大黄素对海人酸致痫小鼠海马神经细胞的保护作用

目的探讨大黄素对海人酸诱导的小鼠癫痫持续状态后海马神经细胞的保护作用。方法 90只ICR雄性小鼠随机分为对照组、癫痫持续状态组、大黄素治疗组(分为100、200和400 mg/kg组),每组18只。采用海人酸建立小鼠癫痫持续状态模型。通过HE染色和TUNEL染色观察大黄素对癫痫鼠海马神经细胞的形态学变化和凋亡情况;比色法测定谷苷胱肽(GSH)和丙二醛(MDA)的含量以及超氧化物歧化酶(SOD)的活力; RT-PCR和Western blot检测海马组织中IL-1β、TNF-α、caspase-3 mRNA和蛋白的表达。结果大黄素(200和400 mg/kg组)可显著减轻癫痫所致的海马神经细胞的损伤和凋亡,提高GSH和SOD的活性,降低MDA的活性(P 0. 05);同时抑制海马中IL-1β、TNF-α及caspase-3mRNA和蛋白的表达量(P 0. 05)。结论大黄素对小鼠癫痫持续状态后海马神经细胞具有抗氧化、抗炎和抗凋亡等神经保护作用,其作用机制可能与提高GSH和SOD的活性,降低MDA的含量,并抑制IL-1β、TNF-α及caspase-3的表达有关。

Protective effect of emodin on hippocampal neural cells in mice with epilepsy induced by kainic acid

Objective To investigate the protective effect of emodin on hippocampal neural cells in mice with epilepsy induced by kainic acid. Methods A total of 90 male ICR mice were randomly divided into control group, status epilepticus (SE) group, and emodin treatment groups (at doses of 100, 200, and 400 mg/kg), with 18 mice in each group. Kainic acid was used to establish a mouse model of SE. HE staining and TUNEL staining were used to observe the effect of emodin on the morphological changes and apoptosis of hippocampal neural cells in mice with epilepsy; colorimetry was used to measure the content of glutathione (GSH) and malondialdehyde (MDA) and the activity of superoxide dismutase (SOD); RT-PCR and Western blot were used to measure the mRNA and protein expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and caspase-3. Results Emodin (200 and 400 mg/kg) significantly alleviated the injury and apoptosis of hippocampal neural cells induced by epilepsy, increased the activities of GSH and SOD, and reduced the activity of MDA (P<0.05). It also reduced the mRNA and protein expression of IL-1β, TNF-α, and caspase-3 in the hippocampus (P<0.05). Conclusions Emodin has antioxidant, anti-inflammatory, and anti-apoptotic effects on hippocampal neural cells in mice after SE, possibly by increasing the activities of GSH and SOD, reducing the content of MDA, and inhibiting the expression of IL-1β, TNF-α, and caspase-3.