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桦褐孔菌多糖可保护小鼠免受弓形虫感染引起的肝损伤。

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

机构信息

Department of Animal Medicine, Agricultural College, Yanbian University, Gongyuan Street, Yanji, Jilin 133002, PR China.

Department of Animal Medicine, Agricultural College, Yanbian University, Gongyuan Street, Yanji, Jilin 133002, PR China.

出版信息

Int J Biol Macromol. 2019 Mar 15;125:1-8. doi: 10.1016/j.ijbiomac.2018.11.114. Epub 2018 Nov 13.

Abstract

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.

摘要

本研究旨在探讨云芝多糖(IOP)对弓形虫(T. gondii)感染小鼠肝损伤的保护作用及其机制。结果表明,IOP 治疗可显著降低肝系数、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、丙二醛(MDA)和一氧化氮(NO)水平,增加抗氧化酶超氧化物歧化酶(SOD)和谷胱甘肽(GSH)的含量。IOP 有效降低了弓形虫感染小鼠血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)、干扰素-γ(IFN-γ)和白细胞介素-4(IL-4)的表达。与这些观察结果一致,IOP 还减轻了弓形虫引起的肝病理损伤。此外,我们发现 IOP 下调了 Toll 样受体 2(TLR2)和 Toll 样受体 4(TLR4)的水平,核因子-κB(NF-κB)p65 和抑制剂 kappaBα(IκBα)的磷酸化水平,而上调了核因子红细胞 2 相关因子 2(Nrf2)和血红素加氧酶-1(HO-1)的表达。这些发现表明,IOP 对弓形虫感染小鼠肝损伤具有保护作用,这种保护至少部分是由于其通过抑制 TLRs/NF-κB 信号通路和诱导 Nrf2/HO-1 信号来发挥抗炎作用。

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