Anti-CXCL8 polyclonal antibody [Biotin]

Previous studies indicate that FGF21 has ability to repair nerve injury, but the specific mechanism is less studied. The present study was designed to investigate the effects of FGF21 on neurodegeneration changes in aging and diabetic mice and its mechanism. The diabetic and aging mice were used to study the effects of FGF21 on neurodegeneration and possible mechanisms. These mice were administrated with PBS, FGF21 or metformin once daily for 4 or 6 months, then the mechanism was studied in SH-SY5Y cells. The relevant gene expression for neurodegeneration was assessed by Quantitative Real Time-PCR, Western blot, H&E staining, immunohistochemistry and ELISA. The Western blot results of NeuN showed that FGF21 inhibited the loss of neurons in diabetic and aging mice. H&E staining results showed that the karyopyknosis and tissue edema around dentate gyrus and Cornu Amonis 3 (CA3) area of hippocampus were also inhibited by FGF21 in aging and diabetes mice. In vivo results revealed that administration of FGF21 suppressed the aggregation of tau and beta-amyloid(1-42) in the brains of diabetic and aging mice. The aggregation resulted in apoptosis of neurons. Meanwhile, FGF21 significantly reduced the expression of Iba1, NF-kappa B, IL6 and IL8 (p < 0.05) and enhanced anti-oxidant enzymes (p < 0.05) in aging and diabetic mice. In addition, the phosphorylation of AKT and AMPK alpha were increased by FGF21 treatment. In vitro experiment showed that the aggregation of tau and beta-amyloid(1-42) were-increased by LPS in SH-SY5Y cells, and FGF21 inhibited the aggregation through inhibiting the expression of NF-kappa B and promoting the phosphorylation of AKT and AMPK alpha. In conclusion, FGF21 attenuates neurodegeneration by reducing neuroinflammation and oxidant stress through regulating the NF-kappa B pathway and AMPK alpha/AKT pathway, which enhances the protective effect on mitochondria in neurons.

Low concentrations of pollutants in surface water challenge the assessment of chronic effects on human health. Human bone mesenchymal stem cells (hBMSCs) were employed as a sensitive and relevant in vitro model to evaluate the potential biological effects caused by mixtures of pollutants in surface water. Organic extracts of surface water collected from Hun River inhibited cell viability in a dose-dependent manner. Surface water extracts at noncytotoxic concentrations induced 533 to 1055 differentially expressed genes (DEGs) in hBMSCs after 48 h of exposure. Total of 370 genes were commonly affected by surface water from different sites and accounted for 35-69% of DEGs impaired by individual sample. Pathways related to human diseases, genetic information processing and organismal systems were enriched based on DEGs. Interleukins (IL1B, IL6 and IL8) were affected and involved in most human diseases related pathways. The significantly downregulation of COL1A1 and the variation of rheumatoid arthritis pathway suggested that surface water potentially inhibited osteogenic differentiation of hBMSCs. Clustering analysis and principle component analysis with DEGs distinguish the surface water from tributary and mainstream. The crossing-species comparison of transcriptomic changes identified 923 and 2715 differentially expressed orthologs in hBMSCs and zebrafish, respectively. After the exposure ceased, the followed osteogenic and adipogenic differentiation in hBMSCs for 14 days were inhibited by the treatment of surface water during undifferentiated period, whereas the non-polar fraction exhibited stronger potency in affecting differentiation than the mid to polar fractions. hBMSCs, combining unsupervised transcriptomic technique and specific endpoints test, are promising in screening the health effects of environmental mixtures in surface water.