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Endogenous Ligands; Hypertension; Doca-Salt Delivery; Dyslipidemia

Introduction

The mice that had received an OA-NO2 pretreatment had less liver damage and less hepatic lipid accumulation. Additionally, the expressions of gp91phox and p47phox dropped concurrently with the liver TBARS [1]. These results demonstrated that the antihyperlipidemic properties of OA-NO2 had a protective impact on liver damage caused by DOCA-salt delivery [2]. The most prevalent cardiovascular illness is hypertension, and it is expected that prevalence will rise across the board, particularly in emerging nations. Researchers are interested in the metabolic anomalies, particularly faulty lipid metabolism, in hypertension patients because of their close relationship [3]. The significant link between Dyslipidemia and hypertension is becoming more and clearer. Many hypertension patients have metabolic problems such as hypertriglyceridemia, hypercholesterolemia, and insulin resistance [4]. The greatest rates of morbidity and death among patients with cardiovascular disease are caused by hypertension and Dyslipidemia, which are significant risk factors for the condition. As a result, several investigations have been devoted to creating therapeutic medicines for hypertension and the lipid metabolism that it is associated with [5]. There are several traditional animal models for the study of hypertension [6]. Animal model of hypertension caused by deoxycorticosterone acetate salt model has been frequently used to research hypertension and the organ damage caused by hypertension. In the past, DOCAsalt hypertensive rats were shown to have rising levels of both circulation and membrane lipids before the onset of hypertension [7].

Discussion

In the meanwhile, DOCA-salt hypertensive mice showed altered levels of membrane phospholipids, phospholipid distribution, and fatty acid saturation [8]. The modifications in the lipid content of the membrane may modify membrane activity over time, affecting the control of blood pressure as well as the function of the heart, liver, and kidney organs [9]. The nitro alkene and nitrooleic acid derivatives of nitrated free fatty acids, in particular, are endogenous compounds with enticing signalling qualities. There are nitro alkenes. Animals we bought male C57BL/6 mice from Shandong University's Animal Center. Standard rat chow was used to feed all animals, and a 12-hour light/dark cycle was maintained [10]. All mice also had full access to water. All mouse-using methods were carried out in compliance with the rules and recommendations of the Provincial Hospital Affiliated to Shandong University's Ethics Committee. Materials two regioisomers of OA-NO2, 9- and 10-nitrooleic acids, are created in vivo by nitrating oleic acid in almost equal amounts. Both substances were bought from Cayman Chemical and utilised as a combination of their isomers after being dissolved in dimethyl sulfoxide. Animals used as sham operators served as controls. Following surgery, animals were given a normal salt diet for three weeks and drinking water containing 1% sodium chloride. Once a week, metabolic cages were used to measure body weight, urine volume, food intake, and water intake.

Conclusion

After the tests were complete, the animals were fasted for an entire night before blood was drawn by cutting a tiny cut in the tail with a razor blade. The mechanism of the hyperlipidaemia in DOCAsalt hypertensive animals was distinct from that of the obese Zucker rats. Hernandez discovered that, in contrast to control rats, DOCAsalt hypertensive rats had higher plasma levels of triglycerides and cholesterol as well as higher glucose, glycogen, and triglyceride levels and decreased citrate synthase and beta-hydroxyacyl-CoA dehydrogenase activities in the soleus muscle. These findings suggested that the hyperlipidaemia of the DOCA-salt hypertensive animals was caused by changes in metabolic enzymes.

Acknowledgement

None

Conflict of Interest

None

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