Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.
Division of General Surgery, Department of Surgery, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City, Taiwan.
Mediators Inflamm. 2019 Jan 27;2019:6848943. doi: 10.1155/2019/6848943. eCollection 2019.
Neurological deficits following neurosurgical procedures are inevitable; however, there are still no effective clinical treatments. Earlier reports revealed that collagen-glycosaminoglycan (CG) matrix implantation promotes angiogenesis, neurogenesis, and functional recovery following surgical brain injury (SBI). The present study was conducted to further examine the potential neuroprotective effects of collagen-glycosaminoglycan (CG) matrix implantation following neurosurgery.
CG implantation was performed in the lesion cavity created by surgical trauma. The Sprague-Dawley rat model of SBI was used as established in the previous study by the author. The rats were divided into three groups as follows: (1) sham (SHAM), (2) surgery-induced lesion cavity (L), and (3) CG matrix implantation following surgery-induced lesion cavity (L+CG). Proinflammatory (tumor necrosis factor-alpha (TNF-), interleukin-6 (IL-6), and NF-B (nuclear factor kappa-light-chain-enhancer of activated B cells)) and anti-inflammatory (IL-10 and granulocyte-macrophage colony-stimulating factor (GMCSF)) cytokine expression was evaluated by enzyme-linked immunosorbent assays. Microglial activation was evaluated by immunohistochemistry, and the neuroprotective effect of CG matrix implantation was evaluated by an immunohistochemical study of microglia ED-1 and IBA-1 (activated microglia) and myeloperoxidase (MPO) and by the analysis of IL-6, IL-10, TNF-, NF-B, and GMCSF cytokine levels. Apoptosis was also assessed using a TUNEL assay.
The results showed that CG matrix implantation following surgically induced lesions significantly decreased the density of ED-1, IBA-1, and MPO (activated microglia). The tissue concentration of proinflammatory cytokines, such as TNF-, IL-6, and NF-B was significantly decreased. Conversely, the anti-inflammatory cytokines GMCSF and IL-10 were significantly increased.
Implantation of the CG matrix following SBI has neuroprotective effects, including the suppression of microglial activation and the production of inflammatory-related cytokines.
神经外科手术后出现神经功能缺损是不可避免的,但目前仍没有有效的临床治疗方法。早期的报道表明,胶原-糖胺聚糖(CG)基质植入可促进手术性脑损伤(SBI)后的血管生成、神经发生和功能恢复。本研究旨在进一步研究 CG 基质植入对神经外科手术后的潜在神经保护作用。
在手术性创伤造成的损伤腔中植入 CG。作者之前使用的 SBI 大鼠模型为 Sprague-Dawley 大鼠模型。将大鼠分为三组:(1)假手术(SHAM),(2)手术致损伤腔(L),和(3)手术致损伤腔后 CG 基质植入(L+CG)。通过酶联免疫吸附试验评估促炎(肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和核因子 κB(NF-κB))和抗炎(IL-10 和粒细胞-巨噬细胞集落刺激因子(GMCSF))细胞因子的表达。通过免疫组织化学评估小胶质细胞的激活,通过对小胶质细胞 ED-1 和 IBA-1(激活的小胶质细胞)和髓过氧化物酶(MPO)的免疫组织化学研究以及对 IL-6、IL-10、TNF-α、NF-κB 和 GMCSF 细胞因子水平的分析来评估 CG 基质植入的神经保护作用。还使用 TUNEL 测定法评估了细胞凋亡。
结果表明,手术致损伤后 CG 基质植入显著降低了 ED-1、IBA-1 和 MPO(激活的小胶质细胞)的密度。促炎细胞因子 TNF-α、IL-6 和 NF-κB 的组织浓度显著降低。相反,抗炎细胞因子 GMCSF 和 IL-10 显著增加。
SBI 后 CG 基质的植入具有神经保护作用,包括抑制小胶质细胞激活和产生与炎症相关的细胞因子。