Pyrroloquinoline quinone (PQQ), as a well-known redox enzyme cofactor, PQQ can protect NS/PCs against glutamate toxicity associated with ROS-mediated mitochondrial pathway,

Pyrroloquinoline quinone（PQQ）预处理显示了其在保护NS/PCs免受谷氨酸诱导的凋亡/坏死中的显著效果。PQQ的神经保护作用与细胞内活性氧（ROS）产生的减少、谷胱甘肽（GSH）水平的增加以及caspase-3活性的降低有关。此外，PQQ预处理还显著提高了暴露于谷氨酸的NS/PCs中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx）的活性[1]。

Pyrroloquinoline quinone(PQQ)，一种存在于多种人类食物中的天然抗氧化剂，在Balb/C小鼠的肝纤维化模型中显示出强大的抗纤维化和清除ROS活性。PQQ的抗氧化作用通过调节肝脏纤维化过程中多个步骤发挥作用，包括慢性肝损伤、肝脏炎症、肝星状细胞的激活以及细胞外基质的产生。PQQ还能在体内外抑制活化的HSCs中RACK1的上调。PQQ对于抑制小鼠的氧化应激和肝脏纤维化具有显著效果[2]。

Healthy male Balb/C mice of 4–6 week were used to induce liver fibrosis and isolate primary HSCs.?The animals were obtained from SLAC Laboratory Animal Corp in SPF microbiological status.?All mice were maintained at 25°C with a 12 h dark/light cycle and completely randomly grouped.?For thioacetamide (TAA)-induced liver fibrosis, which has been shown to be closely resemble the panlobular and parenchymal fibrosis that is found in most human chronic liver disease , TAA was given by intraperitoneal injection ?at 200 mg/kg body weight 3 times each week for 8 weeks.?For bile duct ligation (BDL)-induced liver fibrosis, BDL was performed according to previous report , and mice were sacrificed 2 weeks later.?Administration of PQQ started on the second day when TAA was firstly given or BDL was performed, and PQQ was given at the dose of 0.3 mg/kg or 1 mg/kg by gastrogavage administration daily before mice were sacrificed.?Silymarin (150 mg/kg) was used as the positive control by gastrogavage administration daily.?Total number of 405 mice were used.?Mice were sacrificed by cervical dislocation under anesthesia[2].