The aim of this study was to investigate the effects of the combination of sodium ferulate (SF) and oxymatrine (OMT) on mice with cecal ligation and puncture (CLP)-induced sepsis. Swiss male mice were randomly divided into a control group, CLP group, three SF + OMT groups (3.1+6.9; 6.2+13.8 and 12.3+27.7 mg/kg), SF (6.2 mg/kg) group and OMT (13.8 mg/kg) group. Eight hours after the administration of the drugs, the survival rates and survival times of the animals were monitored. In addition, the lung wet/dry weight (W/D) ratio; alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) levels in the serum; the C-reactive protein (CRP), interleukin-6 (IL-6) and interferon-γ (IFN-γ) levels in the serum and lung and liver homogenates; and the malondialdehyde (MDA) and superoxidase dismutase (SOD) levels in the lung and liver homogenates were measured. The bacterial load in the serum was also studied. Following treatment with the combination of SF and OMT, the survival rate increased and the survival time was prolonged; CLP-induced increases in the lung W/D ratio and the levels of ALT, AST, LDH, CRP, IL-6, IFN-γ and MDA were significantly reduced; and the SOD activity levels were increased, compared with those of the untreated animals with CLP-induced sepsis. These results indicated that the combination of SF and OMT induced protective effects against CLP-induced lethal sepsis of mice. The possible mechanism of these effects may be associated with the alleviation of systemic inflammation and diminishment of oxidative injury.
Chronic cerebral hypoperfusion (CCH) is one of the most common causes of vascular dementia (VaD) and is recognised as an etiological factor in the development of Alzheimer’s disease (AD). CCH can induce severe cognitive deficits, as assessed by the water maze task, along with neuronal loss in the hippocampus. However, there are currently no effective, approved pharmacological treatments available for VaD. In the present study, we created a rat model of CCH using bilateral common carotid artery occlusion and found that (-)-SCR1693, a novel compound, prevented rats from developing memory deficits and neuronal damage in the hippocampus by rectifying cholinergic dysfunction and decreasing the accumulation of the phospho-tau protein. These results strongly suggest that (-)-SCR1693 has therapeutic potential for the treatment of CCH-induced VaD.
Abstract. The present study aimed to investigate the anti-exudative effects of sodium ferulate combined with oxymatrine in a mouse model of acetic acid-induced peritonitis. Furthermore, the underlying mechanisms were explored by determining the effects of these drugs on the volume and aquaporin 1 (AQP1) expression in vascular endothelial cells on omentum majus and human umbilical vein endothelial cells (HUVEC). Treatment with sodium ferulate combined with oxymatrine was shown to significantly inhibit acetic acid-induced vascular permeability in the peritonitis model mice and furthermore to significantly decrease the optical density of Evans blue, the leukocyte number and the levels of interleukin-6, C-reactive protein and interferon-γ in peritoneal lavage fluid. Pathological analysis of the omentum majus revealed that sodium ferulate and oxymatrine combination treatment significantly alleviated vascular endothelial cell edema and capillary loss. In vitro, flow cytometry revealed that the volume of HUVECs was significantly reduced in the drug treatment groups, as reflected in the forward scatter value. The optical density of AQP1 on the membrane of the vascular endothelial cells on omentum majus and HUVECs were significantly increased in the drug treatment groups compared with the model group. These results indicated that sodium ferulate and oxymatrine combination treatment possessed prominent anti-exudative effects and that the underlying mechanisms are likely to include the improvement of vascular endothelial cellular edema, possibly by upregulation of AQP1 expression on their membrane, which requires further exploration.
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