The aim of this study was to fabricate biomatrix/polymer hybrid scaffolds using an electrospinning technique. Then tissue engineered heart valves were engineered by seeding mesenchymal stromal cells (MSCs) onto the scaffolds. The effects of the hybrid scaffolds on the proliferation of seed cells, formation of extracellular matrix and mechanical properties of tissue engineered heart valves were investigated. MSCs were obtained from rats. Porcine aortic heart valves were decellularized, coated with poly(3-hydroxybutyrate-co-4-hydroxybutyrate) using an electrospinning technique, and reseeded and cultured over a time period of 14 days. In control group, the decellularized valve scaffolds were reseeded and cultured over an equivalent time period. Specimens of each group were examined histologically (hematoxylin-eosin [HE] staining, immunohistostaining, and scanning electron microscopy), biochemically (DNA and 4-hydroxyproline) and mechanically. The results showed that recellularization was comparable to the specimens of hybrid scaffolds and controls. The specimens of hybrid scaffolds and controls revealed comparable amounts of cell mass and 4-hydroxyproline (P>0.05). However, the specimens of hybrid scaffolds showed a significant increase in mechanical strength, compared to the controls (P<0.05). This study demonstrated the superiority of the hybrid scaffolds to increase the mechanical strength of tissue engineered heart valves. And compared to the decellularized valve scaffolds, the hybrid scaffolds showed similar effects on the proliferation of MSCs and formation of extracellular matrix. It was believed that the hybrid scaffolds could be used for the construction of tissue engineered heart valves.

This study was aimed to investigate the effects of Shen-Y uan Y i-Qi Huo-Xue (SYYQHX) capsule com-bined with early percutaneous coronary intervention (PCI) on near-term quality of life (QOL) in unstable angina (UA) patients. Seventy-eight patients diagnosed with UA were selected and randomly divided into the treatment group and control group, with 39 patients in each group. Early PCI was undergone after coronary angiography. Before PCI, the control group was given routine western medication. The treatment group was given routine western medication plus SYYQHX capsule, three pills once, three times daily. The treatment lasted for 30 days. The QOL scores were evalu-ated among patients from both groups before and after treatment in order to determine the efficacy on angina, electro-cardiogram (ECG) and traditional Chinese medicine (TCM) main symptom. The results showed that compared to pre-treatment, the scores of physical limitation (PL), angina stability (AS), angina frequency (AF), and treatment satisfac-tion ( TS ) were significantly increased after treatment ( P < 0 . 05 ) . Compared with the control group , after treat-ment with SYYQHX capsule, the AF, duration time and symptoms of palpitation, fatigue and shortness of breath were obviously improved (P< 0.05). The scores of AS, AF and TS in the treatment group were significantly increased (P < 0.05). It was concluded that SYYQHX capsule combined with early PCI can improve the near-term QOL and TCM main symptoms among UA patients.

The aim of this study was to fabricate biomatrix/polymer hybrid scaffolds using an elec-trospinning technique. Then tissue engineered heart valves were engineered by seeding mesenchymal stromal cells (MSCs) onto the scaffolds. The effects of the hybrid scaffolds on the proliferation of seed cells, formation of extracellular matrix and mechanical properties of tissue engineered heart valves were investigated. MSCs were obtained from rats. Porcine aortic heart valves were decellularized, coated with poly(3-hydroxybutyrate-co-4-hydroxybutyrate) using an electrospinning technique, and reseeded and cultured over a time period of 14 days. In control group, the decellularized valve scaffolds were re-seeded and cultured over an equivalent time period. Specimens of each group were examined histologi-cally (hematoxylin-eosin [HE] staining, immunohistostaining, and scanning electron microscopy), bio-chemically (DNA and 4-hydroxyproline) and mechanically. The results showed that recellularization was comparable to the specimens of hybrid scaffolds and controls. The specimens of hybrid scaffolds and controls revealed comparable amounts of cell mass and 4-hydroxyproline (P>0.05). However, the specimens of hybrid scaffolds showed a significant increase in mechanical strength, compared to the controls (P<0.05). This study demonstrated the superiority of the hybrid scaffolds to increase the me-chanical strength of tissue engineered heart valves. And compared to the decellularized valve scaffolds,the hybrid scaffolds showed similar effects on the proliferation of MSCs and formation of extracellular matrix. It was believed that the hybrid scaffolds could be used for the construction of tissue engineered heart valves.

