Hydrogen sulfide attenuates ferric chloride-induced arterial thrombosis in rats

Qin, Yiren; You, Shoujiang; Zhang, Yan; Li, Qian; Wang, Xianhui; Wang, Fen; Hu, Lifang; Liu, Chun‐Feng

doi:10.3109/10715762.2016.1164311

Cited by 13 publications

(10 citation statements)

References 38 publications

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“…Thrombosis of the inferior vena cava (IVC) was induced by applying a piece of filter paper (5 mm × 10 mm) saturated with 10% FeCl 3 (Sigma-Aldrich, St. Louis, USA) solution for 5 min [ 12 ] (Fig. 1 c and d).…”

Section: Methodsmentioning

confidence: 99%

Novel microspheres reduce the formation of deep venous thrombosis and repair the vascular wall in a rat model

Dai

et al. 2017

Blood Coagulation &Amp; Fibrinolysis

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L-Arginine (L-arg), widely known as a substrate for endogenous nitric oxide synthesis, can improve endothelial function associated with the vasculature, inhibit platelet aggregation, and alter the activity of vascular smooth muscle cells. P-selectin is a membrane component of the platelet alpha-granule and the endothelial cell-specific Wiebel–Palade body that plays a central role in mediating interactions between platelets and both leukocytes and the endothelium. The experiment was designed to evaluate the effect of novel microspheres with L-arg targeting P-selectin on the formation of deep vein thrombosis and repair of vascular wall in a rat model. Thrombosis of the inferior vena cava was induced by applying a piece of filter paper (5 mm × 10 mm) saturated with 10% FeCl3 solution for 5 min. Targeted microspheres with L-arg, targeted microspheres with water, and saline were injected into the tail veins of the rats after 30 min of applying the filter paper saturated with 10% FeCl3 solution. The dry weight and length of the thrombus isolated from the inferior vena cava were significantly decreased in the group with L-arg in microsphere after 24 h. No significant differences in prothrombin time, activated partial thromboplastin time, thrombin time, and fibrinogen among the groups were indicated. Images revealed that apoptosis in the vascular wall was less in the group injected with targeted microspheres with L-arg than in the other two groups at 1 and 8 d postsurgery. Meanwhile, cell proliferation was considerably excessive in the group injected with L-arg wrapped in targeted microspheres. Therefore, these novel microspheres could decrease the formation of thrombus in the early stages and in the subsequent periods of thrombosis. The microspheres can also enhance the vitality of impaired endothelial cells and reduce cell apoptosis.

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Section: Methodsmentioning

confidence: 99%

Novel microspheres reduce the formation of deep venous thrombosis and repair the vascular wall in a rat model

Dai

et al. 2017

Blood Coagulation &Amp; Fibrinolysis

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“…In order to confirm the effect of oral administration of Okinawa mozuku on thrombus formation, FeCl3induced arterial thrombosis model was used. FeCl3induced thrombosis model has been well used as the experimental arterial thrombosis model (21)(22)(23). In this model FeCl3, an oxidizing agent, induces denudation of endothelial cells and exposes the subendothelium such as collagen.…”

Section: Discussionmentioning

confidence: 99%

Antithrombotic Effect of Oral Administration of Mozuku (<i>Cladosiphon okamuranus</i>, Brown Seaweed) Extract in Rat

