Zhang Huapeng, Chen Huayong, Wang Wei, Zhang Baoze, Yu Lingzhi
a Department of Pain Management , Jinan Central Hospital Affiliated to Shandong University , Jinan , Shandong , China.
b Department of Anesthesiology , Yidu Central Hospital of Weifang , Weifang , Shandong , China.
J Recept Signal Transduct Res. 2018 Oct-Dec;38(5-6):448-454. doi: 10.1080/10799893.2019.1585451.
To investigate the role of S100B, oxidative stress and the apoptosis signaling pathways in the sevoflurane induced neuroprotective effect on stroke. The brain injury, molecular and cellular damage, and functional recovery were investigated upon ischemic brain injury followed by sevoflurane treatment. Longa rodent stroke scales was used to quantify neurological deficits. TTC staining was used to measure infarct volume of brain tissue. Absolute brain water content was measured by wet/dry weight method. The neuronal morphological change was assessed by H and E staining. The spatial learning and memory ability were measured by water maze test. Serum proteins including S100B, GSH-PX, SOD, Bcl-2, Bax, Caspase-3 were measured by ELISA. The level of NOS and NO in serum was determined by colorimetric method. Compared with control, the serum proteins including S100B, Bax, NO, Caspase-3, and NOS activity in cerebral infarction rats increased significantly while SOD, GSH-PX, and Bcl-2 decreased significantly. Diabetic mellitus complicated with cerebral infarction rats showed more dramatic increase for S100B, Bax, NO, Caspase-3, and NOS activity and dramatic decrease for SOD, GSH-PX, and Bcl-2. Interestingly, sevoflurane reduced the changes significantly. The S100B level positively correlated with brain damage, NO, Bax, caspase-3, and NOS activity but negatively correlated with SOD, Bax, and GSH-PX. Brain damage in sevoflurane groups decreased while behavior outcomes including Longa neurologic score, learning, and memory increased significantly. The neuroprotective effect of sevoflurane is associated with defense mechanisms against free radical-induced oxidative stress and inhibition of apoptosis. S100B protein correlated with oxidative stress and the apoptosis signaling pathways.
探讨S100B、氧化应激及凋亡信号通路在七氟醚诱导的脑缺血神经保护作用中的作用。在缺血性脑损伤后给予七氟醚治疗，观察脑损伤、分子和细胞损伤以及功能恢复情况。采用Longa啮齿动物卒中量表量化神经功能缺损。用TTC染色法测量脑组织梗死体积。采用湿/干重法测量脑组织绝对含水量。通过苏木精-伊红（H&E）染色评估神经元形态变化。用水迷宫试验测量空间学习和记忆能力。采用酶联免疫吸附测定法（ELISA）检测血清中包括S100B、谷胱甘肽过氧化物酶（GSH-PX）、超氧化物歧化酶（SOD）、B细胞淋巴瘤-2（Bcl-2）、Bax、半胱天冬酶-3（Caspase-3）等蛋白质。采用比色法测定血清中一氧化氮合酶（NOS）和一氧化氮（NO）水平。与对照组相比，脑梗死大鼠血清中S100B、Bax、NO、Caspase-3及NOS活性显著升高，而SOD、GSH-PX及Bcl-2显著降低。糖尿病合并脑梗死大鼠S100B、Bax、NO、Caspase-3及NOS活性升高更为显著，SOD、GSH-PX及Bcl-2降低更为显著。有趣的是，七氟醚能显著减轻这些变化。S100B水平与脑损伤、NO、Bax、Caspase-3及NOS活性呈正相关，与SOD、Bcl-2及GSH-PX呈负相关。七氟醚组脑损伤减轻，同时行为学指标包括Longa神经功能评分、学习和记忆能力显著提高。七氟醚的神经保护作用与抗自由基诱导的氧化应激防御机制及抑制细胞凋亡有关。S100B蛋白与氧化应激及凋亡信号通路相关。
