-lead surface electrocardiography. 30 of patients with IPAF were assigned to treatment with amiodrone for 6 months. Pd?Pmax and recurrence of IPAF were observed and compared with control group during the treatment.Results Pmax and Pd were found to be significantly higher in patients with IPAF than in healthy subjects[(126?17)ms vs(102?11)ms; (50?9)vs(29?8)ms,P

A microbial consortium of Trichoderma reesei AS3 3711, Aspergillus niger AS3 316 and Saccharomyces cerevisiae AS2 399 was constructed to decomposed rice chaff on the basis of the characters of each microorganism and the mechanism of cellulases In this experiment, rice chaff was pretreated with NaOH before fermentation so that the lignin structure of rice chaff was degraded and hemi cellulose was dissolved partly, which remove the protection of lignin and hemi cellulose on cellulose and demolish its special crystal structure After pretreatment, rice chaff can be degraded more easily with the microbial consortium The optimal technical paths and technological methods were achieved for intenerating rice chaff with the microbial consortium perfectly through orthogonal experiment According to the technological methods, some experiments were done at 30℃ with pH 4 5 It was found that the highest filter paper enzyme activity (FPA) was 5 64U/g and the ratio of cellulose degradation (RCD) was 28 05%

Nowadays potential preclinical drugs for the treatment of nonalcoholic steatohepatitis (NASH) have failed to achieve expected therapeutic efficacy because the pathogenic mechanisms are underestimated. Inactive rhomboid protein 2 (IRHOM2), a promising target for treatment of inflammation-related diseases, contributes to deregulated hepatocyte metabolism-associated nonalcoholic steatohepatitis (NASH) progression. However, the molecular mechanism underlying Irhom2 regulation is still not completely understood. In this work, we identify the ubiquitin-specific protease 13 (USP13) as a critical and novel endogenous blocker of IRHOM2, and we also indicate that USP13 is an IRHOM2-interacting protein that catalyzes deubiquitination of Irhom2 in hepatocytes. Hepatocyte-specific loss of the Usp13 disrupts liver metabolic homeostasis, followed by glycometabolic disorder, lipid deposition, increased inflammation, and markedly promotes NASH development. Conversely, transgenic mice with Usp13 overexpression, lentivirus (LV)- or adeno-associated virus (AAV)-driven Usp13 gene therapeutics mitigates NASH in 3 models of rodent. Mechanistically, in response to metabolic stresses, USP13 directly interacts with IRHOM2 and removes its K63-linked ubiquitination induced by ubiquitin-conjugating enzyme E2N (UBC13), a ubiquitin E2 conjugating enzyme, and thus prevents its activation of downstream cascade pathway. USP13 is a potential treatment target for NASH therapy by targeting the Irhom2 signaling pathway.