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Arterial thrombosis represents the most commonly feared consequence of cardiovascular disease and a leading cause of death globally. Cardiovascular disease, liver, and kidney are closely linked conditions, and disease in one organ can lead to dysfunction in the other.
The current research aims to examine the therapeutic impact of Ech-A on arterial thrombosis induced by FeCl3 complications on liver and kidney function.
Twenty-four rats were assigned into four sham groups (n= 6), and thrombotic model groups were orally administered 2% DMSO, while the other groups were treated with two dosages of Ech-A (1 and 10 mg/kg, body weight). After seven days of administration, the left common carotid arteries of all groups were exposed to 50% ferric chloride for 10 min, except those of the sham group rats exposed to normal saline.
The oral administration of Ech-A caused a significant increase in partial thromboplastin time, prothrombin time, glutathione, catalase, nitric oxide, and glutathione S-transferase. While aspartate aminotransferase, alkaline phosphatase, and alanine aminotransferase activities as well as creatinine, uric acid, urea, and malondialdehyde concentrations were significantly decreased (p< 0.05). The histological examination revealed a definite improvement in the liver and kidney tissues in the Ech-A groups.
The current investigation revealed that arterial thrombosis induced by FeCl3 in rats causes complications in the kidneys and liver. Additionally, it demonstrates the beneficial impact of Ech-A on coagulation parameters and liver and kidney function. Despite this, the current study has few limitations. Firstly, the molecular mechanism regarding the protective effect of Ech-A on liver and kidney complications caused by arterial thrombosis has not been investigated. Secondly, no reference drug has been utilised to compare with Ech-A.
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