Enhancing adsorption capacity and structural stability of Li1.6Mn1.6O4 adsorbents by anion/cation co-doping.

Modifying the structure of Li1.6Mn1.6O4 (LMO) to enhance its structural stability and adsorption capacity is an effective method to generate materials to recover Li+ ions from mixed solution. Herein, the co-doping of trace non-metal ion (S) and metal ion (Al) into Li1.6Mn1.6O4 (LMO-SAl) is established and shows excellent Li+ adsorption capacity and Mn anti-dissolution properties. The adsorption capacity (when [Li+] is 6 mmol L-1) is increased from 26.1 mg g-1 to 33.7 mg g-1. This is attributed to improved charge density via substitution of S at O sites, which facilitates the adsorption/desorption process. The Mn dissolution is also reduced from 5.4% to 3.0% for LMO-SAl, which may result from the stronger Al-O bonds compared to Li-O bonds that enhance the structural stability of the LMO. The ion-sieving ability of the co-doped material goes by the order of K d (Li+ > Ca2+ > Mg2+ > Na+ > K+), indicating that Li+ can be efficiently separated from Lagoco Salt Lake brine. These results predict that lithium ions are effectively adsorbed from brine by the co-doped LMO material, which manifests the feasibility of lithium recovery and provides basic data for further industrial applications of adsorption.

Morphology-controlled fabrication of magnetic phase-change microcapsules for synchronous efficient recovery of wastewater and waste heat.

Contamination and waste heat are major issues in water pollution. Aiming at efficient synchronous recovery wastewater and waste heat, we designed a novel CaCO3-based phase-change microcapsule system with an n-docosane core and a CaCO3/Fe3O4 composite shell. The system was fabricated through an emulsion-templated in situ precipitation approach in a structure-directing mode, resulting in a controllable morphology for the resultant microcapsules, varying from a peanut hull through ellipsoid to dumbbell shapes. The system has a significantly enlarged specific surface area of approximately 55 m2·g-1 with the CaCO3 phase transition from vaterite to calcite. As a result, the microcapsule system exhibits improved adsorption capacities of 497.6 and 79.1 mg/g for Pb2+ and Rhodamine B removal, respectively, from wastewater. Moreover, increase in the specific surface area of the microcapsule system with a sufficient latent heat capacity of approximately 130 J·g-1 also resulted in an enhanced heat energy-storage capability and thermal conductance for waste-heat recovery. The microcapsule system also exhibits a good leakage-prevention capability and good multicycle reusability owing to the tight magnetic CaCO3/Fe3O4 composite shell. This study provides a promising approach for developing CaCO3-based phase-change microcapsules with enhanced thermal energy storage and adsorption capabilities for efficient synchronous recovery of wastewater and waste heat.

Icarrin prevents cardiomyocyte apoptosis in spontaneously hypertensive rats by inhibiting endoplasmic reticulum stress pathways.

OBJECTIVES: This study aimed to explore whether icarrin (ICA) can protect cardiomyocytes from hypertension-induced damage by inhibiting endoplasmic reticulum stress (ERS). METHODS: Spontaneously hypertensive rats (SHRs) were orally administered water or ICA at 10, 20 and 40 mg/kg once daily for 12 weeks, and Wistar-Kyoto (WKY) rats were used as control. Changes in the growth and blood pressure of rats were assessed. Cardiac function was determined by ultrasound and the left ventricle mass was calculated. Myocardial tissue structure was assessed by haematoxylin and eosin staining, cardiomyocyte apoptosis was observed by TUNEL staining and the expression of ERS-related proteins was determined by western blotting. RESULTS: In the SHR group, blood pressure was significantly high, left ventricular function decreased and left ventricular mass index increased. Additionally, left ventricular cardiomyocyte hypertrophy, disordered myofilament arrangement and increased cardiomyocyte apoptosis were observed by histological staining. ERS-induced proteins associated with apoptosis, including GRP78, PERK, ATF-6, ATF-4, CHOP, DR5, Caspase 12, c-JUN and ASK-1 were found to be highly expressed. ICA treatment reduced blood pressure and regulated the expression of proteins induced by ERS. Cardiomyocyte apoptosis decreased and left ventricular function improved. CONCLUSIONS: ICA can inhibit ERS-induced apoptosis of cardiomyocytes and protect ventricular function in SHR.