Objective: To investigate the effects of different expression of monoacylglycerol lipase (MAGL) in tumor-associated macrophages (TAMs) with the proliferation of MHCC97H human liver cancer cells in vivo and its mechanism. Methods: Human peripheral blood-derived monocyte was induced to differentiate into M2-type TAMs and was identified by flow cytometry. The co-culture model of TAMs and MHCC97H human liver cancer cells was established, and the expression of MAGL in TAMs cells was detected by qRT-PCR. The expression of MAGL in TAMs cells was detected by plasmid transfection. ELISA and qRT-PCR was used to detect the mRNA expression levels and secretion levels of inflammatory factors in TAMs cells. The subcutaneous tumor model of MHCC97H mice was constructed to observe the effect of different expression of MAGL in TAMs cells with the proliferation of MHCC97H human liver cancer cells in vivo. F-test was used for the measurement of homogeneity of variance between two independent samples. A t-test was used for homogeneity of variance, and the corrected t-test was used for non-homogeneity of variance. Results: Human peripheral blood-derived monocytes were successfully induced to differentiate into M2-type TAMs. An in vitro co-culture model was established. qRT-PCR showed that MHCC97H human liver cancer cells significantly down-regulated the expressional level of MAGL in TAMs cells. The constructed subcutaneous tumor model of mice demonstrated that up-regulation up-regulation of MAGL expression in M2-type TAMs inhibited the proliferation of MHCC97H human liver cancer cells in vivo. Furthermore, the mechanistic study illustrated that the high expression of MAGL promoted the transcription and secretion of inflammatory factors such as interleukin-1 beta, interleukin-6 and tumor necrosis factor-alpha in M2-type TAMs cells. Conclusion The overexpression of MAGL inhibits the proliferation of MHCC97H hepatocellular carcinoma cells in vivo, and its mechanism may be associated to the release of inflammatory factors that from TAMs cells.

Based on network pharmacology and in vitro assays,we conducted a collaborative investi-gation into the protective effects of ginsenosides Rg1 and Re on LPS-induced damage of porcine je-junal epithelial cells IPEC-J2.Network pharmacology was used to obtain and screen the intersec-ting targets of Rg1 and Re to alleviate intestinal barrier damage,and molecular docking technique was used to verify the predicted results of network pharmacology.The experiment included the Control group,LPS group,Rg1 group,and Re group.The effects of different concentrations of Rg1 and Re on cell survival rate,apoptosis rate,TEER value,FD4 permeability,and inflammatory fac-tors of IPEC-J2 were observed,and the effects of different concentrations of Rg1 and Re on the mRNA expression levels of apoptosis-related genes were also detected by fluorescence quantitative PCR.The results of network pharmacology showed that the prevention of intestinal barrier damage by Rg1,Re mainly involved the processes of PI3K-Akt and MAPK signaling pathways.The molec-ular docking results showed that the binding energy of Rg1 to all intersecting targets was less than 0,while that of ginsenoside Re to SRC targets only was less than 0.In vitro experiments showed that pretreatment with different concentrations of Rg1 and Re increased the survival rate and TEER value of LPS-treated IPEC-J2 to varying degrees,and reduced the apoptosis,the decrease of FD4 permeability,and the secretion of inflammatory factor TNF-α,suggesting that Re and Rg1 prevented the intestinal barrier from damage.It was shown that Re and Rg1 could effectively re-duce the effects of LPS treatment on IPEC-J2 cells.Rg1 significantly upregulated the mRNA ex-pression levels of MAPK8,MAPK10,HRAS,and significantly down-regulated the mRNA expres-sion levels of MAP2K1,PIK3CG,IL-2 and SRC;and Re significantly upregulated the mRNA ex-pression levels of MAPK8,MAPK10,HRAS,and PIK3R1,BCL2 gene mRNA expression levels.These results suggest that ginsenosides Rg1,Re and ginsenoside products containing Rg1 and Re deserve further investigation in preventing intestinal barrier damage in piglets.

BACKGROUND: Docetaxel is a commonly used anti-tumor drug in clinic, especially as the first-line drug for advanced non-small cell lung cancer (NSCLC). However, the molecular mechanism of docetaxel against NSCLC is still unclear. Increasing studies have shown that metabolic reprogramming of tumor cells plays an important role in tumorigenesis. The aim of this study was to investigate the effects of docetaxel on the metabolic pathway of NSCLC cells based on metabolomics analysis and biological means. METHODS: First, we performed CCK8 assay to analyze the effects of docetaxel on cell viability of NSCLC cells and also to screen the appropriate drug concentration. Then, the differential metabolites of docetaxel-treated and untreated NSCLC cells were analyzed by gas chromatography-mass spectrometry based metabolomics. Finally, the effects of docetaxel on the expression levels of key enzymes that regulate the relevant metabolic pathways were determined by Western blot. RESULTS: Docetaxel inhibited cell viability of A549 and H1299 cells in a concentration- and time-dependent manner. With the prolonged treatment time of docetaxel, the apoptotic sensitive protein poly (ADP-ribose) polymerase (PARP) was gradually activated to form a P89 fragment. Metabolomics analysis showed that eight metabolites were significantly changed in both A549 and H1299 cells following docetaxel treatment, which were mainly in the tricarboxylic acid (TCA) cycle pathway. Moreover, after docetaxel treatment, the protein expression levels of isocitrate dehydrogenases, the key regulators of the TCA cycle, were obviously decreased in both A549 and H1299 cells. CONCLUSIONS Our findings suggest that the effect of docetaxel-induced proliferation inhibition and apoptosis in NSCLC might be associated with down-regulation of isocitrate dehydrogenases and suppression of the TCA cycle pathway.
A549 Cells ; Apoptosis ; drug effects ; Carcinoma, Non-Small-Cell Lung ; pathology ; Docetaxel ; pharmacology ; Humans ; Lung Neoplasms ; pathology ; Metabolomics