Salidroside-pretreated mesenchymal stem cells contribute to neuroprotection in cerebral ischemic injury in vitro and in vivo.

Mesenchymal stem cells (MSCs) are considered a promising tool for treating cerebral ischemic injury. However, their poor survival after transplantation limits their therapeutic effect and applications. Salidroside has been reported to exert potent cytoprotective and neuroprotective effects. This study aimed to investigate whether salidroside could improve MSC survival under hypoxic-ischemic conditions and, subsequently, alleviate cerebral ischemic injury in a rat model. MSCs were pretreated by salidroside under hypoxic-ischemic conditions. The cell proliferation, migratory capacity, and apoptosis were evaluated by means of Cell Counting Kit-8, transwell assay, and flow cytometry. MSCs pretreated with salidroside were transplanted into the rats subsequent to middle cerebral artery occlusion. The grip strength, 2,3,5-triphenyltetrazolium chloride, and hematoxylin-eosin staining were used to analyze the therapeutic efficiency and pathological changes. The mature neuron marker NeuN and astrocyte marker GFAP in the focal area were detected by immunofluorescence. These results indicated that salidroside promoted the proliferation, migration and reduced apoptosis of MSCs under hypoxic-ischemic conditions. In vivo experiments revealed that transplantation of salidroside-pretreated MSCs strengthened the therapeutic efficiency by enhancing neurogenesis and inhibiting neuroinflammation in the hippocampal CA1 area after ischemia. Our results suggest that pretreatment with salidroside could be an effective strategy to enhance the cell survival rate and the therapeutic effect of MSCs in treating cerebral ischemic injury.

Mesenchymal Stem Cells: A Potential Therapeutic Strategy for Neurodegenerative Diseases.

Neurodegenerative disease is a kind of chronic, progressive nervous system disease characterized by neuron degeneration or apoptosis. Current treatments cannot prevent the development of the disease. Possible alternative treatments include cell therapy, especially with the use of mesenchymal stem cells (MSCs). MSCs are pluripotent stem cells with capacities for self-renewal and multidirectional differentiation. MSCs may serve as a reliable source of neural cells for potential cell replacement therapy or regenerative medicine treatment. Here, we summarized the therapeutic mechanisms of MSCs and how they can contribute to the development of treatments for neurodegenerative diseases.

Dimethyloxalyl Glycine Regulates the HIF-1 Signaling Pathway in Mesenchymal Stem Cells.

Mesenchymal stem cells (MSCs) are pluripotent stem cells with self-renewal and multidirectional differentiation capabilities. Dimethyloxalyl glycine (DMOG) mobilizes MSCs, and the hypoxia inducible factor-1 (HIF-1) signaling pathway plays an important role in MSC mobilization. We aimed to investigate the effect of DMOG on the HIF-1 pathway in MSCs. Rats were treated with DMOG, and the numbers of peripheral blood MSCs (PB-MSCs) and bone marrow MSCs (BM-MSCs) were detected by the Colony-forming unit fibroblastic (CFU-F) method. The growth curve, cell cycle and migration ability of PB-MSCs and BM-MSCs were detected by CCK-8, Flow cytometry and Transwell assays. Western blotting and real-time qPCR were used to detect the expression of the HIF-1 pathway. The number of bone marrow microvessels was detected by immunohistochemistry. DMOG significantly increased the numbers of PB-MSCs and BM-MSCs (P < 0.05). Further, the MSCs in peripheral blood and bone marrow still had the ability to proliferate and migrate after mobilization by DMOG. The expression levels of HIF-1α, stromal cell-derived factor-1α (SDF-1α) and vascular endothelial growth factor (VEGF) in MSCs were significantly regulated by DMOG (P < 0.05). The number of bone marrow microvessels decreased after the VEGF/VEGFR signaling pathway was blocked by SU5416 (P < 0.05). Therefore, these findings demonstrated that DMOG regulates the HIF-1α signaling pathway and promotes biological effects in MSCs.

Scattering-initiated parametric noise in optical parametric chirped-pulse amplification.

We experimentally study a new kind of parametric noise that is initiated from signal scattering and enhanced through optical parametric amplification. Such scattering-initiated parametric noise behaves similarly to parametric super-fluorescence in the spatial domain, yet is typically much stronger. In the time domain it inherits the chirp of signal pulses and can be well compressed. We demonstrate that scattering-initiated parametric noise has little influence on the pulse contrast but can degrade the energy conversion efficiency substantially.

Synthesis and antitumor activity of feruloyl and caffeoyl derivatives.

We developed two efficient protocols for the synthesis of feruloyl and caffeoyl derivatives from commercial vanillin and veratraldehyde. Pharmacological activities were assessed against a panel of human cancer cell lines in vitro. Most synthesized compounds demonstrated attractive cytotoxicity. Several new compounds demonstrated significant antiproliferative and cytotoxic activities against HeLa and Bewo tumor cell lines. In particular, 5-nitro caffeic adamantyl ester showed broad spectrum of tumor inhibition in 10 cell lines, and reduced tumor weight by 36.7% in vivo when administered at a dose of 40 mg kg(-1).