ABSTRACT
Hypothermia treatment is one of the neuroprotective strategies that improve neurological outcomes effectively after brain damage. Minimally invasive surgery (MIS) has been an important treatment of intracerebral hemorrhage (ICH). Herein, we evaluated the neuroprotective effect and mechanism of MIS joint local cooling lavage (LCL) treatment on ICH via detecting the inflammatory responses, oxidative injury, and neuronal apoptosis around the hematoma cavity in rats. ICH model was established by type IV collagenase caudatum infusion. The rats were treated with MIS 6 h after injection, and then were lavaged by normothermic (37 °C) and hypothermic (33 °C) normal saline in brain separately. The results indicated that MIS joint LCL treatment showed enhanced therapeutic effects against ICH-induced inflammation injury and apoptosis in rats, as convinced by the decline of TUNEL-positive cells, followed by the decrease of IL-1ß and LDH and increase of IL-10 and SOD. This study demonstrated that the strategy of using MIS joint LCL may achieve enhanced neuroprotection against ICH-induced inflammation injury and apoptosis in rats with potential clinic application.
Subject(s)
Apoptosis/drug effects , Brain Edema/surgery , Cerebral Hemorrhage/complications , Minimally Invasive Surgical Procedures , Animals , Brain Injuries/surgery , Cerebral Hemorrhage/therapy , Inflammation/surgery , Male , Minimally Invasive Surgical Procedures/methods , Neurons/metabolism , Rats, Sprague-Dawley , Recovery of Function/physiology , Therapeutic Irrigation/methodsABSTRACT
<p><b>OBJECTIVE</b>To preliminarily study the changes in CD4CD25regulatory T cells (Tregs) in children with severe purulent meningitis at the early stage and its possible implications.</p><p><b>METHODS</b>A retrospective analysis was performed on the clinical data of 39 children with severe purulent meningitis who were admitted to the pediatric intensive care unit from August 2014 to December 2015. According to whether Tregs count was decreased within 12 hours of hospitalization (considering Tregs count <410/mmas decreased), they were divided into two groups: decrease group and non-decrease group. The associations between the changes in Tregs cells and the clinical manifestations, laboratory marker levels, and prognosis were analyzed.</p><p><b>RESULTS</b>Of the 39 cases, 13 (33%) showed a decrease in the proportion of Tregs cells (<31%) and 18 (46%) showed a decrease in the absolute Tregs cell count (<410/mm). Four deaths were all in the Tregs decrease group. Compared with the non-decrease group, the decrease group showed a significantly higher proportion of children with a peripheral blood leukocyte count lower than the normal range and a significantly greater increase in the level of serum procalcitonin (P<0.05).</p><p><b>CONCLUSIONS</b>Tregs might be suppressed in children with severe purulent meningitis at the early stage. And its suppression could be related to the severer inflammation reaction and higher mortality in those patients.</p>
Subject(s)
Child , Child, Preschool , Female , Humans , Infant , Male , C-Reactive Protein , Calcitonin , Blood , Leukocyte Count , Meningitis , Allergy and Immunology , Suppuration , Allergy and Immunology , T-Lymphocytes, Regulatory , Allergy and ImmunologyABSTRACT
Previously we reported that a polypeptide from Chlamys farreri (PCF) was a potent photoprotective agent against ultraviolet (UV) irradiation in vitro. To understand the mechanism by which PCF protects cells from irradiation, we studied anti-apoptotic effects of PCF against UV irradiation on the murine thymocytes in vitro. MTT and flow cytometric analysis assays showed that 2h pretreatment with PCF completely abolished UV induced cell death. TEM examination showed that PCF fully protected the ultrastructure of thymocytes exposed to UV irradiation. Lipid peroxidation and intracellular reactive oxygen species assays indicated that PCF efficiently blocked production of reactive oxygen intermediates induced by UV irradiation. Further, PCF protected UV-irradiated thymocytes from losing mitochondrial transmembrane potential and DNA fragmentation. Based on these observations we propose that PCF is a potent anti-apoptotic factor, which protects cells from irradiation at multiple steps.