Osthole improves pulmonary artery hypertension by inducing apoptosis in pulmonary artery smooth muscle cells.

OBJECTIVES: The objectives of this study were to explore the effect of Osthole (Ost) on apoptosis in pulmonary artery smooth muscle cells (PASMCs) and investigate the potential mechanism of this effect. METHODS: Rats were injected subcutaneously with monocrotaline (MCT) to establish a PAH model, and Ost were intragastrically administrated from day 1 to day 35. After 35 days administration, the mean pulmonary artery pressure and lung weight index were measured. HE and TUNEL staining were used to observe the morphology of pulmonary artery and the apoptosis of PASMCs. In addition, the apoptosis of PASMCs were detected by flow cytometry in cultured PASMCs. The proteins of Bax and Bcl-2, and the levels of p-ASK1 and cleaved caspase 3 were measured by Western blot. KEY FINDINGS: Ost decreased the mean pulmonary artery pressure and lung weight index in MCT-induced rats, and promoted apoptosis in PASMCs in MCT-induced rats and PDGF-BB stimulated PASMCs. Ost increased the ratio of Bax/Bcl-2 and the levels of p-ASK1, cleaved caspase 3 in MCT-induced rats and PDGF-BB stimulated PASMCs. CONCLUSION: Ost promoted apoptosis in PASMCs in vivo and in vitro, and the mechanism may be associated with upregulation of ASK1 and the Bax/Bcl-2-caspase 3 signalling pathway.

Al-doped H2TiO3 ion sieve with enhanced Li+ adsorption performance.

H2TiO3 (HTO) is considered to be one of the most promising adsorbents for lithium recovery from aqueous lithium resources duo to its highest theoretical adsorption capacity. However, its actual adsorption capacity is much lower owing to its unknown structure and incomplete leaching of lithium. After Al is doped into H2TiO3 (HTO-Al), the adsorption capacity of HTO-Al is 32.12 mg g-1 and the dissolution of Ti is 2.53%. HTO-Al has good adsorption selectivity, and all the separation factors α are ≫1. Furthermore, HTO-Al also exhibits good cyclic stability and solubility resistance. After 5 cycles, the adsorption capacity remains 29.3 mg g-1 and the dissolution rate is 1.7%. Therefore, HTO-Al has potential application value for recovering Li+ from aqueous lithium resources.

The adsorption behavior of lithium on spinel titanium oxide nanosheets with exposed (1-14) high-index facets.

The ion-exchange process is usually influenced by the surface properties of the adsorbents. In particular, the prophase adsorption/desorption process is confined by different crystal facets. In this research, spinel Li4Ti5O12 nanosheets with an exposed (1-14) high-index facet were prepared by a hydrothermal method followed by calcination treatment. Then, a H4Ti5O12 adsorbent was obtained, covered with the same (1-14) facets, after treatment with 0.2 M HCl. This special facet-exposed H4Ti5O12 has high cycling ability, with the adsorption uptake remaining at 96.84% after four cycles, a fast adsorption equilibrium time (equilibrium time < 60 min), excellent ion adsorption selectivity for Li+ uptake (separation factor: Li+ > K+ > Ca2+ > Na+ > Mg2+), and good adsorption capacity for Li+ uptake (21.57 mg g-1 ). With the help of X-ray photoelectron spectroscopy analyses, the Li+ adsorption process on the H4Ti5O12 nanosheets is shown to be an ion-exchange process. In addition, the coordination relationship between lithium and oxygen ions was investigated, illustrating that the four-coordinated structure is more stable than other complexes. These results indicate that hydrogen ions are exchanged for lithium ions at tetrahedral 8a sites, leading to the H4Ti5O12 structure with high stability in the adsorption-desorption cycling process.

