Effects of V2O5 on Proliferation and Differentiation of Limb Bud Cells of Rat

The micromass culture was used to determine the effects of vanadium pentoxide (V2O5 ) on the proliferation and differentiation of limb bud cells of rat. In the in vitro test, the results showed that V2O5 had obvious inhibiting effects on both proliferation and differentiation of limb bud cells with a dosedependent response, its proliferating and differentiating IC50 being 13.64 and 4.77μmol/L, respectively. In the in vivo/in vitro test, the results showed that V2O5 had no obvious effect on cell proliferation but had obvious inhibiting effect on cell differentiation. These results indicated that V2O5 might have a specific inhibiting effect on the differentiation of limb bud cells.

Vanadyl complexes work with cinnamaldehyde in promoting cell viability under the β-amyloid burden in SH-SY5Y neural cells

The Alzheimer＇s disease （AD） is one of the common cognitive disorders in the elderly. AD shares some similar pathological characters with diabetes mellitus （DM）, suggesting potential application of anti-diabetic agents, such as vanadyl complexes, in therapeutic treatment of AD. In the present work, we studied the effects of vanadyl acetylacetonate （VO（acac）2） and cinnamaldehyde （CA） on an AD model based on SH-SY5Y neural cells. The experimental results showed that VO（acac）2 at sub-micromolar concentrations could improve the viability of neural cells with or without increased β-amyloid （Aβ） burden; and the combination of VO（acac）2 and CA showed an additive cell protection effects. Further investigation revealed that for SH-SY5Y neural cells, VO（acac）2 could activate PPART-AMPK signal transduction and inhibit GSK 3β, one of the major kinases for Tau hyperphosphorylation. Meanwhile, CA could correct the abnormal mitochondrial morphology due to Aβ-induced excessive mitochondrial fission, thus restoring/enhancing the mitochondrial function. In addition, both VO（acac）2 and CA decreased intracellular reactive oxygen species （ROS） level and inhibited formation of toxic Aβ oligomers. Overall, VO（acac）2 might work with CA in improving the neural cell viability under the Aβ burden, suggesting application of vanadium metallodrugs in AD treatment.

Vanadium regulates HSP60-induced IL-6 release from RAW264.7 cells in a dose-dependent manner

Vanadium compounds are promising anti-diabetic agents. However, the underlying mechanisms have not been fully elucidated. Inflammation and auto-immune disorders play important roles in the progresses of both type Ⅰ and type Ⅱ diabetes, in which heat shock protein 60 （HSP60） is an important endogenous inflammatory mediator. In the present work, we investigated the effects of vanadium compounds （vanadyl sulfate and sodium metavanadate） on the IL-6 production in RAW264.7 cells upon HSP60 stimulation. Our data revealed that both vanadyl ions regulated the IL-6 expression in a concentration-dependent manner. However, the two common NF-κB and PPAR-γ, signal pathways were not involved in this process. Further works are needed to elucidate the underlying mechanism and significance of the immuno-modification actions for the pharmacological applications of anti-diabetic vanadium compounds.