Background: Stroke, primarily known as ischemic stroke, is a leading cause of mortality and disability worldwide. Reperfusion after the ischemia stroke resolves is necessary for maintaining the health of brain tissues; however, it also induces inflammation and oxidative stress, resulting in brain injury. This study aimed to investigate the role of circ0001679 in the pathology of I/R (Ischemia/Reperfusion)-induced brain injury and explore its therapeutic potential for I/R injury. Methods: The Oxygen-Glucose Deprivation/Re-oxygenation (OGD/R) model was employed in primary mouse astrocytes, and the Middle Cerebral Artery Occlusion (MCAO) model was established in mice to mimic ischemia-reperfusion-induced injury. Si-circ0001679, anti-miR- 216, and TLR4 ORF-clone were transfected either in cells or mice to study the molecular mechanisms during I/R-induced injury. Inflammation and oxidative stress were monitored after treatment. Results: Upregulated gene expression of circ0001679 was noticed in both OGD/R-treated primary mouse astrocytes and MCAO-induced mouse brain tissue. Silencing circ0001679 reduced cellular damage, inflammation, and oxidative stress induced by OGD/R treatment. Knocking down of circ0001679 alone with either miR-216 inhibition or TLR4 overexpression increased the inflammation response and oxidative stress compared to circ0001679 silencing only. Moreover, inhibition of circ0001679 attenuated brain injury in MCAO-treated mice via reduced infarction, neuronal damage, apoptosis, inflammation, and oxidative stress. Conclusion: This study unveiled a novel regulatory axis of circ0001679-miR-216-TLR4 in I/Rinduced brain injury. Targeting circ0001679 may represent a promising therapeutic strategy for I/R-induced brain injury. result: Upregulated gene expression of circ0001679 was noticed in both OGD/R-treated primary mouse astrocytes and MCAO-induced mouse brain tissue. Silencing circ0001679 reduced cellular damage, inflammation, and oxidative stress induced by OGD/R treatment. Knocking down of circ0001679 alone with either miR-216 inhibition or TLR4 overexpression increased the inflammation response and oxidative stress compared to circ0001679 silencing only. Moreover, inhibition of circ0001679 attenuated brain injury in MCAO-treated mice via reduced infarction, neuronal damage, apoptosis, inflammation, and oxidative stress.

Chenrui Zhang

Liaoyu Li

Feng Wang

Hailong Du

Xiaoliang Wang

Xiaoyu Gu

Xinlei Liu

Haie Han

Jianliang Wu

Jianping Sun

Current Neurovascular Research

当前的神经血管研究为发表科学严谨的研究提供了一个跨平台，这些研究解决了神经科学中神经元和血管起源的疾病机制。该杂志作为一个国际论坛，出版新颖和原创作品以及及时的神经科学研究文章、细胞发育障碍、可塑性和退化学科的全长/迷你评论，弥合了基础科学研究和临床发现之间的差距。当前的神经血管研究强调阐明疾病机制，包括细胞和分子，这可能会影响神经元和血管疾病的独特治疗策略的发展。

Current Neurovascular Research is an interdisciplinary platform dedicated to publishing scientifically rigorous research that explores the mechanisms of neuron and vascular-related diseases in neuroscience. As an international forum, the journal publishes novel and original research findings, as well as timely articles, full-length and mini-reviews in the fields of neuroscience, cellular developmental disorders, plasticity, and degeneration, aiming to bridge the gap between basic scientific research and clinical discoveries. Current Neurovascular Research emphasizes elucidating disease mechanisms, including cellular and molecular studies, which may advance the development of unique therapeutic strategies for neuron and vascular diseases.

《Current Neurovascular Research》是一个跨学科的平台，致力于发表科学严谨的研究，探讨神经科学中神经元和血管相关疾病的机制。作为一个国际论坛，该杂志发布新颖且原创的研究成果，以及及时的神经科学研究文章、细胞发育障碍、可塑性和退化领域的全长和迷你评论，旨在弥合基础科学研究与临床发现之间的差距。《Current Neurovascular Research》强调阐明疾病机制，包括细胞和分子层面的研究，这些研究可能会推动针对神经元和血管疾病的独特治疗策略的发展。

Category	Quartile
医学	4
医学, 临床神经病学	4
医学, 神经科学	4

Inhibition of Circ0001679 Alleviates Ischemia/Reperfusion-induced Brain Injury via miR-216/TLR4 Regulatory Axis

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