石竹根水醇提取物的保肝作用西南。慢性应用血管紧张素II引起的过度肝损伤

Zimri Aziel Alvarado-Ojeda, Alejandro Coset Mejia, Gerardo Arrellin Rosas, J. Jimenez-Ferrer, A. Zamilpa, Celeste Trejo-Moreno, Gabriela Castro Martínez, Marisol Méndez Martínez, Jacquelynne Cervantes Torres, Juan Carlos Báez Reyes, G. Fragoso, Gabriela Rosas Salgado
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引用次数: 1

摘要

肝损伤的特征是肝内脂质积累、促氧化/促炎状态、坏死和纤维化。鉴于该疾病的多因素条件和复杂性,以及氧化应激和炎症在其发展中的作用,植物药物是控制其的良好选择。慢性给药血管紧张素II (ANGII) (0.01 μg/kg/d,每日腹腔注射)诱导雄性C57BL/6J小鼠肝损伤。采用以肉桂酸含量为标准的石蒜根(se - ha)水酒精提取物(11 mg/kg/d,口服)来控制小鼠肝损伤的发生率。11周后处死小鼠,取脂肪组织、血清和肝脏。测定肝细胞因子和甘油三酯(TG)浓度,并记录任何组织病理学变化。与此同时,与未治疗的对照组相比,ANGII治疗增加了血清TG浓度(62.8%)、丙氨酸转氨酶(GPT/ALT)水平(206%)、TG积累(82.7%)、肝肿大(32.1%)、炎症(通过TNFα(70%)、IL-1β(103%)、IL-6(92%)和TGFβ(203%)水平以及炎症细胞募集来测量)和纤维化。rSe-HA阻止了这些增加,维持了与对照组相似的所有参数评估值。总的来说,我们的研究结果支持逆转录酶-血凝素对NAFLD和NASH的肝保护作用,这两种疾病通常是更严重的病理的门户。
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Hepatoprotective effect of hydroalcoholic extract from root of Sechium edule (Jacq.) Sw. over hepatic injury induced by chronic application of angiotensin II
Liver damage is characterized by lipid accumulation in the liver, a prooxidant/proinflammatory state, necrosis, and fibrosis. Given the multifactorial conditions and complexity of the disease and the contribution of oxidative stress and inflammation in its development, phytomedicine is a good option for its control. Liver damage was induced in male C57BL/6J mice by chronic administration of angiotensin II (ANGII) (0.01 μg/kg/day, administered daily intraperitoneally). A hydroalcoholic extract of Sechium edule root (rSe-HA), standardized for its cinnamic acid content, was used to control the incidence of liver damage in mice (11 mg/kg/day of rSe-HA, administered orally). After 11 weeks, the mice were sacrificed and adipose tissue, serum, and liver were obtained. Hepatic cytokine and triglyceride (TG) concentrations were determined, and any histopathological changes were recorded. Meanwhile, ANGII treatment increased serum TG concentration (62.8%), alanine aminotransaminase (GPT/ALT) levels (206%), as well as TG accumulation (82.7%), hepatomegaly (32.1%), inflammation (measured by TNFα (70%), IL-1β (103%), IL-6 (92%), and TGFβ (203%) levels, along with inflammatory cell recruitment), and fibrosis with respect to untreated controls. rSe-HA prevented these increases, maintaining all parameters evaluated at values similar to those of the control group. Overall, our results support the hepatoprotective effects of rSe-HA against NAFLD and NASH, which are often the gateway to more severe pathologies.
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