Biomimetic ZrO2-modified seaweed residue with excellent fluorine/ bacteria removal and uranium extraction properties for wastewater purification.

Exploring and developing promising biomass composite membranes for the water purification and waste resource utilization is of great significance. The modification of biomass has always been a focus of research in its resource utilization. In this study, we successfully prepare a functional composite membrane, activated graphene oxide/seaweed residue-zirconium dioxide (GOSRZ), with fluoride removal, uranium extraction, and antibacterial activity by biomimetic mineralization of zirconium dioxide nanoparticles (ZrO2 NPs) on seaweed residue (SR) grafted with oxidized graphene (GO). The GOSRZ membrane exhibits highly efficient and specific adsorption of fluoride. For the fluoride concentrations in the range of 100-400 mg/L in water, the removal efficiency can reach over 99 %, even in the presence of interfering ions. Satisfactory extraction rates are also achieved for uranium by the GOSRZ membrane. Additionally, the antibacterial performance studies show that this composite membrane efficiently removes Escherichia coli (E. coli) and Methicillin-resistant Staphylococcus aureus (MRSA). The high adsorption of F- and U(VI) to the composite membrane is ascribed to the ionic exchange and coordination interactions, and its antibacterial activity is caused by the destruction of bacterial cell structure. The sustainability of the biomass composite membranes is further evaluated using the Sustainability Footprint method. This study provides a simple preparation method of biomass composite membrane, expands the water purification treatment technology, and offers valuable guidance for the resource utilization of seaweed waste and the removal of pollutants in wastewater.

Bear bile powder alleviates Parkinson's disease-like behavior in mice by inhibiting astrocyte-mediated neuroinflammation.

Parkinson's disease (PD) is a common neurodegenerative disease in middle-aged and elderly people. In particular, increasing evidence has showed that astrocyte-mediated neuroinflammation is involved in the pathogenesis of PD. As a precious traditional Chinese medicine, bear bile powder (BBP) has a long history of use in clinical practice. It has numerous activities, such as clearing heat, calming the liver wind and anti-inflammation, and also exhibits good therapeutic effect on convulsive epilepsy. However, whether BBP can prevent the development of PD has not been elucidated. Hence, this study was designed to explore the effect and mechanism of BBP on suppressing astrocyte-mediated neuroinflammation in a mouse model of PD. PD-like behavior was induced in the mice by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (30 mg·kg-1) for five days, followed by BBP (50, 100, and 200 mg·kg-1) treatment daily for ten days. LPS stimulated rat C6 astrocytic cells were used as a cell model of neuroinflammation. THe results indicated that BBP treatment significantly ameliorated dyskinesia, increased the levels of tyrosine hydroxylase (TH) and inhibited astrocyte hyperactivation in the substantia nigra (SN) of PD mice. Furthermore, BBP decreased the protein levels of glial fibrillary acidic protein (GFAP), cyclooxygenase 2 (COX2) and inducible nitric oxide synthase (iNOS), and up-regulated the protein levels of takeda G protein-coupled receptor 5 (TGR5) in the SN. Moreover, BBP significantly activated TGR5 in a dose-dependent manner, and decreased the protein levels of GFAP, iNOS and COX2, as well as the mRNA levels of GFAP, iNOS, COX2, interleukin (IL) -1ß, IL-6 and tumor necrosis factor-α (TNF-α) in LPS-stimulated C6 cells. Notably, BBP suppressed the phosphorylation of protein kinase B (AKT), inhibitor of NF-κB (IκBα) and nuclear factor-κB (NF-κB) proteins in vivo and in vitro. We also observed that TGR5 inhibitor triamterene attenuated the anti-neuroinflammatory effect of BBP on LPS-stimulated C6 cells. Taken together, BBP alleviates the progression of PD mice by suppressing astrocyte-mediated inflammation via TGR5.

Isoliquiritigenin inhibits microglia-mediated neuroinflammation in models of Parkinson's disease via JNK/AKT/NFκB signaling pathway.

Isoliquiritigenin (ISL) is a flavonoid with numerous pharmacological properties, including anti-inflammation, yet its role in Parkinson's disease (PD) with microglia-mediated neuroinflammation remains unknown. In this study, the effects of ISL on inhibiting microglia-mediated neuroinflammation in PD were evaluated in the 1-methyl-4-phenylpyridinium (MPTP)-induced mouse model of PD and in lipopolysaccharide (LPS)-stimulated BV-2 microglia. Our results showed that ISL prevented behavioral deficits and excessive microglial activation in MPTP-treated mice. Moreover, ISL was found to prevent the elevation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and mitigate the phosphorylation of c-Jun N-terminal protein kinase (JNK), protein kinase B (AKT), nuclear factor kappa light-chain enhancer of activated B cells (NFκB), and inhibitor of NFκB protein ɑ (IκBɑ) in the substantia nigra and striatum of MPTP-treated mice and LPS-stimulated BV-2 cells. Meanwhile, in LPS-stimulated BV-2 cells, ISL inhibited the production of inflammatory mediators such as interleukin (IL)-1ß, IL-6 and tumor necrosis factor alpha (TNF-α). In addition, the agonist of JNK partly abolished the inhibitory effects of ISL in LPS-treated BV-2 cells. Our results demonstrated that ISL inhibits microglia-mediated neuroinflammation in PD models probably through deactivating JNK/AKT/NFκB signaling pathways. The novel findings suggest the therapeutic potential of ISL for microglia-mediated neuroinflammation in PD.

