The aims of the present study were to investigate the impact of rapamycin (RAPA) on the endometriosis (EMS) lesions in severe combined immunodeficiency (SCID) mice, and to examine the possible mechanism involved in a novel therapy in EMS. Following the successful establishment of an EMS-SCID mouse model, the mice were randomly assigned into the RAPA, control and saline treatment groups. Subsequent to treatment for 2 weeks, the serum hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) were detected using ELISA. The levels of HIF-1α and VEGF, as well as the size of EMS lesions, were compared among the three groups. In addition, the HIF-1α, VEGF and CD34 protein expression levels, and the microvessel density (MVD) of the lesions were determined by immunohistochemical analysis. Compared with the control and saline groups, the volume of EMS lesions in the RAPA-treated SCID mice was significantly reduced. Furthermore, the serum level and protein expression of VEGF, and the MVD in the lesions of the RAPA-treated group were significantly reduced when compared with the other two groups. These parameters were comparable in the control and saline groups. In conclusion, RAPA may inhibit the growth of endometriotic lesions, most possibly through the inhibition of the expression of VEGF in lesions, thereby inhibiting angiogenesis.
Traumatic brain injury (TBI) is a serious disease that threatens life and health of people. It poses a great economic burden on the healthcare system. Thus, seeking effective therapy to cure a patient with TBI is a matter of great urgency. Microglia are macrophages in the central nervous system (CNS) and play an important role in neuroinflammation. When TBI occurs, the human body environment changes dramatically and microglia polarize to one of two different phenotypes: M1 and M2. M1 microglia play a role in promoting the development of inflammation, while M2 microglia play a role in inhibiting inflammation. How to regulate the polarization direction of microglia is of great significance for the treatment of patients with TBI. The polarization of microglia involves many cellular signal transduction pathways, such as the TLR-4/NF-κB, JAK/STAT, HMGB1, MAPK, and PPAR-γ pathways. These provide a theoretical basis for us to seek therapeutic drugs for the patient with TBI. There are several drugs that target these pathways, including fingolimod, minocycline, Tak-242 and erythropoietin (EPO), and CSF-1. In this study, we will review signaling pathways involved in microglial polarization and medications that influence this process.
Traumatic brain injury (TBI) is still a major public health problem worldwide, and the research of neuroprotective drugs has encountered great difficulties. Whole body vibration (WBV) is a safe and powerful rehabilitative intervention in various clinical settings, but its effect on neurological diseases is not well documented. In this study, we investigated the effects of WBV pretreatment on brain damage following experimental TBI mimicked by controlled cortical impact (CCI) in mice. C57BL/6 J male mice were expose to WBV at 30 Hz twice per day for 20 days and injured by CCI. WBV had no effect on animal body weight, but significantly reduced the TBI-induced brain edema in the cortex. The results of immunostaining showed that the activation of microglia and astrocytes induced by TBI in brain sections was attenuated by WBV. In consistent, WBV markedly inhibited the expression of pro-inflammatory cytokines, while increased the levels of anti-inflammatory cytokine interleukin 10 (IL-10). In addition, WBV pretreatment alleviated neuronal apoptosis in the cortex and suppressed the cleavage of the apoptotic executive molecule caspase-1. The neurological dysfunction following TBI was determined by open field test and Morris Water Maze (MWM) assay. The results showed that motor activity, learning and memory ability were preserved by WBV compared to TBI-injured mice. In summary, our present data identified WBV as a clinically potent strategy with which to attenuate TBI-related brain damage through regulating neuroinflammation.
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