Constructing Hierarchical Zeolites with Highly Complete Framework via Controlled Desilication.

Desilication in alkaline medium has been widely used in construction of hierarchical zeolites for industrially relevant catalytic processes. The built of hierarchy in zeolites, especially with low aluminum stability or high Si/Al ratio, often suffers from uncontrolled destruction of zeolitic framework, accompanied by a significant loss of microporous domains and intrinsic acidity after desilication. Here, we report a novel and simple methodology for preparation of hierarchical zeolites with highly complete framework and minimum sacrifice of microporosity and acidity. The pre-impregnated amines in zeolite micropores act as inner pore-directing agents (iPDAs), largely protecting the zeolitic framework and moderating the silicon extraction during the alkaline treatment. The resulting hierarchical zeolites exhibit high crystallinity, tunable hierarchy, stable framework, and well-preserved acidity, endowing them with significantly improved mass transport properties and enhanced activities in catalytic conversion of methanol or furfural.

ß-Eudesmol induces JNK-dependent apoptosis through the mitochondrial pathway in HL60 cells.

ß-eudesmol, a natural sesquiterpenol present in a variety of Chinese herbs, is known to inhibit the proliferation of human tumor cells. However, the molecular mechanisms of the effect of ß-eudesmol on human tumor cells are unknown. In the present study, we report the cytotoxic effect of ß-eudesmol on the human leukemia HL60 cells and its molecular mechanisms. The cytotoxic effect of ß-eudesmol on HL60 cells was associated with apoptosis, which was characterized by the presence of DNA fragmentation. ß-eudesmol-induced apoptosis was accompanied by cleavage of caspase-3, caspase-9, and poly (ADP-ribose) polymerase; downregulation of Bcl-2 expression; release of cytochrome c from mitochondria; and decrease in mitochondrial membrane potential (MMP). Activation of c-Jun N-terminal kinases (JNK) mitogen-activated protein kinases was observed in ß-eudesmol-treated HL60 cells, and the inhibitor of JNK blocked the ß-eudesmol-induced apoptosis, downregulation of Bcl-2, and the loss of MMP. These data suggest that ß-eudesmol induces apoptosis in HL60 cells via the mitochondrial apoptotic pathway, which is controlled through JNK signaling.

Efficient hydrodeoxygenation of methyl levulinate into pentanoic biofuels over Ru/USY catalysts.

Catalytic hydrodeoxygenation of neat methyl levulinate into pentanoic biofuels is one of the pivotal reactions in biomass valorization. A combined pentanoic acid/methyl pentanoate yield of 92% can be achieved for Ru/USY with a Si/Al ratio of 15 at 220 °C and 40 bar H2. The superior performance of Ru/USY-15 for the efficient production of pentanoic biofuels is attributed to the optimal site balance between the Ru species and strong acid sites (ca. 1 : 5).

JNK-dependent Atg4 upregulation mediates asperphenamate derivative BBP-induced autophagy in MCF-7 cells.

N-Benzoyl-O-(N'-(1-benzyloxycarbonyl-4-piperidiylcarbonyl)-D-phenylalanyl)-D-phenylalaninol (BBP), a novel synthesized asperphenamate derivative with the increased solubility, showed growth inhibitory effect on human breast carcinoma MCF-7 cells in a time- and concentration-dependent manner. The growth inhibitory effect of BBP was associated with induction of autophagy, which was demonstrated by the development of acidic vesicular organelles, cleavage of LC3 and upregulation of Atg4 in BBP-treated MCF-7 cells. Since the application of Atg4 siRNA totally blocked the cleavage of LC3, we demonstrated a central role of Atg4 in BBP-induced autophagy. The further studies showed that BBP increased the levels of reactive oxygen species (ROS), and pretreatment with NAC effectively blocked the accumulation of ROS, autophagy and growth inhibition triggered by BBP. Moreover, BBP induced the activation of JNK, and JNK inhibitor SP600125 reversed autophagy, the increase of Atg4 levels, conversion of LC3 and growth inhibition induced by BBP. Knockdown of JNK by siRNA efficiently inhibited ROS production and autophagy, but antioxidant NAC failed to block JNK activation induced by BBP, indicating that JNK activation may be a upstream signaling of ROS and should be a core component in BBP-induced autophagic signaling pathway. These results suggest that BBP produces its growth inhibitory effect through induction of the autophagic cell death in MCF-7 cells, which is modulated by a JNK-dependent Atg4 upregulation involving ROS production.

