Ganoderma lucidum polysaccharides attenuates pressure-overload-induced pathological cardiac hypertrophy.

Pathological cardiac hypertrophy is an important risk factor for cardiovascular disease. However, drug therapies that can reverse the maladaptive process and restore heart function are limited. Ganoderma lucidum polysaccharides (GLPs) are one of the main active components of G. lucidum (Ganoderma lucidum), and they have various pharmacological effects. GLPs have been used as Chinese medicine prescriptions for clinical treatment. In this study, cardiac hypertrophy was induced by transverse aortic constriction (TAC) in mice. We found that GLPs ameliorate Ang II-induced cardiomyocyte hypertrophy in vitro and attenuate pressure overload-induced cardiac hypertrophy in vivo. Further research indicated that GLPs attenuated the mRNA levels of hypertrophic and fibrotic markers to inhibit cardiac hypertrophy through the PPARγ/PGC-1α pathway. Overall, these results indicate that GLPs inhibit cardiac hypertrophy through downregulating key genes for hypertrophy and fibrosis and attenuate pressure overload-induced pathological cardiac hypertrophy by activating PPARγ. This study provides important theoretical support for the potential of using GLPs to treat pathological myocardial hypertrophy and heart failure.

Syngas production and gas-N evolution over heterogeneously doped La-Fe-O perovskite-type oxygen carriers in chemical looping gasification of microalgae.

Chemical looping gasification (CLG) is a promising technology for syngas production with low pollutant emission. In this study, doped La-Fe-O perovskites including LaFeO3 (LF), LaFe0.5Ni0.5O3 (LN5F5) and La0.3Ba0.7FeO3 (L3B7F) were developed for microalgae CLG. The as-prepared perovskites exhibited an outstanding performance in syngas production with accumulative syngas yield > 33 mol/kg. For gas-N evolution, perovskites were beneficial to the formation of NH3 and HCN, while the iron ore may convert precursors to NO. Below 400 °C, NOx can be stored on the perovskite surface in the form of nitrite/nitrate species. When the temperature was above 700 °C, NOx can be selectively reduced by reducing components in tar or syngas under the catalysis of L3B7F, resulting in the final reduction of NOx emission. Thus, CLG over L3B7F may be a promising way for efficient utilization of microalgae to overcome the intractable nitrogen-related obstacles in the commercial application of biomass gasification technologies.

A new environmentally-friendly route to in situ form a high-corrosion-resistant nesquehonite film on pure magnesium.

Magnesium-based materials are promising lightweight structural materials due to their excellent properties. However, their extensive application has been severely limited due to their high corrosion susceptibility. The inadequate corrosion resistance of Mg is mainly attributed to the porous and unprotective native surface film formed on Mg in aggressive environments. Here, we demonstrated a new environment-friendly route for the growth of a continuous nesquehonite (MgCO3·3H2O) protective film on the surface of pure Mg metal at a relatively low temperature via an in situ reaction of the Mg surface with gaseous phase CO2 in humid environments. The protective film consists solely of highly crystalline MgCO3·3H2O that is compact and has an umbrella-like structure. Electrochemical tests showed that compared to the untreated Mg substrate, the protective film can effectively improve the corrosion resistance of the substrate by nearly two orders of magnitude. Additionally, a possible formation mechanism of the nesquehonite film on the pure Mg was proposed and the effect of the carbonation time on the film was investigated. This environmentally-friendly surface treatment method is promising for use in the protection of magnesium-based materials.

Synergistic effect of bone marrow-derived mesenchymal stem cells and platelet-rich plasma in streptozotocin-induced diabetic rats.

BACKGROUND: Diabetic wounds are a major clinical challenge, because minor skin wounds can lead to chronic, unhealed ulcers and ultimately result in infection, gangrene, or even amputation. Studies on bone marrow derived mesenchymal stem cells (BMSCs) and a series of growth factors have revealed their many benefits for wound healing and regeneration. Platelet-rich plasma (PRP) may improve the environment for BMSC development and differentiation. However, whether combined use of BMSCs and PRP may be more effective for accelerating diabetic ulcer healing remains unclear. OBJECTIVE: We investigated the efficacy of BMSCs and PRP for the repair of refractory wound healing in a diabetic rat model. METHODS: Forty-eight rats with diabetes mellitus induced by streptozotocin were divided into four groups: treatment with BMSCs plus PRP, BMSCs alone, PRP alone, phosphate buffered saline. The rate of wound closure was quantified. A histopathological study was conducted regarding wound depth and the skin edge at 7, 14, and 28 days after surgery. RESULTS: Wound healing rates were significantly higher in the BMSC plus PRP group than in the other groups. The immunohistochemistry results showed that the expression of platelet/endothelial cell adhesion molecule 1, proliferating cell nuclear antigen, and transforming growth factor-ß1 increased significantly in the BMSC plus PRP group compared to the other treatment groups. On day 7, CD68 expression increased significantly in the wounds of the BMSC plus PRP group, but decreased markedly at day 14 compared to the controls. CONCLUSION: The combination of BMSCs and PRP aids diabetic wound repair and regeneration.

