Role of intracranial bone marrow mesenchymal stem cells in stroke recovery: A focus on post-stroke inflammation and mitochondrial transfer.

Stem cell therapy has become a hot research topic in the medical field in recent years, with enormous potential for treating a variety of diseases. In particular, bone marrow mesenchymal stem cells (BMSCs) have wide-ranging applications in the treatment of ischemic stroke, autoimmune diseases, tissue repair, and difficult-to-treat diseases. BMSCs can differentiate into multiple cell types and exhibit strong immunomodulatory properties. Although BMSCs can regulate the inflammatory response activated after stroke, the mechanism by which BMSCs regulate inflammation remains unclear and requires further study. Recently, stem cell therapy has emerged as a potentially effective approach for enhancing the recovery process following an ischemic stroke. For example, by regulating post-stroke inflammation and by transferring mitochondria to exert therapeutic effects. Therefore, this article reviews the therapeutic effects of intracranial BMSCs in regulating post-stroke inflammation and mitochondrial transfer in the treatment of stroke, providing a basis for further research.

Mitochondrial Transplantation and Immune Response of Human Bone Marrow Mesenchymal Stem Cells for the Therapeutic of Ischemic Stroke.

Ischemic stroke is the leading cause of death and disability worldwide, with increasing incidence and mortality, imposing a significant social and economic burden on patients and their families. However, cerebral vascular occlusion leads to acute loss of neurons and destruction of synaptic structures. The limited treatment options cannot adequately address intra-neuronal mitochondrial dysfunction due to stroke. Therefore, stem cell-derived mitochondria transplantation plays an important role in neuronal protection and recovery after stroke, when combined with the intracranial and extracranial immunoregulatory effects of stem cell therapy, revealing the mechanism of transferred mitochondria in stem cells in protecting neurological function among chronic-phase ischemic stroke by affecting the endogenous apoptotic pathway of neuronal cells. This research elaborated on the mitochondrial dysfunction in neurons after ischemic stroke, followed by human bone marrow mesenchymal stem cells (hBMSC) rescued damaged neurons by mitochondrial transfer through tunneling nanotubes (TNTs), and the immunomodulatory effect of the preferential transfer of stem cells to the spleen when transplanted into the body.which created an immune environment for nerve repair, as well as improved neurological recovery after the chronic phase of stroke. This review is expected to provide a novel idea for applying intracranial stem cell transplantation in chronic-phase ischemic stroke treatment.

Immune response treated with bone marrow mesenchymal stromal cells after stroke.

Stroke is a leading cause of death and long-term disability worldwide. Tissue plasminogen activator (tPA) is an effective treatment for ischemic stroke. However, only a small part of patients could benefit from it. Therefore, finding a new treatment is necessary. Bone marrow mesenchymal stromal cells (BMSCs) provide a novel strategy for stroke patients. Now, many patients take stem cells to treat stroke. However, the researches of the precise inflammatory mechanism of cell replacement treatment are still rare. In this review, we summarize the immune response of BMSCs treated to stroke and may provide a new perspective for stem cell therapy.

[Effect of fluo-hydroxyapatite on biological properies of osteosarcoma MG63 cells].

OBJECTIVE: To investigate the effects of 20% fluor-hydroxyapatite (FHA) on proliferation and osteogenic differentiation of human MG63 osteosarcoma cells. METHODS: FHA was prepared by chemical precipitation method, and its structure and surface features were tested by scanning microscope, X-ray diffraction (XRD) and Fourier transform infrared spectroscopy. MG63 cells were cultured and divided into FHA, hydroxyapatite (HA) and control groups (n = 3). The proliferation of the cells was evaluated using methylthiazol tetrazolium (MTT) assay. ALP activity of the cells was assessed. Osteogenic differentiation was evaluated based on the reverse transcription PCR (RT-PCR) of differentiation-related genes, namely, collagen type I (Col I), alkaline phosphatase (ALP), osteocalcin (OCN) and core binding factor α1 (Cbfα1). The data were analyzed statistically by one-way analysis of variance using SPSS 13.0 software. RESULTS: XRD test showed that the main crystalline phase of FHA was similar to that of HA. Absorptance value of cells exposed to FHA(1.87±0.06) measured by MTT was higher than that of the control(1.25±0.02) on the third day(P < 0.05), and there was no statistically significant difference between the cells exposed to FHA and HA(1.84±0.03) (P > 0.05). ALP activity of the cells exposed to FHA(4.62±0.09)was higher than that of the control (1.92 ± 0.05) (P < 0.05). RT-PCR tests showed that compared with the control, FHA up-regulated the expression of Col I, ALP and OCN mRNA, down-regulated the expression of Cbfα1 mRNA. CONCLUSIONS: FHA enhances the proliferation and osteogenic differentiation-related gene expression, and has good biocompatibility.