Synthesis and in vitro antitumor activity of asperphenamate derivatives as autophagy inducer.

In an effort to improve the aqueous solubility and the antitumor activity of natural product asperphenamate, we have designed and synthesized three series of asperphenamate derivatives, including series I (simplifying molecular skeleton series), series II (introducing a hydroxyl group to A-phenyl ring series) and series III (disrupting molecular planarity series). All derivatives have displayed a significantly increased solubility compared with asperphenamate. Their growth inhibitory activities in vitro were screened by the standard MTT method in MCF-7, HeLa, and BEL-7402 cell lines. With the exception of the derivatives in series I, most of derivatives in series II and series III showed growth inhibitory activity. Among all derivatives, IM23b in series III showed the greatest potency in human breast cancer MCF-7 cells. The cellular potency of IM23b was approximately 1.5-fold more potent than that of cisplatin. The mechanism of cell death induced by IM23b in human breast cancer MCF-7 cells was further investigated. We concluded that the cell death was induced by autophagy instead of apoptosis or cell cycle arrest.

Study of optical parameters of polystyrene spheres in dense aqueous suspensions.

We investigated the dependence of the scattering and absorption coefficients of particles in dense suspensions by the low-coherence fiber optic dynamic light scattering (FODLS) technique. The estimated particle size was used to calculate the scattering coefficient of particles suspended in dense suspensions. The path-length resolved intensity distributions of light backscattered from absorbing dense suspensions were investigated experimentally. The absorption coefficient can be obtained by applying the measured path-length resolved intensity distributions to the modified Lambert-Beer law. As a result, the low-coherence FODLS technique can simultaneously measure the scattering and absorption coefficients of particles in absorbing dense suspensions, and the scattering and absorption coefficients are independent of each other in dense suspensions in the low-scattering regime of 2l(d) < 10ℓ*.

Inactivation of PI3K/Akt signaling mediates proliferation inhibition and G2/M phase arrest induced by andrographolide in human glioblastoma cells.

AIMS: Andrographolide, a principal diterpenoid lactone isolated from the traditional herbal medicine Andrographis paniculata, has been reported to show anti-tumor activity. Since the high lipid solubility of andrographolide permits it to penetrate the blood-brain barrier and concentrate in the brain, we hypothesized that andrographolide may be a potential chemotherapeutic agent for the treatment of glioblastomas. To clarify this point, we investigated the growth inhibitory effect and mechanisms of actions of andrographolide on human glioblastoma U251 and U87 cells. MAIN METHODS: MTT assay and trypan blue exclusion assay were used to investigate the proliferation inhibitory and cytotoxic effects of andrographolide, respectively. Cell cycle distribution was analyzed using flow cytometry. Apoptosis analysis proceeded by detecting the cleavage of caspase-3. The levels of proteins were probed by Western blotting. KEY FINDINGS: The results showed that non-toxic concentrations of andrographolide inhibited the proliferation of human glioblastoma cells through induction of G2/M arrest, which was accompanied by down-regulating Cdk1 and Cdc25C proteins. Additionally, andrographolide decreased the activity of PI3K/Akt signaling, as demonstrated by down-regulation of the expression of phos-PI3K, phos-Akt, phos-mTOR and phos-p70s6k in U251 and U87 cells. Furthermore, additive effects on the proliferation inhibition, G2/M arrest and down-regulation of G2/M phase-related proteins were observed, when a combined treatment of andrographolide with PI3K inhibitor LY294002 was used in U251 and U87 cells. SIGNIFICANCE: We prove that andrographolide inhibits the proliferation of human glioblastoma cells via inducing G2/M arrest, which is mediated by inhibiting the activity of PI3K/Akt signaling.