Zoology Department, Faculty of Science, Cairo University, Giza 12613, Egypt.
Int J Biol Macromol. 2020 Dec 1;164:1565-1574. doi: 10.1016/j.ijbiomac.2020.07.212. Epub 2020 Jul 29.
The study aimed to investigate the potential attenuation effect of chitosan in liver ischemia/reperfusion injury (I/R), and its relevant protective mechanisms. Chitosan (200 mg/kg) has been administered orally for 30 days, later animals underwent liver 45 min ischemia and reperfusion for 60 min. Following treatment with chitosan, the levels of serum aminotransferases and lactate dehydrogenase were significantly reduced. Similarly, hepatic (GSH, SOD, CAT, GST and GPx) were enhanced, and the level of tissue malondialdehyde (MDA) was decreased. In addition, inflammatory cytokinesis (TNF-α and TGF-β) have recorded a significant decrease in their mRNA expression and protein levels using qPCR and ELISA respectively. Marked reduction of apoptosis has been indicated by the elevation in BCL2, and decreasing in BAX, Caspace-3 and Cytochrome-c expression levels, which furthermore confirmed by DNA fragmentation assay. The enhancement of the previous parameters resulted in a marked improvement in the liver architectures after chitosan administration. In conclusion, chitosan has proved its efficiency as an anti-inflammatory and antioxidant agent through its inhibitory effect of cytokines and reducing ROS respectively. In addition, chitosan could modulate the changes in histological structure and alleviate apoptosis induced by liver I/R, which recommend it as an efficient agent for protection against liver I/R injury.
本研究旨在探讨壳聚糖对肝脏缺血再灌注损伤（I/R）的潜在衰减作用及其相关保护机制。壳聚糖（200mg/kg）已口服给药 30 天，随后动物经历 45 分钟肝脏缺血和 60 分钟再灌注。用壳聚糖治疗后，血清转氨酶和乳酸脱氢酶水平显著降低。同样，肝组织（GSH、SOD、CAT、GST 和 GPx）水平升高，组织丙二醛（MDA）水平降低。此外，使用 qPCR 和 ELISA 分别检测到炎性细胞因子（TNF-α 和 TGF-β）的 mRNA 表达和蛋白水平显著降低。通过 DNA 片段化测定进一步证实，BCL2 水平升高，BAX、 Caspace-3 和 Cytochrome-c 表达水平降低，表明细胞凋亡明显减少。这些参数的增强导致壳聚糖给药后肝脏结构明显改善。总之，壳聚糖通过抑制细胞因子和减少 ROS 分别作为一种抗炎和抗氧化剂证明了其功效。此外，壳聚糖可以调节组织学结构的变化，并减轻肝脏 I/R 诱导的细胞凋亡，这表明它是一种有效的肝脏 I/R 损伤保护剂。
