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Bone marrow is full of mitochondria. However, the role of bone marrow mitochondrial protein in bone marrow damage and related signal transduction mechanism remains to be further studied. OPA is a newly discovered mitochondrial transmembrane protein. Its expression pattern and function in the physiological and pathological conditions of bone marrow are still elusive. The purpose of this study is to investigate the potential role of OPA in osteoporosis.A mouse osteoporosis model was established by radiation. The OPA expression was tested by Western blot and qRT-PCR. The P38 signaling activity was evaluated by enzymatic activity kit. The mitochondrial ATP production was determined by flow cytometry. The bone marrow cell apoptosis was detected by flow cytometry. U0126 was used to pretreat mouse before modeling. Bone marrow tissue was collected from patients who received osteoporosis surgery to test the OPA expression, P38 activation and cell apoptosis. The OPA and P38 levels were analyzed by correlation.The mouse osteoporosis model was successfully established by radiation induction. In this osteoporosis model, the expression of OPA was increased. The P38 signaling was activated while the mitochondrial ATP production was reduced, with the increase of apoptosis of bone marrow cells. By contrast, U0126 pretreatment markedly inhibited the OPA expression, restrained the P38 signaling pathway, enhanced mitochondrial ATP production and suppressed the bone marrow cell apoptosis in mouse osteoporosis model. A significantly positive correlation was found between OPA and P38.The down-regulation of OPA inhibits cell apoptosis and improves osteoporosis via inducing mitochondrial ATP production and suppressing the P38 signaling pathway.

The occurrence rate of delayed fracture healing in diabetes mellitus patients is high. Transforming growth factor β1 (TGF-β1) is an important regulatory factor in bone tissue repair and regeneration. However, TGF-β1 expression and its function in diabetic patient fracture have not been fully elucidated.Type 2 diabetes fracture patients (T2DM group), fracture patients without diabetes (non-T2DM group), and healthy volunteers (Control group) were selected for the research. TGF-β1 expression in peripheral blood was detected by using enzyme-linked immunosorbent assay (ELISA). Osteoblast cell line, MG-63 cells, were randomly divided into Control, high glucose group, and TGF-β1 group. TGF-β1 expression was evaluated by using Real Time-PCR (RT-PCR). Cell proliferation was evaluated by using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell apoptosis activity was determined with caspase-3 activity and flow cytometry assay. The effect of TGF-β1 on NF-κB was detected by using Western blot.TGF-β1 was significantly reduced in patients of T2DM and non-T2DM groups compared with Control (p0.05), while it was lower in T2DM group (p0.05). TGF-β1 expression was declined, cell proliferation was inhibited, caspase-3 activity was enhanced, cell apoptosis was elevated, and NF-κB expression was reduced in MG-63 cells of high glucose group compared to Control group (p0.05). TGF-β1 significantly promoted cell proliferation, suppressed caspase-3 activity, alleviated cell apoptosis, and elevated NF-κB expression in MG-63 cells compared with high glucose group (p0.05).TGF-β1 decreased in diabetes fracture patients. Up-regulation of TGF-β1 regulates cell apoptosis and caspase-3 activity, and it facilitates osteoblasts proliferation.

To observe the one-year neurologic prognostic outcome of newborns with moderate and severe hypoxic-ischemic encephalopathy (HIE) who received recombinant human erythropoietin (rhuEPO) combined with exogenous monosialotetrahexosylganglioside (GM1) treatment to provide new guidelines for clinical treatment.Seventy-six newborns with moderate and severe HIE were selected from February 2011 to February 2014 in our hospital. This study received the informed consent of our hospital's Ethics Committee and the newborns' guardians. The newborns were divided to an observation group (n = 34 cases) and a control group (n = 42 cases). All newborns underwent hypothermia and conventional treatment for their conditions. The control group received GMl treatment and observation group received rhuEPO combined with GMl treatment. The curative differences and neural behavior from these two groups were compared.The excellent, efficient proportion and total effective rate of the newborns from the observation group were higher than the control group. The death rate, cerebral palsy and the invalid ratio of the newborns from the observation group were lower than that of the control group. Awareness, muscle tension, primitive reflex and increased intracranial pressure recovery time of the newborns in the observation group were less than those of the control group. The Neonatal Behavior Neurological Assessment (NBNA) score of both groups after the treatment of 7, 14 and 28 days were significantly higher and increased with time (p0.05). The MDI, PDI and DQ score of newborns from the two groups all increased after treatment of 3, 6 and 12 months than those of before, which increased with time (p0.05).The rhuEPO + GMl treatment in newborns with HIE improves short-term clinical effects and long-term neurological symptoms.