Yao Xie, Leyi Wei, Jiashi Guo, Qingsong Jiang, Yang Xiang, Yan Lin, Huang Xie, Xinru Yin, Xia Gong, Jingyuan Wan
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引用次数: 0
摘要
背景：非酒精性脂肪性肝炎（NASH非酒精性脂肪性肝炎（NASH）是一种与代谢失调相关的疾病，通常以脂质代谢功能障碍和过度炎症反应为特征。目前，还没有获得授权的专门用于治疗 NASH 的药物干预措施。据报道，银杏内酯 C 具有抗炎作用，并能调节脂质代谢。然而，银杏内酯 C 在饮食诱导的 NASH 中的影响和功能尚不清楚：在这项研究中，小鼠通过西式饮食（WD）与不同剂量的银杏内酯 C（5'-单磷酸腺苷（AMP）激活的蛋白激酶（AMPK）抑制剂）或不与化合物 C（5'-单磷酸腺苷（AMP）激活的蛋白激酶（AMPK）抑制剂）进行诱导。通过评估肝损伤、脂肪变性、肝纤维化和 AMPK 表达来评价银杏内酯 C 的作用：结果表明，银杏内酯 C 能明显减轻 WD 诱导小鼠的肝损伤、脂肪变性和纤维化。此外，银杏内酯 C 还能明显改善胰岛素抵抗，减轻肝脏炎症。重要的是，银杏内酯 C 通过激活 AMPK 信号通路发挥保护作用，而抑制 AMPK 则会逆转这种作用：结论：银杏内酯 C 可通过激活 AMPK 信号通路缓解 WD 诱导的小鼠 NASH。
Ginkgolide C attenuated Western diet-induced non-alcoholic fatty liver disease via increasing AMPK activation.
Background: Non-alcoholic steatohepatitis (NASH) is a metabolic dysregulation-related disorder that is generally characterized by lipid metabolism dysfunction and an excessive inflammatory response. Currently, there are no authorized pharmacological interventions specifically designed to manage NASH. It has been reported that Ginkgolide C exhibits anti-inflammatory effects and modulates lipid metabolism. However, the impact and function of Ginkgolide C in diet-induced NASH are unclear.
Methods: In this study, mice were induced by a Western Diet (WD) with different doses of Ginkgolide C with or without Compound C (adenosine 5 '-monophosphate (AMP)-activated protein kinase (AMPK) inhibitor). The effects of Ginkgolide C were evaluated by assessing liver damage, steatosis, fibrosis, and AMPK expression.
Results: The results showed that Ginkgolide C significantly alleviated liver damage, steatosis, and fibrosis in the WD-induced mice. In addition, Ginkgolide C markedly improved insulin resistance and attenuated hepatic inflammation. Importantly, Ginkgolide C exerted protective effects by activating the AMPK signaling pathway, which was reversed by AMPK inhibition.
Conclusion: Ginkgolide C alleviated NASH induced by WD in mice, potentially via activating the AMPK signaling pathway.
期刊介绍：
Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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