Hydrothermal synthesis and adsorption behavior of H4Ti5O12 nanorods along [100] as lithium ion-sieves.

The adsorption method is a promising route to recover Li+ from waste lithium batteries and lithium-containing brines. To achieve this goal, it is vital to synthesize a stable and high adsorption capacity adsorbent. In this work, Li4Ti5O12 nanorods are prepared by two hydrothermal processes followed by a calcination process. Then the prepared Li4Ti5O12 nanorods are treated with different HCl concentrations to obtain a H4Ti5O12 adsorbent with 5 µm length along the [100] direction. The maximum amount of extracted lithium can reach 90% and the extracted titanium only 2.5%. The batch adsorption experiments indicate that the H4Ti5O12 nanorod maximum adsorption capacity can reach 23.20 mg g-1 in 24 mM LiCl solution. The adsorption isotherms and kinetics fit a Langmuir model and pseudo-second-order model, respectively. Meanwhile, the real adsorption selectivity experiments show that the maximum Li+ adsorption capacity reaches 1.99 mmol g-1, which is far higher than Mg2+ (0.03 mmol g-1) and Ca2+ (0.02 mmol g-1), implying these nanorods have higher adsorption selectivity for Li+ from Lagoco Salt Lake brine. The adsorption capacity for Li+ remains 91% after five cycles. With the help of XPS analyses, the adsorption mechanism of Li+ on the H4Ti5O12 nanorods is an ion exchange reaction. Therefore, this nanorod adsorbent has a potential application for Li+ recovery from aqueous lithium resources.

Bone marrow mesenchymal stem cells conditioned medium protects VSC4.1 cells against 2,5-hexanedione-induced autophagy via NGF-PI3K/Akt/mTOR signaling pathway.

We aimed to investigate the effects of bone marrow mesenchymal stem cell conditioned medium (BMSC-CM) in preventing 2,5-hexanedione (HD)-induced damage to motoneurons, and examined the molecular mechanisms that mediate these effects. VSC4.1 cells were exposed to 25 mM HD for 24 h followed by incubation with DMEM for 24 h. HD-treated cells were incubated with BMSC-CM at varied concentrations. Incubation with BMSC-CM ameliorated the decreased cell viability and reduced LDH release from cells exposed to HD. BMSC-CM suppressed the elevated number of autophagic vacuoles, cells with LC3 puncta, increased LC3-II/LC3-I ratio, and decreased p62 caused by HD exposure. BMSC-CM elevated NGF and p-TrkA expressions in HD-treated cells. Administration of NGF inhibited autophagy, an effect that was similar to that observed after BMSC-CM treatment; this effect was abolished by the addition of NGF-neutralizing antibodies. BMSC-CM or NGF elevated p-protein kinase B (Akt) and p-mammalian target of rapamycin (mTOR) in HD-exposed cells, which was interrupted by TrkA inhibitor, K252a and mTOR inhibitor, rapamycin. BMSC-CM prevented HD-induced autophagic cell damage in VSC4.1 cells. The neuroprotective effect of BMSC-CM appeared to be at least partly associated with its ability to trigger the NGF-phosphatidylinositol-3-kinase (PI3K)/Akt/mTOR signaling pathway.

Bone marrow mesenchymal stem cells protect against n-hexane-induced neuropathy through beclin 1-independent inhibition of autophagy.

