The Shapiro Family Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, 714 Tiverton Ave., Los Angeles, CA 90095, USA.
Section of Oral Biology, UCLA School of Dentistry, 714 Tiverton Avenue, Los Angeles, CA 90095, USA.
Int J Mol Sci. 2024 Jun 1;25(11):6126. doi: 10.3390/ijms25116126.
GV1001, an anticancer vaccine, exhibits other biological functions, including anti-inflammatory and antioxidant activity. It also suppresses the development of ligature-induced periodontitis in mice. (), a major human oral bacterium implicated in the development of periodontitis, is associated with various systemic disorders, such as atherosclerosis and Alzheimer's disease (AD). This study aimed to explore the protective effects of GV1001 against -induced periodontal disease, atherosclerosis, and AD-like conditions in ()-deficient mice. GV1001 effectively mitigated the development of -induced periodontal disease, atherosclerosis, and AD-like conditions by counteracting -induced local and systemic inflammation, partly by inhibiting the accumulation of DNA aggregates, lipopolysaccharides (LPS), and gingipains in the gingival tissue, arterial wall, and brain. GV1001 attenuated the development of atherosclerosis by inhibiting vascular inflammation, lipid deposition in the arterial wall, endothelial to mesenchymal cell transition (EndMT), the expression of Cluster of Differentiation 47 (CD47) from arterial smooth muscle cells, and the formation of foam cells in mice with -induced periodontal disease. GV1001 also suppressed the accumulation of AD biomarkers in the brains of mice with periodontal disease. Overall, these findings suggest that GV1001 holds promise as a preventive agent in the development of atherosclerosis and AD-like conditions associated with periodontal disease.
GV1001 是一种抗癌疫苗,具有其他生物学功能,包括抗炎和抗氧化活性。它还能抑制结扎诱导的牙周炎在小鼠中的发展。牙龈卟啉单胞菌()是一种主要的人类口腔细菌,与牙周炎等多种系统性疾病有关,如动脉粥样硬化和阿尔茨海默病(AD)。本研究旨在探讨 GV1001 对()缺陷小鼠牙周炎、动脉粥样硬化和 AD 样疾病的保护作用。GV1001 通过对抗 - 诱导的局部和全身炎症,有效减轻了 - 诱导的牙周病、动脉粥样硬化和 AD 样疾病的发展,部分通过抑制龈组织、动脉壁和大脑中 DNA 聚集物、脂多糖(LPS)和牙龈蛋白酶的积累。GV1001 通过抑制血管炎症、动脉壁脂质沉积、内皮到间充质细胞转化(EndMT)、动脉平滑肌细胞中 Cluster of Differentiation 47(CD47)的表达以及牙周炎小鼠中泡沫细胞的形成,抑制了动脉粥样硬化的发展。GV1001 还抑制了牙周病小鼠大脑中 AD 生物标志物的积累。总之,这些发现表明 GV1001 有望成为预防牙周炎相关动脉粥样硬化和 AD 样疾病发展的一种药物。
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