Guangxi Medical University, Nanning, China.
Biol Pharm Bull. 2012;35(9):1574-80. doi: 10.1248/bpb.b12-00494.
This study was designed to investigate the protective effects of the polysaccharide isolated from Tarphochlamys affinis (PTA) against CCl4-induced hepatotoxicity in rats. Liver injury was induced in rats by the administration of CCl4 twice a week for 2 weeks. During the experiment, the model group received CCl4 only; the treatment groups received various drugs plus CCl4, whereas the normal control group received an equal volume of saline. Compared with the CCl4 group, PTA significantly decreased the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) in the serum and increased the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) in the liver. Moreover, the content of hepatic malondialdehyde (MDA) was reduced. Histological findings also confirmed the anti-hepatotoxic characterisation. In addition, PTA significantly inhibited the proinflammatory mediators, such as prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and myeloperoxidase (MPO). Further investigation showed that the inhibitory effect of PTA on the pro-inflammatory cytokines was associated with the down-regulation of nuclear factor-kappa B (NF-κB). In brief, our results show that the protective effect of PTA against CCl4-induced hepatic injury may rely on its ability to reduce oxidative stress and suppress inflammatory responses.
本研究旨在探讨从 Tarphochlamys affinis(PTA)中分离得到的多糖对 CCl4 诱导的大鼠肝损伤的保护作用。通过每周两次给予 CCl4 2 周诱导大鼠肝损伤。实验过程中,模型组仅给予 CCl4;治疗组给予不同药物加 CCl4,而正常对照组给予等量生理盐水。与 CCl4 组相比,PTA 显著降低了血清中天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)和碱性磷酸酶(ALP)的活性,同时增加了肝中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)的活性。此外,肝组织丙二醛(MDA)含量降低。组织学发现也证实了其抗肝毒性作用。此外,PTA 还显著抑制了促炎介质,如前列腺素 E2(PGE2)、诱导型一氧化氮合酶(iNOS)、环氧化酶-2(COX-2)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和髓过氧化物酶(MPO)。进一步研究表明,PTA 对促炎细胞因子的抑制作用与核因子-κB(NF-κB)的下调有关。总之,我们的研究结果表明,PTA 对 CCl4 诱导的肝损伤的保护作用可能与其降低氧化应激和抑制炎症反应的能力有关。