Laboratory of Functional Morphology, Graduate School of Human Health Sciences, Tokyo Metropolitan University, Tokyo 116-8551, Japan.
Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan 250062, Shandong Province, China.
World J Gastroenterol. 2020 Mar 28;26(12):1286-1297. doi: 10.3748/wjg.v26.i12.1286.
(TCL) is a shrub that usually grows in arid or semiarid desert areas and saline-alkali fields. It is a traditional Chinese herbal medicine with hepatoprotective, antioxidant, antibacterial, and antitumor activities.
To investigate the possible protective effects of TCL against liver injury induced by chronic ethanol intake.
C57BL/6J male mice were fed a Lieber-DeCarli lipid diet containing alcohol and received (by gavage) a water-alcohol extract (80%) of TCL (100 and 200 mg/kg BW) or distilled water for 4 wk. After euthanasia, liver tissues were observed histologically with hematoxylin and eosin staining and Oil red O staining, and the levels of alanine aminotransferase, aspartate transaminase, hepatic lipids, reactive oxygen species, malondialdehyde, and superoxide dismutase were measured. In addition, expression of the NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome and downstream proinflammatory cytokines were determined.
Compared with the ethanol group, mice in the TCL-treated group (200 mg/kg) had significantly lower serum levels of alanine aminotransferase (mean, 34.1 IU/L 45.3 IU/L, < 0.01) and aspartate transaminase (mean, 89.6 IU/L 115.7 IU/L, < 0.01), as well as marked reduction of hepatic tissue reactive oxygen species (decreased by 27.5%, < 0.01) and malondialdehyde (decreased by 76.6%, < 0.01) levels, with a significant increase of superoxide dismutase (Increased by 73.2%, < 0.01). Expression of the NLRP3 inflammasome and its downstream cytokines [interleukin (IL)-1β, tumor necrosis factor-α, and IL-6], and recruitment of natural killer T cells to the liver, were reduced in the TCL-treated incubation with a Lieber-DeCaril ethanol lipid diet group.
These findings suggest that a TCL extract (200 mg/kg) protects against chronic ethanol-induced liver injury, probably by inhibiting the NLRP3-caspase-1-IL-1β signaling pathway and suppressing oxidative stress.
（TCL）是一种灌木，通常生长在干旱或半干旱沙漠地区和盐碱地。它是一种传统的中草药，具有保肝、抗氧化、抗菌和抗肿瘤作用。
研究 TCL 对慢性乙醇摄入引起的肝损伤的可能保护作用。
C57BL/6J 雄性小鼠给予含酒精的 Lieber-DeCarli 脂质饮食，并通过灌胃给予 TCL（100 和 200mg/kg BW）水-醇提取物或蒸馏水 4 周。安乐死后，用苏木精-伊红染色和油红 O 染色观察肝组织的组织学变化，测定丙氨酸氨基转移酶、天冬氨酸氨基转移酶、肝脂质、活性氧、丙二醛和超氧化物歧化酶的水平。此外，还测定了 NOD 样受体家族、含吡喃结构域蛋白 3（NLRP3）炎性小体和下游促炎细胞因子的表达。
与乙醇组相比，TCL 治疗组（200mg/kg）小鼠血清丙氨酸氨基转移酶（均值 34.1IU/L vs 45.3IU/L，<0.01）和天冬氨酸氨基转移酶（均值 89.6IU/L vs 115.7IU/L，<0.01）水平明显降低，肝组织活性氧（减少 27.5%，<0.01）和丙二醛（减少 76.6%，<0.01）水平明显降低，超氧化物歧化酶（增加 73.2%，<0.01）水平明显升高。TCL 治疗组 NLRP3 炎性小体及其下游细胞因子[白细胞介素（IL）-1β、肿瘤坏死因子-α和 IL-6]表达以及自然杀伤 T 细胞向肝脏的募集减少。
这些发现表明，TCL 提取物（200mg/kg）可预防慢性乙醇诱导的肝损伤，可能通过抑制 NLRP3-半胱天冬酶-1-IL-1β 信号通路和抑制氧化应激。