Chronic exposure to n-hexane, a widely used organic solvent in industry, induces central-peripheral neuropathy, which is mediated by its active metabolite, 2,5-hexanedione (HD). We recently reported that transplantation of bone marrow-mesenchymal stem cells (BMSC) significantly ameliorated HD-induced neuronal damage and motor deficits in rats. However, the mechanisms remain unclear. Here, we reported that inhibition of HD-induced autophagy contributed to BMSC-afforded protection. BMSC transplantation significantly reduced the levels of microtubule-associated protein 1 light chain 3-II (LC3-II) and the degradation of sequestosome-1 (p62) in the spinal cord and sciatic nerve of HD-intoxicated rats. Downregulation of autophagy by BMSC was also confirmed in VSC4.1 cells exposed to HD. Moreover, inhibition of autophagy by PIK III mitigated the neurotoxic effects of HD and, meanwhile, abolished BMSC-afforded neuroprotection. Furthermore, we found that BMSC failed to interfere with Beclin 1, but promoted activation of mammalian target of rapamycin (mTOR). Unc-like kinse 1 (ULK1) was further recognized as the downstream target of mTOR responsible for BMSC-mediated inhibition of autophagy. Altogether, BMSC transplantation potently ameliorated HD-induced autophagy through beclin 1-independent activation of mTOR pathway, providing a novel insight for the therapeutic effects of BMSC against n-hexane and other environmental toxicants-induced neurotoxicity.

Icariside II attenuates myocardial fibrosis by inhibiting nuclear factor-κB and the TGF-ß1/Smad2 signalling pathway in spontaneously hypertensive rats.

Studies have demonstrated that icariin plays important roles in preventing hypertension and improving myocardial hypertrophy, inflammatory and infiltration. Icariside (ICS II) is the main metabolite of icariin, which has anti-inflammatory and anti-oxidant activities and protects against ischaemic brain injury. Whether ICS II improves myocardial fibrosis in spontaneously hypertensive rats (SHRs) and the related mechanism remain unknown. Some studies have suggested that TGF-ß and the nuclear factor κB signalling pathway play a key role in the progression of myocardial fibrosis. Therefore, in the current study, we aimed to evaluate the effects of ICS II on induced myocardial fibrosis in SHRs and explore the mechanism underlying this activity. The SHRs were treated with ICS II (4, 8, and 16 mg/kg) via daily gavage for 12 weeks. Left ventricular function was detected using the Vevo2100 system, and the collagen area was measured by Masson staining. The results indicated that ICS II markedly improved left ventricular function and decreased the left ventricular myocardial collagen area compared with the SHR group. To further investigate the mechanism underlying this activity, we measured the protein expression of interleukin-1ß (IL-1ß), tumour necrosis factor-α (TNF-α), transforming growth factor-ß1 (TGF-ß1), Smad2, inhibitory κB (IκB), and nuclear factor κB (NF-κB) p65 by Western blot. The results showed that ICS II inhibited NF-κB p65 expression and the TGF-ß1/Smad2 signalling pathways. In conclusion, the present results suggest that ICS II suppresses myocardial fibrosis in SHRs, and this effect might be at least partially mediated through suppression of NF-kB signalling and the TGF-ß1/Smad2 signalling pathway.

IcarisideII improves left ventricular remodeling in spontaneously hypertensive rats by inhibiting the ASK1-JNK/p38 signaling pathway.

Inhibition or removal of excess reactive oxygen species can effectively protect cellular function or reduce cell death because oxidative stress is the main cause of cellular damage in many diseases. The flavonoid compound IcarisideII having a slight inhibitory effect on PDE5, is the main active components of epimedium in vivo and has a wide range of pharmacological effects on oxidation and apoptosis. However, whether IcarisideII has the same protective effect on ventricular remodeling in spontaneously hypertensive rats (SHR) is unknown. We found that compared with WKY rats, SHRs exhibited noticeable arterial hypertension. Additionally, echocardiography showed that the diameter of the left ventricle was enlarged, wall thickness was increased, and ejection fraction and short axis shortening rate were reduced. H&E staining demonstrated that SHR cells were disordered and noticeably hypertrophic. Masson trichrome staining revealed significant myocardial fibrosis in the myocardium. Tunel staining indicated that 4.39 times the percent of apoptotic cells were present in SHRs compared to WKY rats. In our study, intra-gastric administration of IcarisideII decreased blood pressure, promoted heart function recovery and improved ventricular remodeling in SHRs. Additionally, it reduced myocardial fibrosis, inhibited myocardial apoptosis, decreased the generation of reactive oxygen species and improved SOD activity. IcarisideII down-regulated the activation of the oxidative stress associated proteins ASK1, p38 and JNK; inhibited the expression of p53, Bax and cleaved-caspase3 in the mitochondrial apoptosis pathway; and up-regulated the expression of Bcl-2. In conclusion, this study indicates that IcarisideII can inhibit myocardial apoptosis and improve left ventricular remodeling in SHRs. It can be inferred that this mechanism may be related to the inhibition of the ASK1-JNK/p38 signaling pathway.