Yasuzawa

Mima

Ueshima

2019

J Nutr Sci Vitaminol

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Dysfunction of vascular endothelial cells causes the risk of thrombosis. Aim of this study is to evaluate the antithrombotic effect of Okinawa mozuku (brown seaweed, Cladosiphon okamuranus) extract by using cultured vascular endothelial cells and rat carotid arterial thrombosis model induced by ferric chloride (FeCl3). The cell line (TKM-33) established from human umbilical vein endothelial cells were cultured with or without Okinawa mozuku extract. After incubation for 24 h, the conditioned medium was collected to evaluate urokinase-type plasminogen activator (u-PA) activity. Next, rats were fed with water or water containing 5% of Okinawa mozuku extract for 8 wk. After 8 wk of treatments, the rats were provided for the carotid arterial thrombosis model, and fibrinolytic factor and coagulation factor in blood were measured. Okinawa mozuku extract significantly augmented u-PA activity in the conditioned medium. The decrease of carotid artery blood flow induced by 40% FeCl3 injury in rats fed with Okinawa mozuku extract was less than that in control rats. Thus, oral administration of Okinawa mozuku extract prevented thrombus formation in this model. Oral administration of Okinawa mozuku extract significantly increased u-PA activity in euglobulin fraction, compared with control group. On the other hand, platelet aggregation activity, activated partial thromboplastin time, and active PAI-1 level in plasma exhibited no significant differences between control and Okinawa mozuku groups. These results indicate that oral administration of Okinawa mozuku enhances fibrinolytic activity in plasma and prevents thrombus formation which is induced by injury of vascular endothelial cells.

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“…ClC‐3 can inhibit the specific endoplasmic reticulum calcium‐ATPase inhibitor thapsigargin (TG)‐induced Pheochromocytoma‐derived cell line, PC12), mainly morphological changes (including cytoplasmic contraction, nuclear chromatin, condensation and the formation of apoptotic bodies), DNA ladder, and activation of caspase‐3 in PC12 cells (Zhang et al, ; Zhu et al, ). ClC‐3 regulates H 2 O 2 ‐induced apoptosis via mitochondrial pathway in basilar artery smooth muscle cells BASMCs (Qin et al, ). B‐cell lymphoma‐2 (Bcl‐2) and Bcl‐2 associated X protein (Bax), members of the Bcl‐2 family of proteins, are antiapoptotic and proapoptotic factors, respectively (Ciardiello and Tortora, ; Kim et al, ).…”

Section: Discussionmentioning

confidence: 99%

Aggravated intestinal apoptosis by ClC‐3 deletion is lethal to mice endotoxemia

Huang

et al. 2018

Cell Biology International

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Our previous study found that ClC-3 chloride channel functioned differently in the vascular and intestinal inflammation, the loss of ClC-3 reduced vascular inflammation but exacerbated intestinal inflammation. To furtherly clarify the role of ClC-3 chloride channels in systemic inflammation, we used LPS-induced endotoxemia model to investigate the response of wild-type and ClC-3 knockout mice to systemic inflammation. The results showed that in the LPS-induced endotoxemia model, the mortality of mice with ClC-3 deletion was significantly higher than that of wild-type mice. The liver and lung inflammations in mice with ClC-3 deletion were significantly less than those in wild-type mice, and the levels of TNF-α and MIP-2 in serum were lower than those of wild-type mice. However, intestinal inflammatory cytokines contents and intestinal permeability were higher than wild-type mice. After transfection of THP-1 cells with ClC-3 siRNA, the contents of TNF-α and IL-8 in LPS-induced cell supernatants were significantly decreased. Further experiments revealed that the level of Bax and Cleaved Caspase 3 in intestinal tissue of mice with ClC-3 deletion was significantly increased, while the level of Bcl2 did not change, which indicated that the intestinal apoptosis was increased after LPS-induced mice intestinal integrity destruction. Therefore, the regulation of intestinal tissue integrity by ClC-3 is crucial for maintaining LPS-induced survival in mice with endotoxemia.

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Hydrogen sulfide attenuates ferric chloride-induced arterial thrombosis in rats

Cited by 13 publications

References 38 publications

Novel microspheres reduce the formation of deep venous thrombosis and repair the vascular wall in a rat model

Novel microspheres reduce the formation of deep venous thrombosis and repair the vascular wall in a rat model

Antithrombotic Effect of Oral Administration of Mozuku (<i>Cladosiphon okamuranus</i>, Brown Seaweed) Extract in Rat

Aggravated intestinal apoptosis by ClC‐3 deletion is lethal to mice endotoxemia

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