Titin Andri Wihastuti1, Fitria Nugraha Aini2,3, Cholid Tri Tjahjono4, Yuni Hendrati Sulfia3, Zuhrotus Sholichah3, Teuku Heriansyah5. 1. Department of Basic Science in Nursing, Faculty of Medicine, University of Brawijaya, Malang, East Java, Indonesia. 2. Faculty of Medicine, University of Islam Malang, Malang, East Java, Indonesia. 3. Master Programme of Biomedicine, Faculty of Medicine, Brawijaya University, Malang, East Java, Indonesia. 4. Department of Cardiology and Vascular Medicine, Faculty of Medicine, Brawijaya University, Malang, East Java, Indonesia. 5. Department of Cardiology and Vascular Medicine, Faculty of Medicine, University of Syiah Kuala, Banda Aceh, Aceh, Indonesia.
Abstract
PURPOSE: The aim of this study is to prove that type 2 diabetes mellitus can induce increasing inflammation marker in renal and that the provision of darapladib as Lp-LA2 Inhibitor agents can inhibit inflammation that were measured from the expression of IL-1B and IL-6- type cytokine in renal. This study also discusses the correlation between IL-1B and IL-6- type cytokine expression in renal. METHODS: Thirty Sprague-Dawley (SD) rats were divided into three main groups; those are negative control group (NC), Type 2 Diabetes Mellitus group (T2DM) given high fat diet (HFD) with streptozotocin intraperitoneal injection (35mg/kg BW) and diabetes mellitus + darapladib group (DM + DP). Each group was treated within two serial treatment time: 8 weeks and 16 weeks. Expressions of IL-1B and IL-6- type cytokine in renal were the markers that we measured by immunofluorosense method. RESULTS: The administration of darapladib can significantly decrease the expression of IL-1B- type cytokine (p ANOVA = 0.029, p < 0.005) measured in rats' renal both at weeks 8 and 16 in the T2DM group. The Expression of IL-6- type cytokine also showed a significant difference after treated with darapladib both at weeks 8 and 16 in T2DM group with p-value of ANOVA = 0.033, p < 0.005. The Pearson correlation showed a strong correlation (linear regression value was r2 = 0.743). CONCLUSION: Our results show that atherosclerosis caused by inflammation in renal T2DM SD rats could be inhibited by the administration of darapladib.
PURPOSE: The aim of this study is to prove that type 2 diabetes mellitus can induce increasing inflammation marker in renal and that the provision of darapladib as Lp-LA2 Inhibitor agents can inhibit inflammation that were measured from the expression of IL-1B and IL-6- type cytokine in renal. This study also discusses the correlation between IL-1B and IL-6- type cytokine expression in renal. METHODS: Thirty Sprague-Dawley (SD) rats were divided into three main groups; those are negative control group (NC), Type 2 Diabetes Mellitus group (T2DM) given high fat diet (HFD) with streptozotocin intraperitoneal injection (35mg/kg BW) and diabetes mellitus + darapladib group (DM + DP). Each group was treated within two serial treatment time: 8 weeks and 16 weeks. Expressions of IL-1B and IL-6- type cytokine in renal were the markers that we measured by immunofluorosense method. RESULTS: The administration of darapladib can significantly decrease the expression of IL-1B- type cytokine (p ANOVA = 0.029, p < 0.005) measured in rats' renal both at weeks 8 and 16 in the T2DM group. The Expression of IL-6- type cytokine also showed a significant difference after treated with darapladib both at weeks 8 and 16 in T2DM group with p-value of ANOVA = 0.033, p < 0.005. The Pearson correlation showed a strong correlation (linear regression value was r2 = 0.743). CONCLUSION: Our results show that atherosclerosis caused by inflammation in renal T2DM SD rats could be inhibited by the administration of darapladib.
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