The polysaccharide from Inonotus obliquus protects mice from Toxoplasma gondii-induced liver injury

• Published in: International journal of biological macromolecules Vol. 125; pp. 1 - 8
• Main Authors: Xu, Lu, Sang, Rui, Yu, Yifan, Li, Jinxia, Ge, Bingjie, Zhang, Xuemei
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 15.03.2019
• Subjects: Inonotus obliquus polysaccharide; Liver injury; Nrf2/HO-1; TLRs/NF-κB; Toxoplasma gondii; TLRs/NF-κB; Inonotus obliquus polysaccharide; Toxoplasma gondii; Liver injury; Nrf2/HO-1
• ISSN: 0141-8130; 1879-0003
• DOI: 10.1016/j.ijbiomac.2018.11.114

The study aimed to explore the protective effects and mechanism of Inonotus obliquus polysaccharide (IOP) on liver injury caused by Toxoplasma gondii (T. gondii) infection in mice. The results showed that treatment with IOP significantly decreased the liver coefficient, the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA) and nitric oxide (NO), and increased the contents of antioxidant enzyme superoxide dismutase (SOD) and glutathione (GSH). IOP effectively decreased the expression of serum tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), interferon-γ (IFN-γ) and interluekin-4 (IL-4) in T. gondii-infected mice. In agreement with these observations, IOP also alleviated hepatic pathological damages caused by T. gondii. Furthermore, we found that IOP down-regulated the levels of toll-like receptor 2 (TLR2) and toll-like receptor 4 (TLR4), phosphorylations of nuclear factor-κappaB (NF-κB) p65 and inhibitor kappaBα (IκBα), whereas up-regulated the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). These findings suggest that IOP possesses hepatoprotective effects against T. gondii-induced liver injury in mice, and such protection is at least in part due to its anti-inflammatory effects through inhibiting the TLRs/NF-κB signaling axis and the activation of an antioxidant response by inducing the Nrf2/HO-1 signaling.