2,5-Hexanedione induces autophagic death of VSC4.1 cells via a PI3K/Akt/mTOR pathway.

2,5-Hexanedione (HD) is an important bioactive metabolite of n-hexane, which mediates the neurotoxicity of the parent compound. Increasing evidence suggests that over-activated autophagy can lead to autophagic neuronal death; however, whether the excessive autophagy is involved in HD-induced neurotoxicity remains unknown. To investigate the effect of HD on autophagy and to find its underlying mechanism, we respectively treated VSC4.1 cells with 5, 15 and 25 mM HD for 24 h. Our results show that HD induced excessive autophagy of VSC4.1 cells in a dose-dependent manner, also, the over-activated autophagy was significantly mitigated in the presence of PI3K activator or Akt activator or mTOR activator. These results indicate that HD induces excessive autophagy of VSC4.1 cells by repressing the PI3K/Akt/mTOR signaling pathway. LDH assay showed that HD contributed to a concentration dependent increase in VSC4.1 cell death, which was significantly reduced by the administration of PIK-III, an autophagy inhibitor. These results also indicate that HD induces autophagic death of VSC4.1 cells via the signaling pathway.

Osthole attenuates pulmonary arterial hypertension in monocrotaline­treated rats.

Pulmonary arterial hypertension (PAH) is an insidious and progressive disease that is triggered by various cardiopulmonary diseases. Inflammation has an important role in the progression of PAH. Osthole (Ost) is a coumarin that has clear anti­inflammatory properties. The present study aimed to investigate the effects of Ost on PAH, and to explore the mechanism underlying this effect. Using the monocrotaline (MCT)­induced PAH rat model, the effects of Ost on PAH were investigated. Rats were subcutaneously administered a single dose of MCT (50 mg/kg) to establish the PAH model, followed by daily treatment with Ost (10 or 20 mg/kg) by gavage for 28 days. The mean pulmonary arterial pressure (mPAP) was measured and histological analysis was performed. The results demonstrated that Ost significantly decreased mPAP, and reduced thickening of the pulmonary artery, compared with in rats in the MCT group. To further determine whether the effects of Ost on MCT­induced PAH were associated with inflammatory responses, the nuclear factor­κB (NF­κB) p65 signaling pathway was investigated by western blot analysis. The results demonstrated that Ost increased inhibition of the NF­κB p65 signaling pathway. In conclusion, the results of the present study demonstrate that Ost may suppress the progression of MCT­induced PAH in rats, which may be, at least partially, mediated through modulation of the NF­κB p65 signaling pathway.

Osthole inhibits intimal hyperplasia by regulating the NF-κB and TGF-ß1/Smad2 signalling pathways in the rat carotid artery after balloon injury.

