Abstract：
BACKGROUND: Diabetic hepatopathy is a serious complication of poorly controlled diabetes mellitus. An efficient antidiabetic drug which keeps normal liver tissues is not available. The renin-angiotensin system has been reported to be involved in both diabetic state and liver function. Aliskiren is a direct renin inhibitor and a recently antihypertensive drug with poly-pharmacological properties. The aim of the current study is to explore the possible hepatoprotective effects and mechanisms of action of aliskiren against streptozotocin (STZ) induced liver toxicity.
METHODS: Mice were distributed to 3 groups; first: the normal control group, second: the diabetic control group, third: the diabetic group which received aliskiren (25 mg/kg; oral) for 4 weeks. At the end of the treatment period, plasma glucose, insulin, lipid profile, oxidative stress, and liver function tests were evaluated spectrophotometrically. ELISA technique was used to measure the expression levels of TNF-α and adiponectin. Furthermore, a Histopathological examination of liver samples was done.
RESULTS: It was shown that aliskiren treatment ameliorated the STZ-induced oxidative stress and elevated inflammatory biomarkers, hypercholesterolemia, serum aminotransferases and alkaline phosphatase levels in diabetic mice. In addition, hepatocellular necrosis, and fibrosis were improved by aliskiren treatment.
CONCLUSIONS: aliskiren protects against the liver damage caused by STZ-induced diabetes. This can be explained by its ability to block angiotensin-II, and its anti-diabetic, hypocholesterolemic, antioxidant and anti-inflammatory effects. Aliskiren could be a novel therapeutic strategy to prevent liver diseases associated with hypertension and diabetes mellitus.
METHODS: Mice were distributed to 3 groups; first: the normal control group, second: the diabetic control group, third: the diabetic group which received aliskiren (25 mg/kg; oral) for 4 weeks. At the end of the treatment period, plasma glucose, insulin, lipid profile, oxidative stress, and liver function tests were evaluated spectrophotometrically. ELISA technique was used to measure the expression levels of TNF-α and adiponectin. Furthermore, a Histopathological examination of liver samples was done.
RESULTS: It was shown that aliskiren treatment ameliorated the STZ-induced oxidative stress and elevated inflammatory biomarkers, hypercholesterolemia, serum aminotransferases and alkaline phosphatase levels in diabetic mice. In addition, hepatocellular necrosis, and fibrosis were improved by aliskiren treatment.
CONCLUSIONS: aliskiren protects against the liver damage caused by STZ-induced diabetes. This can be explained by its ability to block angiotensin-II, and its anti-diabetic, hypocholesterolemic, antioxidant and anti-inflammatory effects. Aliskiren could be a novel therapeutic strategy to prevent liver diseases associated with hypertension and diabetes mellitus.
摘要：
背景：糖尿病肝病是糖尿病控制不佳的严重并发症。一种有效的抗糖尿病药物，保持正常的肝组织是不可用的。据报道，肾素-血管紧张素系统与糖尿病状态和肝功能有关。阿利吉仑是一种直接的肾素抑制剂，最近是一种具有多药理学特性的抗高血压药物。本研究的目的是探讨阿利吉仑对链脲佐菌素（STZ）诱导的肝毒性的可能的保护作用和作用机制。
方法:小鼠分为3组,第二：糖尿病对照组，第三：接受阿利吉仑（25mg/kg；口服）治疗4周的糖尿病组。在治疗期结束时，血浆葡萄糖，胰岛素，血脂谱,氧化应激，和肝功能检查用分光光度法进行评估。ELISA技术检测TNF-α和脂联素的表达水平。此外，a对肝脏样本进行组织病理学检查。
结果：显示阿利吉仑治疗可改善STZ诱导的氧化应激和炎症生物标志物的升高，高胆固醇血症,糖尿病小鼠血清转氨酶和碱性磷酸酶水平。此外,肝细胞坏死，阿利吉仑治疗可改善纤维化。
结论：阿利吉仑可预防STZ诱导的糖尿病引起的肝损伤。这可以解释为其阻断血管紧张素II的能力，和它的抗糖尿病药，低胆固醇血症，抗氧化和抗炎作用。阿利吉仑可能是预防与高血压和糖尿病相关的肝脏疾病的一种新的治疗策略。
方法:小鼠分为3组,第二：糖尿病对照组，第三：接受阿利吉仑（25mg/kg；口服）治疗4周的糖尿病组。在治疗期结束时，血浆葡萄糖，胰岛素，血脂谱,氧化应激，和肝功能检查用分光光度法进行评估。ELISA技术检测TNF-α和脂联素的表达水平。此外，a对肝脏样本进行组织病理学检查。
结果：显示阿利吉仑治疗可改善STZ诱导的氧化应激和炎症生物标志物的升高，高胆固醇血症,糖尿病小鼠血清转氨酶和碱性磷酸酶水平。此外,肝细胞坏死，阿利吉仑治疗可改善纤维化。
结论：阿利吉仑可预防STZ诱导的糖尿病引起的肝损伤。这可以解释为其阻断血管紧张素II的能力，和它的抗糖尿病药，低胆固醇血症，抗氧化和抗炎作用。阿利吉仑可能是预防与高血压和糖尿病相关的肝脏疾病的一种新的治疗策略。