Natural bear bile powder suppresses neuroinflammation in lipopolysaccharide-treated mice via regulating TGR5/AKT/NF-κB signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: According to the Tang Dynasty classics Dietetic Material Medica and the Ming Dynasty classics Compendium of Materia Medica records, bear bile powder (BBP) has been used to treat a variety of diseases, such as febrile seizures, the pathogenesis of which is associated to neuroinflammation. However, the mechanism of BBP on alleviating neuroinflammation remains unclear. AIMS OF THE STUDY: Microglia can be activated by peripheral lipopolysaccharide (LPS) and play an important role in the pathogenesis of neuroinflammation. The purpose of this study is to investigate the effects and mechanism of BBP in inhibiting LPS-induced microglia inflammation in vitro and in vivo. MATERIALS AND METHODS: The anti-microglia inflammatory effects and mechanism of BBP were assessed in LPS-treated BV2 microglial cells and in LPS-treated mice. The mRNA expression levels of the inflammatory factor and the protein expressions of cyclooxygenase-2 (COX2), inducible nitric oxide synthase (iNOS), takeda G-protein coupled receptor 5 (TGR5), nuclear factor-κB (NF-κB), inhibitor of NF-κB (IκBɑ), protein kinase B (AKT) in BV2 cells, mouse hippocampus and cortex were detected. The NF-κB transcription activity and NF-κB nuclear translocation were observed. RESULTS: Our findings showed that BBP reduces branched process retraction and NO in LPS-treated BV2 cells, inhibits the protein expression of ionized calcium binding adaptor molecule 1 in the hippocampus of LPS-treated mice. Moreover, we observed that BBP decreases tumor necrosis factor α, interleukin (IL)-6 and IL-1ß mRNA levels, deceases iNOS and COX-2 protein levels, increases TGR5 protein levels, suppresses the phosphorylation of AKT, NF-κB and IκBɑ protein in microglia both in vitro and in vivo. Further, we found that triamterene, the inhibitor of TGR5, abolishes the effects of BBP in LPS- treated BV2 cells. CONCLUSION: BBP inhibits LPS-induced microglia activation, and the mechanism of its action is partly through TGR5/AKT/NF-κB signaling pathway.

Combination of curcuma zedoary and kelp inhibits growth and metastasis of liver cancer in vivo and in vitro via reducing endogenous H2S levels.

The combination of traditional Chinese medicines can improve the efficacy of cancer treatment. Furthermore, the combination of the traditional Chinese medicine curcuma zedoary and kelp was used to enhance the effect of the dissipation of blood stasis in pediatrics during the Song Dynasty. Curcumenol and laminarin, the main components of curcuma zedoary and kelp, are also reported to have a wide range of biological activities. Therefore, we hypothesize that the combination of curcuma zedoary and kelp may prevent the development of cancer. The aim of this research was to confirm whether a combination of curcuma zedoary and kelp could inhibit the proliferation and metastasis of hepatoma cells and consequently improve prognosis. In this study, we firstly found in H22-bearing mice that the combination of curcuma zedoary and kelp inhibited tumor growth and the expression of metastasis-related proteins (MMPs, VEGF, pAkt, pERK1/2). Meanwhile, the decreased cystathionine beta synthase (CBS, an endogenous hydrogen sulfide (H2S) synthetase) level was also observed in H22-bearing mice admistrated with the combination of curcuma zedoary and kelp. It was also observed that the combination of curcumenol and laminarin inhibited the proliferation, migration and invasion in human hepatoma HepG2 cells. Furthermore, we investigated the potential inhibiting mechanism of the combination of curcumenol and laminarin on HepG2 cell proliferation and metastasis. Our previous research showed that a CBS/H2S system was vital for maintaining the proliferation in hepatoma cells. Here, we found that the levels of pSTAT3 and BCL-2 were decreased in CBS knockdown HepG2 cells and the combination of curcumenol and laminarin significantly decreased the H2S level in a dose-dependent manner and down-regulated the levels of pSTAT3 and BCL-2 in HepG2 cells. Angiogenesis, positively regulated by the vascular endothelial growth factor (VEGF), is essential for human cancer metastasis. In the present study, we found that the combination of curcumenol and laminarin could significantly down-regulate the expression levels of VEGF and its downstream key genes pAkt and pERK1/2. Furthermore, previous research showed that hydrogen sulfide could stimulate angiogenesis. Here, we also observed the reduction of the VEGF, Akt, pAkt, ERK1/2 and pERK1/2 proteins levels and the inhibition of proliferation and metastasis in CBS knockdown HepG2 cells. Moreover, exogenous H2S rescued the cytological results caused by the combination of curcumenol and laminarin. Taken together, the combination of curcuma zedoary and kelp could inhibit the proliferation and metastasis of liver cancer cells in vivo and in vitro by inhibiting endogenous H2S production and down-regulating the pSTAT3/BCL-2 and VEGF pathway, which provides strong evidence for the application of curcuma zedoary and kelp in treatments of liver cancer.