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Up to now, the member of zeolite family has expanded to more than 230. However, only little part of them have been reported as catalysts used in reactions. Discovering potential zeolites for reactions is significantly important, especially in industrial applications. A carbonylation zeolite catalyst Al-RUB-41 has special morphology and channel orientation. The 8-MR channel of Al-RUB-41 is just perpendicular to its thin sheet, making a very short mass-transfer distance along 8-MR. This specific nature endows Al-RUB-41 with efficient catalytic ability to dimethyl ether carbonylation reaction with beyond 95% methyl acetate selectivity. Compared with the most widely accepted carbonylation zeolite catalysts, Al-RUB-41 behaves a much better catalytic stability than H-MOR and a greatly enhanced catalytic activity than H-ZSM-35. A space-confined deactivation mechanism over Al-RUB-41 is proposed. By erasing the acid sites on outer surface, Al-RUB-41@SiO2 catalyst achieves a long-time and high-efficiency activity without any deactivation trend.

To investigate the effect of curcumol on NOD-like receptor thermoprotein domain 3 (NLRP3) inflammasomes, and analyze the mechanism underlying curcumol against liver fibrosis. Thirty Kunming mice were divided into a control group, a model group and a curcumol group according to a random number table, 10 mice in each group. Mice were intraperitoneally injected with 40% carbon tetrachloride (CCl4:peanut oil, 2:3 preparation) at 5 mL/kg for 6 weeks, twice a week, for developing a liver fibrosis model. The mice in the control group were given the same amount of peanut oil twice a week for 6 weeks. The mice in the curcumol group were given curcumol (30 mL/kg) intragastrically, and the mice in the model and control groups were given the same amount of normal saline once a day for 6 weeks. Changes in liver structure were observed by hematoxylin and eosin (HE) and Masson staining. Liver function, liver fiber indices, and the expression of interleukin (IL)-10 and tumor necrosis factor-α (TNF-α) levels were determined by automatic biochemical analyzer and enzyme linked immunosorbent assay kit. Immunoblotting and reverse transcription-quantitative PCR (RT-qPCR) were performed to detect the expression of NLRP3 inflammasome-related molecules, TGF-β and collagen. HE and Masson staining results showed that the hepatocytes of the model group were arranged irregularly with pseudo-lobular structure and a large amount of collagen deposition. The mice in the curcumol group had a significant decrease in liver function and liver fibers indices compared with the model group (P

Improving the selectivity of light olefins remains a longstanding challenge in Fischer–Tropsch to light olefins reaction (FTO). Toward this objective, we designed and prepared a newly catalyst with core-shell-like structure by using a simple and facile method named physically adhesive method. This core-shell-like catalyst Fe@SAPO-34 was characterized by XRD, SEM, EDS, N2 sorption and NH3-TPD respectively. The characterization results indicated that the SAPO-34 zeolite shell was comparatively uniform, homogeneous and defect-free, and it encapsulated the Fe catalyst entirely. Fischer–Tropsch synthesis reaction of syngas to light olefins was selected to test the catalytic performance of the zeolite capsule catalyst. In comparison with the simple mixture catalyst Fe/SAPO-34 and bare Fe catalyst, the newly Fe@SAPO-34 catalyst has demonstrated ability of the highest selectivity of light olefins 52.6% and O/P ratio 6.4. The SAPO-34 zeolite shell acted an important role for the improvement of light olefins selectivity.

Aims The purpose of this study was to investigate plumbagin (PL) on liver fibrosis in vitro and in vivo and to explore the underlying mechanisms. Methods Carbon tetrachloride (CCl4) was used to establish a rat liver fibrosis model, primary hepatic stellate cells (HSCs) were isolated from the rat liver, and fibrosis-related indicators were detected. Results The results revealed that PL significantly prevented CCl4-induced liver fibrosis, as evidenced by the attenuation of histopathological changes, the decrease of MDA and the increase of SOD and GSH-P X . In addition, PL downregulated the mRNA levels of NOX4 and procollagen I; the protein expression levels of NOX4 and p-IκB; and the transcriptional activity of NF-κB in liver fibrosis rats. Moreover, PL significantly decreased ROS expression, protein expression of α-SMA and collagen III, and activation of NF-κB and inhibited the nuclear translocation of NF-κB p65 in IL-1β-stimulated HSCs in vitro. Conclusion The results of our study indicate that PL can mitigate liver fibrosis in vitro and in vivo, which may be related to the ROS-mediated NF-кB signaling pathway.

