ABSTRACT
It is still an important and hard work to diagnose anaphylactic shock in forensic practice. However, no breakthrough progresses in the diagnosis of anaphylactic shock and relevant research have been made so far due to the problems we used to meet in actual postmortem examination ,which are short of specific pathological changes in autopsy, the condition progress of patients who occur anaphylactic shock and history of allergy. Furthermore, patients suffer from diseases such as coronary heart disease, pneumonia, asthma, skin irritation, etc, and blood serum allergy biomarkers degrade after hemolysis on account of a long time from death to autopsy ,which are also the difficulties we have to cope with. The aim of this review is to focus on present situation and diagnostic index of anaphylactic shock including the pathological changes and some experimental methods such as special stain, immunohistochemical and serological test to provide reference for diagnosis and study of anaphylactic shock.
ABSTRACT
This study examined the neuroprotective effect of cluster of differentiation molecule 200 (CD200) against methamphetamine (METH)-induced neurotoxicity. In the in vitro experiment, neuron-microglia cultures were treated with METH (20 μmol/L), METH (20 μmol/L)+CD200-Fc (10 μg/mL) or CD200-Fc (10 μg/mL). Those untreated served as control. Microglia activation expressed as the ratio of MHC-II/CD11b was assessed by flow cytometry. The cytokines (IL-1β, TNF-α) secreted by activated microglia were detected by enzyme-linked immunosorbent assay (ELISA). In the in vivo experiment, 40 SD rats were divided into control, METH, METH+CD200-Fc and CD200-Fc groups at random. Rats were intraperitoneally injected with METH (15 mg/kg 8 times at 12 h interval) in METH group, with METH (administered as the same dose and time as the METH group) and CD200-Fc (1 mg/kg at day 0, 2, 4 after METH injection) in METH+CD200-Fc group, with CD200-Fc (1 mg/kg injected as the same time as the METH+CD200-Fc group) or with physiological saline solution in the control group. The level of striatal dopamine (DA) in rats was measured by high-performance liquid chromatography (HPLC). The microglial cells were immunohistochemically detected for the expression of Iba-1, a marker for microglial activation. The results showed that METH could increase the microglia activation in the neuron-microglia cultures and elevate the secretion of IL-1β and TNF-α, which could be attenuated by CD200-Fc. Moreover, CD200-Fc could partially reverse the striatal DA depletion induced by METH and reduce the number of activated microglia, i.e. Iba-1-positive cells. It was concluded that CD200 may have neuroprotective effects against METH-induced neurotoxicity by inhibiting microglial activation and reversing DA depletion in striatum.
Subject(s)
Animals , Male , Rats , Animals, Newborn , Antigens, CD , Cells, Cultured , Coculture Techniques , Corpus Striatum , Cell Biology , Allergy and Immunology , Cytokines , Allergy and Immunology , Dopamine , Allergy and Immunology , Drug Interactions , Methamphetamine , Toxicity , Microglia , Allergy and Immunology , Neurons , Metabolism , Rats, Sprague-DawleyABSTRACT
This study examined the neuroprotective effect of cluster of differentiation molecule 200 (CD200) against methamphetamine (METH)-induced neurotoxicity. In the in vitro experiment, neuron-microglia cultures were treated with METH (20 μmol/L), METH (20 μmol/L)+CD200-Fc (10 μg/mL) or CD200-Fc (10 μg/mL). Those untreated served as control. Microglia activation expressed as the ratio of MHC-II/CD11b was assessed by flow cytometry. The cytokines (IL-1β, TNF-α) secreted by activated microglia were detected by enzyme-linked immunosorbent assay (ELISA). In the in vivo experiment, 40 SD rats were divided into control, METH, METH+CD200-Fc and CD200-Fc groups at random. Rats were intraperitoneally injected with METH (15 mg/kg 8 times at 12 h interval) in METH group, with METH (administered as the same dose and time as the METH group) and CD200-Fc (1 mg/kg at day 0, 2, 4 after METH injection) in METH+CD200-Fc group, with CD200-Fc (1 mg/kg injected as the same time as the METH+CD200-Fc group) or with physiological saline solution in the control group. The level of striatal dopamine (DA) in rats was measured by high-performance liquid chromatography (HPLC). The microglial cells were immunohistochemically detected for the expression of Iba-1, a marker for microglial activation. The results showed that METH could increase the microglia activation in the neuron-microglia cultures and elevate the secretion of IL-1β and TNF-α, which could be attenuated by CD200-Fc. Moreover, CD200-Fc could partially reverse the striatal DA depletion induced by METH and reduce the number of activated microglia, i.e. Iba-1-positive cells. It was concluded that CD200 may have neuroprotective effects against METH-induced neurotoxicity by inhibiting microglial activation and reversing DA depletion in striatum.
ABSTRACT
AIM:To explore the protective effect of ischemic preconditioning on myocardial capillary bed. METHODS: Anesthetized open-chest dogs in ischemic preconditioning (IP) group ( n =6) were subjected to 5 min ischemia and 5 min reperfusion for 4 times in left descending coronary artery (LDA) while the dogs in sham-operated (SO) group ( n =6) were observed for 40 min without any stimulating. Myocardial contrast echocardiography (MCE) was performed before the surgery, at the end of the first and the fourth ischemia and reperfusion period, respectively. Myocardial samples in ischemic area were obtained for capillaries ultrastructure examination and their quantitative analysis was conducted by corresponding imagine analyzing system, then compared within group and between control group. RESULTS: (1) Comparing fourth 5 min ischemia with first one, the percents of area defect in minimum (AD min%) by MCE decreased from 32.6%?5.7% to 21.8%?5.2%( P
ABSTRACT
Objective To study the changes in activity of NADPH oxidase, the effects of signal molecules on membrane potential and ROS production of mitochondria in apoptotic murine peritoneal macrophages. Methods Laser scanning confocal microscopy, flow cytometry and fluorescence labeling were used. Results 1 The macrophages treated with dexamethasone developed apoptosis quickly and presented concomitant apoptotic changes. 2 Mitochondria membrane depolarized quickly, the activity of NADPH oxidase declined sharply, and ROS production decreased rapidly. The erasers of ROS promoted macrophage apoptosis. 3 PKC favored, and cAMP inhibited the macrophage apoptosis and the rapid drop in ROS and mitochondrial membrane depolarization. cGMP and TPK which slightly inhibited macrophage apoptosis, had no effects on ROS. Conclusion 1 The activity of NADPH oxidase declined sharply, hence the ROS decreased rapidly, which promoted apoptosis in macrophages treated with dexamethasone. 2 The signal molecules affected apoptosis by modulating ROS decline and mitochondria depolarization. The results suggested that, mitochondria variations, especially the variations of ROS and membrane potential, mainly affected macrophage apoptosis.;