Zhu Qingmao, Jiang Dianming, Tang Li, Meng Chunyang, Hu Yunjiu
Department of Orthopedics, First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China.
Department of Life Sciences, Chongqing Medical University, Chongqing 400016, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2015 Apr;31(4):437-42.
To explore the neuroprotective effects of preconditioning with low-dose lipopolysaccharide (LPS) in rats after spinal cord injury and its possible mechanism.
Forty-eight female SD rats were randomly divided into four groups as follows: empty virus (EV), LPS combined with empty virus (LPS-EV), nuclear factor erythroid 2-related factor 2 (Nrf2) interference virus (NIV), and LPS combined with Nrf2 interference virus (LPS-NIV) (n=12 per group). The model of traumatic spinal cord injury (TSCI) was established by the modified Allen's method. Hind limb motor function of the rats was assessed by the Basso, Beattie and Bresnahan (BBB) score 3 days after the operation. The injured spinal cord tissues were harvested after the operation. The pathological changes of spinal cord were observed by HE staining. The Nissl body and neuron survival index were assessed by Nissl staining. The expressions of Nrf2, NF-κB and associated pro-inflammatory cytokines (IL-1β, TNF-α) were detected by immunohistochemical staining and Western blotting.
NIV group showed descended Nrf2 protein expression and ascended NF-κB, IL-1β, TNF-α protein levels compared with EV group, and no significant difference from LPS-NIV group. The Nrf2 protein expression of LPS-EV group increased significantly compared with EV group and LPS-NIV group, and NF-κB, TNF-α and IL-1β protein expression decreased significantly at the same time. Compared with those of EV group and LPS-NIV group, the neuron survival index of LPS-EV group was improved. The morphological change of LPS-EV group was also obviously alleviated. The BBB score had no statistical significance among these groups.
Low-dose LPS preconditioning had neuroprotective effects on spinal cord injury. This protective effect was mediated by activating the Nrf2 to down-regulate expressions of NF-κB and pro-inflammatory cytokines and alleviate inflammatory response.
探讨低剂量脂多糖（LPS）预处理对大鼠脊髓损伤后的神经保护作用及其可能机制。
48只雌性SD大鼠随机分为四组：空病毒组（EV）、LPS联合空病毒组（LPS-EV）、核因子红细胞2相关因子2（Nrf2）干扰病毒组（NIV）、LPS联合Nrf2干扰病毒组（LPS-NIV）（每组n = 12）。采用改良的Allen法建立创伤性脊髓损伤（TSCI）模型。术后3天通过Basso、Beattie和Bresnahan（BBB）评分评估大鼠后肢运动功能。术后取损伤的脊髓组织。通过HE染色观察脊髓的病理变化。通过Nissl染色评估Nissl体和神经元存活指数。通过免疫组织化学染色和蛋白质印迹法检测Nrf2、NF-κB及相关促炎细胞因子（IL-1β、TNF-α）的表达。
与EV组相比，NIV组Nrf2蛋白表达下降，NF-κB、IL-1β、TNF-α蛋白水平升高，与LPS-NIV组无显著差异。与EV组和LPS-NIV组相比，LPS-EV组Nrf2蛋白表达显著增加，同时NF-κB、TNF-α和IL-1β蛋白表达显著降低。与EV组和LPS-NIV组相比，LPS-EV组的神经元存活指数得到改善。LPS-EV组的形态学变化也明显减轻。这些组之间的BBB评分无统计学意义。
低剂量LPS预处理对脊髓损伤具有神经保护作用。这种保护作用是通过激活Nrf2来下调NF-κB和促炎细胞因子的表达并减轻炎症反应介导的。
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