PDF(Pubmed)
Abstract：
UNASSIGNED: Non-alcoholic fatty liver disease (NAFLD) is a chronic steatohepatitis disorder. If left untreated, it can progress to hepatocellular carcinoma. Several studies have shown that saroglitazar, a PPARα/γ dual agonist, and curcumin (the principal constituent of turmeric) may be effective in the treatment of NAFLD. This research aimed to study the pharmacological mechanism of these compounds in rats with NAFLD.
UNASSIGNED: NAFLD was induced in male Wistar rats (aged 6-8 weeks) by feeding them a high-fat diet (HFD) for 6 weeks. Subsequently, the rats were divided into four groups, with Group 1 continuing on HFD, while groups 2, 3, and 4 received HFD supplemented with saroglitazar, curcumin, and both saroglitazar and curcumin, respectively. We evaluated the expression of Nrf2, ERK1/2, NOX1,2,4, antioxidant enzymes, PPARα, γ, and genes regulating lipid metabolism in the liver. Histopathology of liver tissue was also examined. Furthermore, we analyzed serum levels of lipid profiles and hepatic enzymes.
UNASSIGNED: Rats with NAFLD that received treatment involving saroglitazar and curcumin showed a significant decrease in the expression of ERK1/2, SREBP1, PPARγ, pro-inflammatory cytokines, NOXs, and ROS levels. Additionally, the levels of Nrf2, PPARα, and antioxidant enzymes showed a significant increase. The serum levels of lipid profiles and hepatic enzymes also decreased significantly after drug treatment.
UNASSIGNED: Our results confirm that both saroglitazar and curcumin ameliorate NAFLD by regulating the Nrf2 and ERK1/2 signaling pathways. These findings suggest that curcumin could serve as a suitable substitute for saroglitazar, although they appear to have a synergistic effect.
UNASSIGNED: NAFLD was induced in male Wistar rats (aged 6-8 weeks) by feeding them a high-fat diet (HFD) for 6 weeks. Subsequently, the rats were divided into four groups, with Group 1 continuing on HFD, while groups 2, 3, and 4 received HFD supplemented with saroglitazar, curcumin, and both saroglitazar and curcumin, respectively. We evaluated the expression of Nrf2, ERK1/2, NOX1,2,4, antioxidant enzymes, PPARα, γ, and genes regulating lipid metabolism in the liver. Histopathology of liver tissue was also examined. Furthermore, we analyzed serum levels of lipid profiles and hepatic enzymes.
UNASSIGNED: Rats with NAFLD that received treatment involving saroglitazar and curcumin showed a significant decrease in the expression of ERK1/2, SREBP1, PPARγ, pro-inflammatory cytokines, NOXs, and ROS levels. Additionally, the levels of Nrf2, PPARα, and antioxidant enzymes showed a significant increase. The serum levels of lipid profiles and hepatic enzymes also decreased significantly after drug treatment.
UNASSIGNED: Our results confirm that both saroglitazar and curcumin ameliorate NAFLD by regulating the Nrf2 and ERK1/2 signaling pathways. These findings suggest that curcumin could serve as a suitable substitute for saroglitazar, although they appear to have a synergistic effect.
摘要：
■非酒精性脂肪性肝病（NAFLD）是一种慢性脂肪性肝炎。如果不及时治疗，它可以进展为肝细胞癌。一些研究表明saroglitazar,PPARα/γ双激动剂，姜黄素（姜黄的主要成分）可能对NAFLD的治疗有效。本研究旨在研究这些化合物对NAFLD大鼠的药理机制。
■在雄性Wistar大鼠（6-8周龄）中通过喂食高脂饮食（HFD）6周来诱导NAFLD。随后，大鼠被分成四组,第1组继续HFD，而第2、3和4组接受补充了saroglitazar的HFD，姜黄素,还有saroglitazar和姜黄素,分别。我们评估了Nrf2，ERK1/2，NOX1，2，4，抗氧化酶的表达，PPARα,γ,和调节肝脏脂质代谢的基因。还检查了肝组织的组织病理学。此外，我们分析了血脂谱和肝酶的血清水平。
■接受包括saroglitazar和姜黄素的治疗的NAFLD大鼠显示ERK1/2，SREBP1，PPARγ的表达显着降低，促炎细胞因子，NOX,和ROS水平。此外,Nrf2、PPARα、和抗氧化酶表现出显著的增加。药物治疗后，血脂谱和肝酶的血清水平也显着降低。
■我们的结果证实，saroglitazar和姜黄素通过调节Nrf2和ERK1/2信号通路改善NAFLD。这些发现表明，姜黄素可以作为saroglitazar的合适替代品，尽管它们似乎有协同作用。
■在雄性Wistar大鼠（6-8周龄）中通过喂食高脂饮食（HFD）6周来诱导NAFLD。随后，大鼠被分成四组,第1组继续HFD，而第2、3和4组接受补充了saroglitazar的HFD，姜黄素,还有saroglitazar和姜黄素,分别。我们评估了Nrf2，ERK1/2，NOX1，2，4，抗氧化酶的表达，PPARα,γ,和调节肝脏脂质代谢的基因。还检查了肝组织的组织病理学。此外，我们分析了血脂谱和肝酶的血清水平。
■接受包括saroglitazar和姜黄素的治疗的NAFLD大鼠显示ERK1/2，SREBP1，PPARγ的表达显着降低，促炎细胞因子，NOX,和ROS水平。此外,Nrf2、PPARα、和抗氧化酶表现出显著的增加。药物治疗后，血脂谱和肝酶的血清水平也显着降低。
■我们的结果证实，saroglitazar和姜黄素通过调节Nrf2和ERK1/2信号通路改善NAFLD。这些发现表明，姜黄素可以作为saroglitazar的合适替代品，尽管它们似乎有协同作用。
