| 刘梦佳，
，陆兆丰
，李海荣
，朱义通
，杨家发.高渗冰盐水改善大鼠创伤性脑损伤后半暗带脑水肿[J].神经损伤功能重建,2024,(7):379-384 |
| 高渗冰盐水改善大鼠创伤性脑损伤后半暗带脑水肿 |
| Hypertonic Ice Saline Improve Penumbra Brain Edema after Traumatic Brain Injury in Rats |
| |
| DOI： |
| 中文关键词: 细胞焦亡 高渗冰盐水 水通道蛋白4 NLRP3 |
| 英文关键词: pyroptosis hypertonic ice saline aquaporin 4 NLRP3 |
| 基金项目:河南省医学科技攻
关计划省部共建重
点项目（SBGJ2021
02198) |
|
| 摘要点击次数: 324 |
| 全文下载次数: 382 |
| 中文摘要: |
| 目的：应用高渗冰盐水（hypertonic ice saline，HIS）治疗创伤性脑损伤（traumatic brain injury，TBI）大
鼠以探讨HIS通过调节水通道蛋白4（aquaporin 4，AQP4）和NLRP3炎症小体的表达抑制大鼠半暗带脑水
肿形成和焦亡，并探究HMGB1/NF-κB信号通路调控的分子机制。方法：60只SD大鼠被随机分为假手术
组、对照组和HIS组，每组20只。通过改进的菲尼自由落体法构建TBI模型，假手术组不造成打击。对照
组术后予生理盐水治疗，HIS组术后予HIS治疗。水迷宫试验用于检测大鼠认知能力，脑水肿通过脑组织含
水量检测，Western blot用于检测AQP4、NLRP3、焦亡途径相关蛋白（Caspase-1、GSDMD）、HMGB1/NF-κB
信号通路相关蛋白（HMGB1、NF-κB、p- IκBα）的表达；采用实时荧光定量PCR检测AQP4以及炎症细胞因
子IL-1β和TNF-α的水平。结果：水迷宫试验结果显示与对照组相比，HIS组大鼠逃逸潜伏期缩短（P＜0.05）
和经过原平台象限次数增加（P＜0.05）；Western blot结果显示，与假手术组相比，对照组和HIS组AQP4表
达水平均升高（P＜0.05）；与对照组相比，HIS组AQP4表达下调（P＜0.05）；与对照组相比，HIS组焦亡相关
蛋白NLRP3、Caspase-1、GSDMD表达下调；与假手术组相比，对照组和HIS组炎症因子IL-1β和TNF-α的水
平显著上调（P＜0.05），与对照组相比，HIS组炎症因子水平下调（P＜0.05）；Western blot结果显示HIS能抑
制HMGB1/NF-κB信号通路的激活。结论：创伤性脑损伤能诱导半暗带炎症水平升高和脑水肿及AQP4表
达上调，应用HIS治疗则能改善缓解大鼠创伤性脑损伤后半暗带炎症和脑水肿并降低AQP4表达，其调节
机制涉及抑制焦亡相关蛋白表达和抑制HMGB1/NF-κB信号通路激活。 |
| 英文摘要: |
| To investigate whether hypertonic ice saline (HIS) treatment can inhibit penumbra brain
edema formation and pyroptosis in rats with traumatic brain injury (TBI) by regulating the expression of
aquaporin 4 (AQP4) and NLRP3 inflammasome, and to explore the molecular mechanism involving the
regulation of the HMGB1/NF-κ B signaling pathway. Methods: Sixty Sprague-Dawley rats were randomly
divided into three groups: sham, TBI control, and HIS , with 20 rats in each group. The TBI model was
constructed using a modified Feeney's free-fall method, while the sham group underwent the same procedure
without the impact. Postoperatively, the control group received normal saline treatment, and the HIS group
received HIS treatment. The Morris water maze test was used to assess the cognitive ability of the rats. Brain
edema was measured by determining the water content of brain tissue. Western blot was used to detect the
expression of AQP4, NLRP3, pyroptosis-related proteins (Caspase-1, GSDMD), and HMGB1/NF-κB signaling
pathway-related proteins (HMGB1, NF-κB, p-IκBα). Real-time quantitative PCR was used to measure the levels
of AQP4 and the inflammatory cytokines IL-1β and TNF-α. Results: The water maze test results showed that,
compared with the control group, the escape latency of rats in the HIS group was shortened (P<0.05) and the
number of times they passed through the original platform quadrant increased (P<0.05). Western blot results
showed that, compared with the sham group, AQP4 expression levels in both the control and HIS groups were
increased (P<0.05). However, compared with the control group, AQP4 expression in the HIS group was
significantly down-regulated (P<0.05). Additionally, compared with the control group, the expressions of
pyroptosis-related proteins NLRP3, Caspase-1 and GSDMD were down-regulated in the HIS group.
Furthermore, compared with the sham group, the levels of inflammatory factors IL-1 β and TNF-α were
significantly up-regulated in both the control and HIS groups (P<0.05), while the levels of these inflammatory
factors were significantly down-regulated in the HIS group compared with the control group (P<0.05). Western
blot results also showed that HIS inhibited the activation of the HMGB1/NF-κ B signaling pathway.
Conclusion: TBI can induce an increase in penumbra inflammation, brain edema and up-regulation of AQP4
expression. HIS treatment can significantly alleviate the inflammation and brain edema of the penumbra and reduce the expression of
AQP4 after TBI in rats. The regulatory mechanism involves inhibiting the expression of pyroptosis-related proteins and blocking the
activation of the HMGB1/NF-κB signaling pathway. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|