Lycium barbarum polysaccharides improve CCl4-induced liver fibrosis, inflammatory response and TLRs/NF-κB signaling pathway expression in wistar rats
Lycium barbarum polysaccharides improve CCl4-induced liver fibrosis, inflammatory response and TLRs/NF-κB signaling pathway expression in wistar rats
复制标题
枸杞多糖改善 CCl4 诱导的 Wistar 大鼠肝纤维化、炎症反应和 TLRs/NF-kB 信号通路表达。
DOI：
10.1016/j.lfs.2017.11.047
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发表时间：
2018-01-01
期刊：
影响因子：
6.1
通讯作者：
Huang, Kehe
中科院分区：
文献类型：
--
作者：
Gan, Fang;Liu, Qing;Huang, Kehe
枸杞多糖具有抗氧化、抗炎、抗癌等多种生物学和药理学功能。本研究旨在探讨枸杞多糖是否能减轻四氯化碳（CCl 4）诱导的肝纤维化及其可能的信号通路机制。将50只雄性Wistar大鼠随机分为对照组、CCl 4组和CCl 4 + LBPs组（分别为400、800和1600 mg/kg），每组10只。实验结束时，每组每只Wistar大鼠用于血液和组织收集。结果表明，CCl 4可诱导肝纤维化，表现为肝组织病理学损伤、α-平滑肌肌动蛋白表达、天冬氨酸转氨酶活性、碱性磷酸酶活性和丙氨酸转氨酶活性增加。LBP补充减轻CCl 4诱导的肝纤维化，如通过逆转上述参数所证明的。此外，CCl 4处理诱导了氧化损伤，增加了肿瘤坏死因子-α、单核细胞趋化蛋白-1和白细胞介素-1 β的mRNA水平，上调了Toll样受体4（TLR 4）、TLR 2、髓样分化因子88、核因子-κ B（NF-κ B）和p-p65的蛋白表达。补充LBPs可通过逆转上述指标，减轻CCl 4诱导的氧化损伤、炎症反应和TLRs/NF-κ B信号通路的表达。提示枸杞多糖可能通过抑制TLRs/NF-κ B信号通路的表达，减轻四氯化碳诱导的大鼠肝纤维化。
Lycium barbarum polysaccharides (LBPs) have multiple biological and pharmacological functions, including antioxidant, anti-inflammatory and anticancer activities. This research was conducted to evaluate whether LBPs could alleviate carbon tetrachloride (CCl4)-induced liver fibrosis and the underlying signaling pathway mechanism. Fifty male wistar rats were randomly allocated to five groups (n = 10): control, CCl4 and CCl4 with 400, 800 or 1600 mg/kg LBPs, respectively. Each wistar rat from each group was used for blood and tissue collections at the end of experiment. The results showed that CCl4 induced liver fibrosis as demonstrated by increasing histopathological damage, alpha-smooth muscle actin expression, aspartate transaminase activities, alkaline phosphatase activities and alanine aminotransferase activities. LBPs supplementation alleviated CCl4-induced liver fibrosis as demonstrated by reversing the above parameters. In addition, CCl4 treatment induced the oxidative injury, increased the mRNA levels of tumor necrosis factor-alpha, monocyte chemoattractant protein-1 and interleukin-1 beta, and up-regulated the protein expressions of toll-like receptor 4 (TLR4), TLR2, myeloid differentiation factor 88, nuclear factor-kappa B (NF-kappa B) and p-p65. LBPs supplementation alleviated CCl4-induced oxidative injury, inflammatory response and TLRs/NF-kappa B signaling pathway expression by reversing the above some parameters. These results suggest that the alleviating effects of LBPs on CCl4-induced liver fibrosis in wistar rats may be through inhibiting the TLRs/NF-kappa B signaling pathway expression.