Attenuation of high-glucose-induced inflammatory response by a novel curcumin derivative B06 contributes to its protection from diabetic pathogenic changes in rat kidney and heart.

There is increasing evidence indicating that inflammatory processes are involved in the development and progression of diabetic complications. However, effective anti-inflammatory treatments for patients who have diabetic complications have yet been practically identified. Curcumin is a main component of Curcuma longa with numerous pharmacological activities. Previously, we synthesized a novel curcumin analogue (B06) that exhibited an improved pharmacokinetic and enhanced anti-inflammatory activity compared to curcumin. The present study aimed to test the hypothesis that B06 may reduce high-glucose-induced inflammation and inflammation-mediated diabetic complications. In vitro, pretreatment with B06 at a concentration of 5 µM significantly reduced the high-glucose-induced overexpression of inflammatory cytokines in macrophages. This anti-inflammatory activity of B06 is associated with its inhibition of c-Jun N-terminal kinase/nuclear factor κB activation. In vivo, despite that B06 administration at 0.2 mg · kg(-1) · d(-1) for 6 weeks did not affect the blood glucose profile of diabetic rats, the B06-treated animals displayed significant decreases in inflammatory mediators in the serum, kidney, and heart and renal macrophage infiltration. This was accompanied with an attenuation of diabetes-induced structural and functional abnormalities in the kidney and heart. Taken together, these data suggest that the novel derivative B06 might be a potential therapeutic agent for diabetic complications via an anti-inflammatory mechanism and support the potential application in diabetic complication therapy via anti-inflammatory strategy.

bFGF inhibits ER stress induced by ischemic oxidative injury via activation of the PI3K/Akt and ERK1/2 pathways.

Extensive research has focused on finding effective strategies to prevent or improve recovery from brain ischemia and reperfusion (I/R) injury. The basic fibroblast growth factor (bFGF) has been shown to have therapeutic potential in some central nervous system (CNS) disorders, including ischemic injury. In this study, we demonstrate that bFGF administration can improve locomotor activity and inhibit the ER stress induced in the CA1 region of the hippocampus in a mouse model of I/R injury. In vitro, bFGF exerts a protective effect by inhibiting the ER stress response proteins CHOP, XBP-1, ATF-6 and caspase-12 that are induced by H(2)O(2) treatment. Both of these in vivo and in vitro effects are related to the activation of two downstream signaling pathways, PI3K/Akt and ERK1/2. Inhibition of the PI3K/Akt and ERK1/2 pathways by specific inhibitors, LY294002 and U0126, respectively, partially reduce the protective effect of bFGF. Taken together, our results indicate that the neuroprotective role of bFGF involves the suppression of ER stress in the ischemic oxidative damage models and oxidative stress-induced PC12 cell injury, and these effects is underlying the activation of the PI3K/Akt and ERK1/2 signal pathway.

[Effect of bufalin on cellular proliferation and apoptosis in human esophageal squamous carcinoma EC9706 cells].

OBJECTIVE: To investigate the effect of bufalin on nucleus-mitochondria localization of human telomerase reverse transcriptase(hTERT) by exploring its effect on proliferation and apoptosis in human esophageal squamous carcinoma EC9706 cells. METHODS: EC9706 cells were treated with bufalin at various concentrations, and then the cell growth inhibition of EC9706 cells was examined by CCK-8 assay and the 50% inhibitory concentration (IC(50)) was calculated.Cell cycle analysis was performed by flow cytometry with PI staining, and nucleus morphology of apoptosis were observed by fluorescence microscopy with Hoechst 33342 staining. The apoptotic index was measured by flow cytometry with Annexin V-FITC/PI double staining. hTERT subcellular localization and protein expression were determined by Western blotting and multiple immunofluorescence labling combined with laser confocal scanning microscopy. RESULTS: The proliferation of EC 9706 cells was significantly inhibited by bufalin along with the increase of processing time and concentrations (p<0.01). After the EC9706 cells were exposed to 100 nmol/L bufalin,the number of cells gradually decreased in G(1) phase and increased in S and G(2)/M phases(p<0.05). The typical nucleus morphological changes of apoptosis were observed and the apoptotic index was increased(p<0.01). The expression of hTERT decreased in nucleus but increased in mitochondria(p<0.05). CONCLUSIONS: Bufalin can inhibit the proliferation of human esophageal squamous carcinoma EC9706 cells in a time- and dose-dependent manner. It can arrest cell cycle in S and G(2)/M phases and induce the apoptosis of EC 9706 cells. hTERT is localized in both nucleus and mitochondria,and can be partially translocated from nucleus to mitochondria during the bufalin-induced apoptosis.