To evaluate magnetic resonance (MR) T1 mapping for quantifying brain manganese (Mn) deposition in type C hepatic encephalopathy (CHE) rats and to investigate the mechanism of magnesium sulfate (MgSO₄) therapy. Thirty Sprague–Dawley rats were randomly assigned into normal control group (NC, n = 6) and CHE groups (n = 24). Thioacetamide (TAA) was used for modeling CHE rats. CHE groups were further divided into 4 subgroups: TAA group, MgSO₄ low dose (Mg-L) group, MgSO₄ high dose (Mg-H) group and deionized water (DW) group (n = 6 for each group). TAA, Mg-L, Mg-H and DW groups were received intraperitoneal injections of 250 mg TAA/kg, twice a week for 8 weeks. Mg-L and Mg-H groups were orally received MgSO₄ of 124 and 248 mg/kg daily, respectively, for another 8 weeks (without TAA). MR T1 mapping was performed in NC, TAA, Mg-L, Mg-H and DW groups at various time points. T1 value and Mn content in basal ganglia, hippocampus, cerebral cortex and cerebellum were evaluated. Morris water maze (MWM) and narrow beat test (NBT) were utilized to evaluate rats' learning, memory and motor ability. Contents of interleukin-6 (IL-6), tumor necrosis factor-a (TNF-a) and calcium-binding adaptor 1 protein (Iba1) were evaluated. Reduced T1 values in basal ganglia, hippocampus and cerebral cortex (P < 0.01, P < 0.05 and P < 0.05, respectively); increased Mn content in basal ganglia, hippocampus and cerebral cortex (all P < 0.05); reduced times of head contacting with region of interest (ROI), reduced times of entrance into the target quadrant (both P < 0.05); increased NBT total time (P < 0.05); increased brain contents of IL-6 (P < 0.001), TNF-α (P < 0.01) and over-expression of Iba1 were found in TAA group compared to NC group. After treated by MgSO₄, increased T1 value and reduced Mn content in basal ganglia, hippocampus and cerebral cortex (all P < 0.01); increased times of head contacting with ROI, increased times of entrance into the target quadrant (both P < 0.05); reduced NBT total time (P < 0.01); reduced brain content of IL-6, TNF-α (both P < 0.05) and reduced expression of Iba1 were found. T1 values were negatively correlated with Mn contents in basal ganglia (r = − 0.834, P < 0.01), hippocampus (r = − 0.739, P < 0.05), cortex (r = − 0.801, P < 0.05) and cerebellum (r = − 0.788, P < 0.05). T1 mapping could quantify brain Mn deposition in CHE rats. MgSO₄ could improve cognition and motor ability of CHE rats by reducing brain Mn deposition, alleviating neurological inflammation and achieve the effective therapy for CHE. Mn may participate in the pathogenesis of CHE through neuroinflammation.

评估磁共振 (MR) T1 映射在 C 型肝性脑病 (CHE) 大鼠中量化脑锰 (Mn) 沉积并研究硫酸镁 (MgSO ₄ ) 治疗的机制。将 30 只 Sprague-Dawley 大鼠随机分配到正常对照组（NC，n = 6）和 CHE 组（n = 24）。硫代乙酰胺 (TAA) 用于模拟 CHE 大鼠。CHE组进一步分为4个亚组：TAA组、MgSO ₄低剂量（Mg-L）组、MgSO ₄高剂量（Mg-H）组和去离子水（DW）组（每组n = 6）。TAA、Mg-L、Mg-H 和 DW 组接受 250 mg TAA/kg 的腹腔注射，每周两次，持续 8 周。Mg-L和Mg-H组口服MgSO ₄每天 124 和 248 mg/kg，分别为另外 8 周（不含 TAA）。在不同时间点在 NC、TAA、Mg-L、Mg-H 和 DW 组中进行 MR T1 映射。评价基底节、海马、大脑皮层和小脑的T1值和Mn含量。莫里斯水迷宫（MWM）和窄跳动测试（NBT）被用来评估大鼠的学习、记忆和运动能力。评估了白细胞介素 6 (IL-6)、肿瘤坏死因子-a (TNF-a) 和钙结合接头 1 蛋白 (Iba1) 的含量。基底节、海马和大脑皮层 T1 值降低（分别为P  < 0.01、P  < 0.05 和P  < 0.05）；基底节、海马和大脑皮层 Mn 含量增加（所有P < 0.05); 减少头部接触感兴趣区域（ROI）的次数，减少进入目标象限的次数（均P  < 0.05）；NBT总时间增加（P  < 0.05）； 与NC组相比，TAA组脑内IL-6（P  <0.001）、TNF-α（P <0.01）和Iba1过表达增加。经MgSO ₄处理后，基底节、海马和大脑皮层T1值升高，Mn含量降低（均P  < 0.01）；头部接触 ROI 的次数增加，进入目标象限的次数增加（均P  < 0.05）；减少 NBT 总时间 ( P < 0.01); 发现脑内 IL-6、TNF-α 含量降低（均P  < 0.05）和 Iba1 表达降低。T1 值与基底神经节 (r = - 0.834, P  < 0.01)、海马 (r = - 0.739, P  < 0.05)、皮质 (r = - 0.801, P  < 0.05) 和小脑 (r = − 0.788, P  < 0.05)。T1 映射可以量化 CHE 大鼠的脑锰沉积。MgSO ₄可通过减少脑内锰沉积，减轻神经炎症，提高CHE大鼠的认知和运动能力，实现对CHE的有效治疗。Mn可能通过神经炎症参与CHE的发病机制。