Objective The aim of this study was to establish a reasonable protocol for a rat model of ferric chloride-induced carotid arterial thrombosis by ultrasonic continuous evaluation.Methods Twenty SD rats were randomly divided into four groups and then treated with 20％,30％,40％ or 50％ concentrations of FeCl3,respectively.The vascular conditions were evaluated by 14L ultrasonic probe,at 10 mins,15 mins,and 20 mins.We then selected the best group through the examination of the rate of spontaneous reperfusion of blood vessels and the rate of reperfusion after intravenous injection of urokinase.At the end of the experiment,vessels were fixed in 10％ formalin solution and stained with HE.Results After external application of FeCl3 on rat common carotid artery for 20 mins,the artery occlusion rate was 100％,20％,0％ and 0％ in animals receiving 50％,40％,30％ and 20％ FeCl3,respectively.After external application of FeCl3 on rat common carotid artery for 120 mins,the spontaneous revascularization rate was 0％ in 50％ concentration group whereas were 100％ in rest other groups (P＜ 0.001).In 50％ concentration group,the partial recanalization rate was 40％ after intravenous injection of urokinase.HE staining revealed that the thrombus was dense and the lumen was partially recanalized after the urokinase intervention in 50％ concentration group.Conclusion By use of uultrasonic continuous evaluation of ferric chloride-induced thrombosis of rat common carotid artery,we have demonstrated that external application of 50％ ferric chloride solution for 20 mins is effective for the formation of thrombus model,which may be suitable for the studv of thrombolysis.

BACKGROUND/OBJECTIVES: Previous research has shown maternal betaine supplementation alleviates fetal-derived hepatic steatosis. Therefore, this study examined the anti-inflammatory effect of maternal betaine intake in offspring mice and its mechanism.MATERIALS/METHODS: Female C57BL/6J mice and their offspring were randomly divided into 3 groups according to the treatment received during gestation and lactation: control diet (CD), fatty liver disease (FLD), and fatty liver disease + 1% betaine (FLD-BET). The FLD group was given a high-fat diet and streptozotocin (HFD + STZ), and the FLD-BET group was treated with HFD + STZ + 1% betaine. After weaning, the offspring mice were given a normal diet for 5 weeks and then dissected to measure the relevant indexes. RESULTS: Compared to the CD group, the offspring mice in the FLD group revealed obvious hepatic steatosis and increased serum levels of alanine aminotransferase, interleukin (IL)-6, and tumor necrosis factor (TNF)-α; maternal betaine supplementation reversed these changes. The hepatic mRNA expression levels of IL-6, IL-18, and Caspase-1 were significantly higher in the FLD group than in the CD group. Maternal betaine supplementation reduced the expression of IL-1β, IL-6, IL-18, and apoptosis-associated speck-like protein containing C-terminal caspase recruitment domain (ASC). Maternal betaine supplementation also reversed the increasing protein expressions of nitric oxide dioxygenase-like receptor family pyrin domain containing 3 (NLRP3), ASC, Caspase-1, IL-1β, and IL-18 in offspring mice exposed to HFD + STZ. Maternal betaine supplementation decreased the homocysteine (Hcy) and s-adenosine homocysteine (SAH) levels significantly in the livers. Furthermore, the hepatic Hcy concentrations showed significant inverse relationships with the mRNA expression of TNF-α, NLRP3, ASC, and IL-18. The hepatic SAH concentration was inversely associated with the IL-1β mRNA expression. CONCLUSIONS The lipotropic and anti-inflammatory effect of maternal betaine supplementation may be associated with the inhibition of NLRP3 inflammasome in the livers of the offspring mice.