Effect of Bevacizumab on traumatic penumbra brain edema in rats at different time points.

IF 3.6 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Li Ai, Chen Xin, Muhammad Usman, Yu Zhu, Hong Lu
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Abstract

Traumatic penumbra (TP) is a secondary injury area located around the core area of traumatic brain injury after brain trauma, and is an important factor affecting the outcome of traumatic brain injury (TBI). The main pathological change caused by TP is brain edema, including (cellular brain edema and vascular brain edema). The formation and development of brain edema in the TP area are closely related to the blood-brain barrier (BBB) and vascular endothelial growth factor (VEGF). VEGF is a vascular permeability factor that can promote angiogenesis and increase BBB permeability, and there is a debate on the pros and cons of its role in early TBI. Therefore, in the early stage of TBI, when using the VEGF inhibitor bevacizumab to treat TP area brain edema, the timing of bevacizumab administration is particularly important, and there are currently no relevant literature reports. This article explores the treatment time window and optimal treatment time point of bevacizumab in the treatment of cerebral edema in the TP area by administering the same dose of bevacizumab at different time points after brain injury in rats. The results showed that there was traumatic brain edema in TP area, BBB structure and function were damaged, VEGF expression and angiogenesis were increased. Compared with TBI + NS Group, after Bevacizumab treatment, brain edema in TP area was alleviated, BBB structure and function were improved, VEGF expression and angiogenesis were decreased in each treatment group, and the effect of TBI + Bevacizumab 1 h group was the most significant. Bevacizumab can be used as a targeted therapy for traumatic brain edema. The therapeutic time window of bevacizumab for traumatic brain edema is within 12 hours after TBI, and 1 h is the optimal therapeutic time point.

贝伐单抗对不同时间点大鼠创伤性半影脑水肿的影响
创伤性半影(Traumatic penumbra,TP)是位于脑外伤后创伤性脑损伤核心区域周围的继发性损伤区,是影响创伤性脑损伤(TBI)预后的重要因素。TP 引起的主要病理变化是脑水肿,包括(细胞性脑水肿和血管性脑水肿)。TP 区域脑水肿的形成和发展与血脑屏障(BBB)和血管内皮生长因子(VEGF)密切相关。血管内皮生长因子是一种血管通透性因子,可促进血管生成并增加 BBB 的通透性,关于其在早期 TBI 中作用的利弊存在争议。因此,在 TBI 早期使用血管内皮生长因子抑制剂贝伐单抗治疗 TP 区脑水肿时,贝伐单抗的给药时机尤为重要,目前尚无相关文献报道。本文通过在大鼠脑损伤后的不同时间点给予相同剂量的贝伐珠单抗,探讨贝伐珠单抗治疗TP区脑水肿的治疗时间窗和最佳治疗时间点。结果显示,TP区存在创伤性脑水肿,BBB结构和功能受损,VEGF表达和血管生成增加。与TBI+NS组相比,贝伐单抗治疗后,各治疗组TP区脑水肿减轻,BBB结构和功能改善,VEGF表达和血管生成减少,其中TBI+贝伐单抗1 h组效果最显著。贝伐单抗可作为创伤性脑水肿的靶向治疗药物。贝伐珠单抗治疗创伤性脑水肿的时间窗为创伤性脑损伤后12小时内,1小时是最佳治疗时间点。
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来源期刊
Tissue Barriers
Tissue Barriers MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
6.60
自引率
6.50%
发文量
25
期刊介绍: Tissue Barriers is the first international interdisciplinary journal that focuses on the architecture, biological roles and regulation of tissue barriers and intercellular junctions. We publish high quality peer-reviewed articles that cover a wide range of topics including structure and functions of the diverse and complex tissue barriers that occur across tissue and cell types, including the molecular composition and dynamics of polarized cell junctions and cell-cell interactions during normal homeostasis, injury and disease state. Tissue barrier formation in regenerative medicine and restoration of tissue and organ function is also of interest. Tissue Barriers publishes several categories of articles including: Original Research Papers, Short Communications, Technical Papers, Reviews, Perspectives and Commentaries, Hypothesis and Meeting Reports. Reviews and Perspectives/Commentaries will typically be invited. We also anticipate to publish special issues that are devoted to rapidly developing or controversial areas of research. Suggestions for topics are welcome. Tissue Barriers objectives: Promote interdisciplinary awareness and collaboration between researchers working with epithelial, epidermal and endothelial barriers and to build a broad and cohesive worldwide community of scientists interesting in this exciting field. Comprehend the enormous complexity of tissue barriers and map cross-talks and interactions between their different cellular and non-cellular components. Highlight the roles of tissue barrier dysfunctions in human diseases. Promote understanding and strategies for restoration of tissue barrier formation and function in regenerative medicine. Accelerate a search for pharmacological enhancers of tissue barriers as potential therapeutic agents. Understand and optimize drug delivery across epithelial and endothelial barriers.
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