Osthole (7-methoxy-8-isopentenoxy-coumarin), a compound extracted from Cnidiummonnieri (L.) Cusson seeds, has been found to exhibit potent therapeutic effects in cancer due to its ability to inhibit inflammation and cell proliferation. However, its effects on arterial wall hypertrophy-related diseases remain unclear. Therefore, in this study, we aimed to investigate the effects of Osthole on intimal hyperplasia in a rat model of carotid artery balloon injury. We established the balloon-induced carotid artery injury rat model in male Sprague-Dawley rats, after which we administered Osthole (20mg/kg/day or 40mg/kg/day) or volume-matched normal saline orally by gavage for 14 consecutive days. Intimal hyperplasia and the degree of vascular smooth muscle cell proliferation were then evaluated by histopathological examination of the changes in the carotid artery, as well as by examination of proliferating cell nuclear antigen (PCNA) expression. Tumour necrosis factor-ɑ (TNF-α), interleukin-1ß (IL-1ß), transforming growth factor-beta (TGF-ß1) and PCNA mRNA expression levels were examined by real-time RT-PCR, while nuclear factor-κB (NF-κB (p65)), IκB-α, TGF-ß1 and phospho-Smad2 (p-Smad2) protein expression levels were analysed by immunohistochemistry or western blot analysis. We found that Osthole significantly attenuated neointimal thickness and decreased the elevations in PCNA protein expression induced by balloon injury. Moreover, Osthole down-regulated the pro-inflammatory factors TNF-α and IL-1ß and NF-κB (p65), whose expression had been upregulated after balloon injury. Moreover, IκB-α protein expression levels increased following Osthole treatment. In addition, the elevations in TGF-ß1 and p-Smad2 protein expression induced by balloon injury were both significantly attenuated by Osthole administration. We concluded that Osthole significantly inhibited neointimal hyperplasia in balloon-induced rat carotid artery injury and that the mechanism by which this occurs may involve NF-κB, IL-1ß and TNF-ɑ down-regulation, which alleviates the inflammatory response, and TGF-ß1/Smad2 signalling pathway inhibition.

Icariin prevents hypertension-induced cardiomyocyte apoptosis through the mitochondrial apoptotic pathway.

A prior study demonstrated that icariin (ICA) could repress angiotensin II-induced apoptosis in H9c2 cells. The activation of mitochondrial apoptotic pathways may play a crucial role in this phenomenon. In this study, we explored the potential protective roles of ICA in apoptosis in cardiomyocytes, cardiac remodelling, and the underlying mechanisms with regard to the mitochondrial apoptotic pathway in rats with spontaneous hypertension. The oral administration of ICA (20 and 40mg/kg/d) inhibited cardiomyocyte apoptosis and ameliorated left heart ventricle remodelling and abnormal mitochondria. ICA also decreased the blood pressure of model rats. ICA treatment increased the expression of Bcl-2 and decreased the expression of p53, Bax, Bok and cleaved caspase 3 in model rats, which suggests the potential mechanism underlying this effect. In summary, ICA inhibits the apoptosis of cardiomyocytes and ameliorates cardiac remodelling. The potential mechanism may relate to the inhibition of the mitochondrial apoptotic pathway.

Taurine inhibits 2,5-hexanedione-induced oxidative stress and mitochondria-dependent apoptosis in PC12 cells.

2,5-hexanedione (HD) is the ultimate neurotoxic metabolite of hexane, causing the progression of nerve diseases in human. It was reported that HD induced apoptosis and oxidative stress. Taurine has been shown to be a potent antioxidant. In the present study, we investigated the protection of taurine against HD-induced apoptosis in PC12 cells and the underlying mechanism. Our results showed the decreased viability and increased apoptosis in HD-exposed PC12 cells. HD also induced the disturbance of Bax and Bcl-2 expression, the loss of MMP, the release of mitochondrial cytochrome c and caspase-3 activation in PC12 cells. Moreover, HD resulted in an increase in reactive oxygen species (ROS) level and a decline in the activities of superoxidedismutase and catalase in PC12 cells. However, taurine pretreatment ameliorated the increased apoptosis and the alterations in key regulators of mitochondria-dependent pathway in PC12 exposed to HD. The increased ROS level and the decreased activities of the antioxidant enzymes in HD group were attenuated by taurine. These results indicate that pretreatment of taurine may, at least partly, prevent HD-induced apoptosis via inhibiting mitochondria-dependent pathway. It is also suggested that the potential of taurine against HD-induced apoptosis may benefit from its anti-oxidative property.