Department of Ultrasound, The First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China.
Department of Geriatrics, The First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China.
World J Gastroenterol. 2017 Dec 21;23(47):8334-8344. doi: 10.3748/wjg.v23.i47.8334.
To investigate whether morin can reduce hepatic fibrosis by activating the NF-E2-related factor 2 (Nrf2) signaling pathway.
Twenty male Sprague-Dawley rats were randomly divided into four groups: control group, morin group, carbon tetrachloride (CCl) group, and morin + CCl group. Rats in both the CCl and morin + CCl groups were injected intraperitoneally with CCl at a dose of 2 mL/kg twice a week. Rats in both the morin and morin + CCl groups were treated orally with morin at a dose of 50 mg/kg twice a week. Control rats were treated with vehicle only twice a week. At the end-point of the 8 wk of the experimental period, serum AST, ALT, and ALP were measured, and the liver specimens were obtained for pathological assessment. Real-time PCR and Western blot methods were used to analyze the expression of α-smooth muscle actin (α-SMA), collagen I, collagen III, Nrf2, heme oxygenase (HO-1), and quinone oxidoreductase 1 (NQO1) using frozen liver specimens.
Morin-treated rats in the morin + CCl group had less hyperplasia of fiber tissue, minimal inflammatory cells, and less body weight loss with favorable liver enzyme measurements compared to rats treated with CCl only. Additionally, morin-treated rats had significantly lower mRNA and protein expression of α-SMA, collagen I, and collagen III, but significantly higher mRNA and protein expression of Nrf2, HO-1, and NQO1 compared to rats treated with CCl only ( < 0.05).
Morin could play a protective role by inducing the expression of Nrf2 and its downstream antioxidant factors (HO-1 and NQO1) and reducing the expression of α-SMA, collagen I, and collagen III in CCl-induced liver fibrosis rats.
研究桑色素是否可以通过激活核因子 E2 相关因子 2（Nrf2）信号通路来减少肝纤维化。
将 20 只雄性 Sprague-Dawley 大鼠随机分为四组：对照组、桑色素组、四氯化碳（CCl）组和桑色素+CCl 组。CCl 组和桑色素+CCl 组大鼠每周两次腹腔注射 CCl4，剂量为 2 mL/kg。桑色素组和桑色素+CCl 组大鼠每周两次口服桑色素，剂量为 50 mg/kg。对照组大鼠每周两次给予载体。在实验 8 周结束时，测量血清天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）和碱性磷酸酶（ALP），并获取肝组织标本进行病理评估。使用冷冻肝组织标本，通过实时 PCR 和 Western blot 方法分析α-平滑肌肌动蛋白（α-SMA）、I 型胶原、III 型胶原、Nrf2、血红素加氧酶（HO-1）和醌氧化还原酶 1（NQO1）的表达。
与仅用 CCl 处理的大鼠相比，用桑色素+CCl 处理的大鼠纤维组织增生较少，炎症细胞最少，体重减轻较少，肝酶测量结果较好。此外，与仅用 CCl 处理的大鼠相比，用桑色素处理的大鼠 α-SMA、I 型胶原和 III 型胶原的 mRNA 和蛋白表达明显降低，但 Nrf2、HO-1 和 NQO1 的 mRNA 和蛋白表达明显升高（<0.05）。
桑色素可能通过诱导 Nrf2 及其下游抗氧化因子（HO-1 和 NQO1）的表达，减少 CCl 诱导的肝纤维化大鼠中 α-SMA、I 型胶原和 III 型胶原的表达，发挥保护作用。
