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Rev. Assoc. Med. Bras. (1992, Impr.) ; 68(8): 1011-1016, Aug. 2022. tab, graf
Article in English | LILACS-Express | LILACS | ID: biblio-1406628

ABSTRACT

SUMMARY OBJECTIVE: Heart attack is one of the most common causes of sudden death in adults. Therefore, early detection of heart attack and investigation of potential new biomarkers are of great importance. We investigated whether perilipin-5 is a potential biomarker by examining changes in perilipin-5 serum levels along with high-sensitivity cardiac troponin I during a heart attack. METHODS: The subjects were divided into two groups: (1) control group and (2) patients with heart attack, with 150 people in each group. High-sensitivity cardiac troponin I, perilipin-5, total oxidant status, malondialdehyde, reduced glutathione, and superoxide dismutase levels in serum samples were measured. In addition, perilipin-5 mRNA expressions and protein levels were analyzed. RESULTS: There was no overall statistical difference between the demographic characteristics of the groups. However, high-density lipoprotein, creatine kinase, Creatine kinase myocardial band, aspartate amino transferase, lactate dehydrogenase, and calcium levels were higher in the heart attack group compared to the control group. We found that the high-sensitivity cardiac troponin I and perilipin-5 levels increased in the patients with heart attack (p<0.0001) compared to control. Although there was an insignificant increase in malondialdehyde levels in the heart attack group (p>0.05), there was a 35.9% increase in total oxidant status levels and a 33.5 and 24.1% decrease in glutathione and superoxide dismutase levels, respectively (p<0.01), compared to control. Perilipin-5 mRNA and protein levels in heart attack patients increased by 48.2 and 23.6%, respectively, compared to the control group (p<0.01). CONCLUSION: Our results showed that perilipin-5 together with high-sensitivity cardiac troponin I could be a promising biomarker in heart attack.

2.
Medical Journal of Chinese People's Liberation Army ; (12): 1045-1050, 2017.
Article in Chinese | WPRIM | ID: wpr-694055

ABSTRACT

Objective To investigate the effects and mechanisms of perilipin-5 (Plin5) on the apoptosis of mouse cardiac microvascular endothelial cells induced by high fat and high glucose.Methods The mouse cardiac microvascular endothelial cells (MCMECs) cultured with high glucose medium were respectively given 0,100,300 and 500μmol/L palmitic acid for 24 hours.In order to explore the effects and mechanisms of Plin5 on MCMECs injuries induced by high fat and high glucose,MCMECs exposed to 300μmol/L palmitic acid for 24 hours were divided into control group,Scra siRNA group and Plin5 siRNA group.The control group was only treated with transfection reagent,the Scra siRNA group was given treatment of transfection reagent and garbled RNA,the Plin5 siRNA group was given treatment of transfection reagent and Plin5 specific siRNA.In order to further confirm the specific mechanism of Plin5 in high fat/glucose inducing MCMECs injury,MCMECs in Plin5 siRNA group were divided into vehicle group and N-acetyl cysteine (NAC) group,and given the same intervention of high fat.The apoptotic rate was detected by flow cytometry,qRT-PCR and Western blotting were respectively used to detect the mRNA and protein expression of Plin5,and the intracellular reactive oxygen species (ROS) level was tested by DHE staining and ELISA kit.Results The apoptotic rate of MCMECs was increased in a fat concentration-dependent manner (P<0.05).Compared with 0μmol/L palmitic acid group,the intracellular ROS content and the expression of Plin5 increased significantly in 300μmol/L palmitic acid group (P<0.05).Compared with the control group and the Scra siRNA group,the intracellular ROS content and apoptotic rate increased significantly in Plin5 siRNA group under the action of 300μmol/L palmitic acid (P<0.05).Compared with the vehicle group,the intracellular ROS content and apoptotic rate decreased remarkably in NAC group (P<0.05).Conclusion With inhibition of oxidative stress,Plin5 may reduce the apoptosis of MCMECs induced by high fat and high glucose.

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