Anti-inflammatory cytokine interleukin-10 (IL-10) plays a crucial role in controlling the resolution of inflammation. In this study, we aimed to assess gene expression and the level of IL-10 in the hippocampus and prefrontal cortex of rats, after a single injection of neurotoxicant trimethyltin chloride (TMT). It was shown that 4 weeks after the treatment with TMT, the level of IL-10 in the prefrontal cortex, but not in the hippocampus of TMT-treated rats, was increased. However, expression level of IL-10 mRNA was upregulated both in the hippocampus and in the prefrontal cortex 3 weeks after the injection. Concomitantly, within the same post-treatment period, the expression level of the cyclooxygenase-2 was upregulated in both brain structures, indicating the induction of neuroinflammation. Considering that TMT leads to the death of neurons mainly in the hippocampus, we assume that in contrast to the prefrontal cortex, the level of anti-inflammatory cytokine IL-10 in the hippocampus is not sufficiently increased to prevent the damaging effect of the neurotoxicant. Therefore, an exogenous increase in the level of IL-10 may be useful for the survival of neurons in conditions of neurotoxic damage to the hippocampus.

抗炎细胞因子白细胞介素 10 (IL-10) 在控制炎症消退方面起着至关重要的作用。在这项研究中，我们旨在评估单次注射神经毒剂三甲基氯化锡 (TMT) 后大鼠海马和前额叶皮层中的基因表达和 IL-10 水平。结果表明，在用 TMT 治疗 4 周后，前额叶皮层中的 IL-10 水平升高，但在 TMT 治疗的大鼠的海马中没有升高。然而，注射后 3 周，海马和前额叶皮层中 IL-10 mRNA 的表达水平上调。同时，在相同的治疗后时期内，环氧合酶-2 的表达水平在两个大脑结构中均上调，表明诱导了神经炎症。考虑到 TMT 主要导致海马神经元死亡，我们假设与前额叶皮层相比，海马中抗炎细胞因子 IL-10 的水平没有充分增加以防止神经毒物的破坏作用。因此，IL-10 水平的外源性增加可能有助于神经元在海马神经毒性损伤条件下的存活。