// YanFei Wei 1, * , Qi Yang 2, * , Yuan Zhang 3, * , TieJian Zhao 1 , XueMei Liu 1 , Jing Zhong 1 , Jing Ma 1 , YongXin Chen 1 , Chuan Zhao 1 , JunXuan Li 1 1 Department of Physiology, Faculty of Basic Medicine, Guangxi University of Chinese Medicine, Nanning, Guangxi, 530200, China 2 Department of Emergency, Tianjin Fifth Central Hospital, Binhai New Area, Tianjin 300450, China 3 Department of State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, Tianjin, 710032, China * These authors contributed equally to this work Correspondence to: Yan-Fei Wei, email: weiyanfei@163.com Keywords: plumbagin, HCC, angiogenesis, vascular endothelial cells, PI3K/AKT Received: July 02, 2016 Accepted: January 10, 2017 Published: January 20, 2017 ABSTRACT Tumor occurrence and development are very complicated processes. In addition to the roles of exogenous carcinogenic factors, the body’s internal factors also play important roles. These factors include the host response to the tumor and the tumor effect on the host. In particular, the proliferation, migration and activation of endothelial cells are involved in tumor angiogenesis. Angiogenesis is one of the hallmarks of cancer. In this study, we investigate whether plumbagin can abrogate angiogenesis-mediated tumor growth in hepatocellular carcinoma (HCC) and, if so, through which molecular mechanisms. We observed that in co-cultures of the human endothelial cell line EA.hy926 and the human hepatoma cell line SMMC-7721 and Hep3B, the hepatoma cells induced migration, invasion, tube formation and viability of the EA.hy926 cells in vitro , and these processes were inhibited by plumbagin. Real-Time PCR, Western Blot and Immunofluorescence staining showed that plumbagin treatment suppressed expression of angiogenesis pathways (PI3K-Akt, VEGF/KDR and Angiopoietins/Tie2) and angiogenic factors (VEGF, CTGF, ET-1, bFGF),which is associated with tumor angiogenesis in cancer cells and xenograft tumor tissues. Furthermore, plumbagin was also found to significantly reduce tumor growth in an orthotopic HCC mouse model and to inhibit tumor-induced angiogenesis in HCC patient xenografts. Taken together, our findings strongly suggest that plumbagin might be a promising anti-angiogenic drug with significant antitumor activity in HCC.

Critical roles for liver sinusoidal endothelial cells (LSECs) in liver fibrosis have been demonstrated, while little is known regarding the underlying molecular mechanisms of drugs delivered to the LSECs. Our previous study revealed that plumbagin plays an antifibrotic role in liver fibrosis. In this study, we investigated whether plumbagin alleviates capillarization of hepatic sinusoids by downregulating endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), laminin (LN), and type IV collagen on leptin-stimulated LSECs. We found that normal LSECs had mostly open fenestrae and no organized basement membrane. Leptin-stimulated LSECs showed the formation of a continuous basement membrane with few open fenestrae, which were the features of capillarization. Expression of ET-1, VEGF, LN, and type IV collagen was enhanced in leptin-stimulated LSECs. Plumbagin was used to treat leptin-stimulated LSECs. The sizes and numbers of open fenestrae were markedly decreased, and no basement membrane production was found after plumbagin administration. Plumbagin decreased the levels of ET-1, VEGF, LN, and type IV collagen in leptin-stimulated LSECs. Plumbagin promoted downregulation of ET-1, VEGF, LN, and type IV collagen mRNA. Altogether, our data reveal that plumbagin reverses capillarization of hepatic sinusoids by downregulation of ET-1, VEGF, LN, and type IV collagen.

Purpose: To investigate the protective effects of plumbagin against liver fibrosis and explore the influence of plumbagin on the proliferation of hepatic stellate cells (HSCs).Methods: HSC-LX2 cells were divided into blank/control group, 100 ng/ml leptin group, 100 ng/ml leptin + 2 μmol/L plumbagin group, 100 ng/ml leptin + 8 μmol/L plumbagin group and 100 ng/ml leptin + 6.25 μg/ml colchicines group. The expressions of leptin receptor protein (OB-Rb), p-JAK2, p-STAT3, JAK2, STAT3, p-ERK1/2, ERK1/2 and MMP-1 were detected by Western blot assay. The content of type I collagen in the supernatant of HSCs was also measured after stimulation by leptin.Results: Leptin induced OB-Rb expression in HSCs, which reached a peak level at 24 h (p < 0.01). Leptininduced OB-Rb expression was significantly inhibited by plumbagin at concentrations of 2 μmol/L and 8 μmol/L, respectively. Western blot assay revealed that plumbagin significantly decreased pJAK2 expression in leptin-treated HSCs (p < 0.01). Leptin induced expression of pSTAT3 significantly decreased after plumbagin treatment in HSC-LX2 (p < 0.01). p-ERK1/2 expression markedly decreased in plumbagin-treated HSCs (p < 0.01). Plumbagin significantly increased MMP-1 expression in leptin-treated HSCs (p < 0.01).Conclusion: Plumbagin has an anti-fibrotic effect and may decrease the protein expressions of components in JAK2-STAT3 pathway to inhibit HSC proliferation. Thus, plumbagin may be useful in the clinical prevention and treatment of liver fibrosis.Keywords：Plumbagin, Leptin, Hepatic stellate cell, Proliferation, Signal transduction pathway, Antiinflammatory