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Effects and Mechanism of Mouse Nerve Growth Factor on Diffuse Brain Injury in Rats with Traumatic Brain Injury Combined with Seawater Drowning

生理盐水 创伤性脑损伤 神经生长因子 医学 水肿 B组 A组 腹腔注射 内分泌学 免疫组织化学 内科学 麻醉 脑水肿 化学 受体 精神科
作者
Zihuan Zeng,Hao Zhang,Jianwu Wu,Liangfeng Wei,Weiqiang Chen,Shousen Wang
出处
期刊:Journal of Biomaterials and Tissue Engineering [American Scientific Publishers]
卷期号:11 (12): 2321-2328 被引量:1
标识
DOI:10.1166/jbt.2021.2832
摘要

To investigate the effect of mouse nerve growth factor (mNGF) on axonal injury after traumatic brain injury (TBI) combined with seawater drowning (SWD) in rats and the possible mechanism, we assigned 78 SD rats by random into sham group (Group A, n = 14), TBI+SWD group (Group B, n = 32), and mNGF group (Group C, n = 32). The compound injury model of rats was established by Marmarou method (450 g×1.5 m) and intratracheal pumping seawater (3 ml/kg). Rats in Group C were subject to intraperitoneal injection of mNGF (3 ug/kg) immediately after injury, and Group A as well as Group B were intraperitoneally injected the same amount of normal saline. Modified neurological severity scores(mNSS) was performed on rats at 12 h, 24 h, 72 h as well as 168 h, respectively after injury. HE staining showed that 24 h after injury, the swelling of nerve cells in Group C was relatively milder and the tissue edema was similar to that in Group B. At 72 h and 168 h after injury, the matrix looseness, cell swelling, and nuclear condensation in Group C were improved in comparison with Group B. (2) Compared with group B, mNSS of group C decreased signally at 72 h and 68 h after injury ( P <0.05). (3) IHC staining showed that the protein expressions of β -APP, NF-L, and AQP4 were decreased in Group C in comparison with Group B at 12 h, 24 h, 72 h and 168 h after injury. (4) Brain water content in Group C was similar to that in Group B ( P >0.05). (5) At 12 h after injury, the expression of TNF- α in Group C was signally lower than that in Group B ( P < 0.05). Our reseache showed that mNGF might play a neuroprotective role by reducing cerebral edema and inflammatory response after TBI+SWD injury in rats, thereby restoring part of the injured axons in TBI+SWD rats.

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